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  • 93
    Millipore calbindin d 28k
    The cerebella of HTRA2 KO and NesKO mice appeared grossly normal. ( A–D ) Calbindin <t>D-28K</t> staining of HTRA2 WT ( A ), KO ( B ), NesWT ( C ) and NesKO ( D ) cerebellum did not reveal any differences in Purkinje cell organization in P35 cerebellum ( n = 3). ( E–H ) Cerebellar neuronal populations did not appear altered in HTRA2 KO or NesKO mice compared to WT controls by Nissl staining at P30 ( n = 3). ( I–L ) PLP staining for myelinated axons appeared comparable between HTRA2 KO and WT controls, and NesKO and NesWT controls at P30 ( n = 3). ( M–P ) The cerebellar granule cell layer of P30 WT and HTRA2 KO, and NesKO and NesWT did not appear different upon staining for Pax6 ( n = 3). KO denotes HTRA2 KO, WT denotes HTRA2 WT, nKO denotes NesKO and nWT denotes NesWT. Scale bars: A–P: 500 µm.
    Calbindin D 28k, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 282 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc calbindin
    CD44 expression in neuron-lineage cells during postnatal development. A–C: Double immunostaining of CD44 and <t>calbindin</t> in the cerebellum at P7. D–L: Double immunostaining of CD44 and NeuN at P7 (D–H) and P42 (I–L). H: Negative controle. G L: High magnification of F K. Nucleus was counterstained with TO-PRO-3 (blue). J: Quantitative analysis of the number of CD44-positive neuron-lineage cells by FACS at P3, P7 and P10. *p
    Calbindin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti calbindin
    The transcriptome of cerebellar lobule X is distinct from other lobules, regardless of Npc1 expression. ( A – D ) <t>Calbindin</t> 1 staining of Purkinje neurons in representative sagittal cerebellar sections of a Npc1 +/+ mouse at nine weeks of age ( A ), and Npc1 −/− mice at 4.5 weeks ( B ), seven weeks ( C ), or nine weeks of age ( D ). The Purkinje neuron marker, Calbindin 1, is shown in red and a DAPI (4’,6-diamidino-2-phenylindole) counterstain in blue. Scale bar = 500 µm. ( E ) Principal component analysis of RNA-sequencing data sets from cerebellar lobules III, VI, and X from 4.5 weeks old Npc1 +/+ and Npc1 −/− transgenic mice.
    Anti Calbindin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Cell Signaling Technology Inc antibodies against calbindin antibody
    Neuroanatomical and histological examination of the brain . A. Brain weight. Brain weight analysis was perform in 24 weeks GSK-3α KO (n = 19-10) and WT (n = 14-10) animals. Values are mean (± SEM). *p ≤ 0.05; **p ≤ 0.001. B. Rotarod. GSK-3α KO (n = 13) and WT (n = 11) mice were tested on an accelerating rotarod in 3-day trials. Significant differences between the groups (p.value = 0.013) were found on day1 in the balance and coordination; however no changes were found in motor learning. C-D. Decrease in Purkinje cell density and size in GSK-3α KO mice. C . Purkinje cells image. Immunohistochemistry against <t>Calbindin</t> antibody of WT and GSK-3α KO cerebellum (shown original magnification, ×4 (upper panel) and ×10 (lower panel)). D . Statistical analysis of Purkinje cell density. Average cell density was determined by taking the ratio of the number of Purkinje cells to the length of cerebellar cortex segments. Cell density is significantly decreased in the GSK-3α KO (p
    Antibodies Against Calbindin Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Abcam calbindin
    Immunohistochemical analysis for <t>calbindin</t> expression using TMA technology. Immunohistochemical staining of the TMA representing the four major RCC subtypes along with corresponding tumor-adjacent renal epithelium was performed using a human anti-calbindin-specific
    Calbindin, supplied by Abcam, used in various techniques. Bioz Stars score: 92/100, based on 301 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore calbindin
    Normal postnatal cerebellar development in L7Dpl and wild-type mice. Normal foliation and thickness of the EGL in Tg15 L7Dpl and wild-type mice (P1 in A and B and P8 in G and H ). At P1, no loss of Purkinje cells as determined by <t>Calbindin</t> immunostaining ( C and D ) and regular thickness of the external (eEGL) and inner (iEGL) part of the EGL, as identified by p27 immunostaining, which identifies committed postmitotic EGL neurons, in contrast to the still-proliferating p27-negative eEGL ( E and F ). At P8, no loss of Purkinje cells (Calbindin, I and J ) and a normal EGL, split into proliferating eEGL and postmitotic iEGL ( K and L ); see labels. [Bar = 550 μm ( A and B ), 950μm ( G and H ), and 80 μm ( C - F and I - L ).]
    Calbindin, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 1197 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam calbindin ab108404
    Normal postnatal cerebellar development in L7Dpl and wild-type mice. Normal foliation and thickness of the EGL in Tg15 L7Dpl and wild-type mice (P1 in A and B and P8 in G and H ). At P1, no loss of Purkinje cells as determined by <t>Calbindin</t> immunostaining ( C and D ) and regular thickness of the external (eEGL) and inner (iEGL) part of the EGL, as identified by p27 immunostaining, which identifies committed postmitotic EGL neurons, in contrast to the still-proliferating p27-negative eEGL ( E and F ). At P8, no loss of Purkinje cells (Calbindin, I and J ) and a normal EGL, split into proliferating eEGL and postmitotic iEGL ( K and L ); see labels. [Bar = 550 μm ( A and B ), 950μm ( G and H ), and 80 μm ( C - F and I - L ).]
    Calbindin Ab108404, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Neuromics mouse anti calbindin
    Normal postnatal cerebellar development in L7Dpl and wild-type mice. Normal foliation and thickness of the EGL in Tg15 L7Dpl and wild-type mice (P1 in A and B and P8 in G and H ). At P1, no loss of Purkinje cells as determined by <t>Calbindin</t> immunostaining ( C and D ) and regular thickness of the external (eEGL) and inner (iEGL) part of the EGL, as identified by p27 immunostaining, which identifies committed postmitotic EGL neurons, in contrast to the still-proliferating p27-negative eEGL ( E and F ). At P8, no loss of Purkinje cells (Calbindin, I and J ) and a normal EGL, split into proliferating eEGL and postmitotic iEGL ( K and L ); see labels. [Bar = 550 μm ( A and B ), 950μm ( G and H ), and 80 μm ( C - F and I - L ).]
    Mouse Anti Calbindin, supplied by Neuromics, used in various techniques. Bioz Stars score: 94/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    Abcam calbindin 28
    Histology of explants cultured for six days. Representative images for 3–5 organs in each condition. All sections counterstained with hematoxylin (blue nuclei). A–D. Note lack of cysts in control ( Vehicle ) explants and the progressively greater size (a typical cyst is boxed in each image) and extent of cysts per organs exposed to 470 nM dexamethasone ( Dex )-alone, 100 µM 8-Br-cAMP ( cAMP )-only, or both chemicals. E–H. Brown color indicates immunoreactivity to megalin antibody. Note patchy reactivity of cyst epithelia in organs exposed to 470 nM dexamethasone-alone, 100 µM 8-Br-cAMP-alone or both chemicals. I–L. Uromodulin immunoreactivity (brown); note that cysts are not labeled. M–P. Immunostaining with antibody to <t>calbindin-28.</t> Most cyst epithelia are unreactive (M, O and P) but a small subset of cysts in cAMP-exposed organs were positive and one such is depicted in O′. Q–T. These sections were probed with Dolichos biflorus lectin. Note that the lectin prominently labeled non-dilated tubules between cysts; in addition, the great majority of cysts did not bind the lectin. In (R), an asterisk indicates a rare, labeled cyst. Bar in A–D is 500 µm, and bar for other frames is 50 µm.
    Calbindin 28, supplied by Abcam, used in various techniques. Bioz Stars score: 96/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Abcam rabbit calbindin
    MtDNA loss in astrocytes depletes <t>Calbindin-positive</t> interneurons in cortex, upper neuronal layers. Immunofluorescnece staining of mid-sagittal sections of 7–8 months old mice, brain graph shows sampling site. a Neuronal nuclei (NeuN, green), Calbindin-positive neurons (red) and nucleus (DAPI, blue). b Quantification of NeuN-and Calbindin-positive neurons in somatosensory cortex, cortical layers I and II are boxed. Scale bars: 20 μm. The data are presented as mean and error bars indicate standard deviation. Statistical significance: *** p
    Rabbit Calbindin, supplied by Abcam, used in various techniques. Bioz Stars score: 91/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Swant calbindin cbn
    MtDNA loss in astrocytes depletes <t>Calbindin-positive</t> interneurons in cortex, upper neuronal layers. Immunofluorescnece staining of mid-sagittal sections of 7–8 months old mice, brain graph shows sampling site. a Neuronal nuclei (NeuN, green), Calbindin-positive neurons (red) and nucleus (DAPI, blue). b Quantification of NeuN-and Calbindin-positive neurons in somatosensory cortex, cortical layers I and II are boxed. Scale bars: 20 μm. The data are presented as mean and error bars indicate standard deviation. Statistical significance: *** p
    Calbindin Cbn, supplied by Swant, used in various techniques. Bioz Stars score: 88/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Millipore calbindin d
    Astrocytic IP-10 gene expression in the CNS of BDV-infected rats. Rats were infected as adults (A) or neonates (B to F) and euthanatized 11 days (A), 33 days (C to F), or 75 days (B) later. Following perfusion of rats using either 4% buffered paraformaldehyde (A) or Bouin's fixative (B to F), brains were removed and processed for analysis by ISH. ISH with a 33 P-radiolabeled IP-10 antisense probe was combined with IHC for GFAP as a marker for astrocytes (A, B, D, and F) or <t>Calbindin-D</t> as a marker for Purkinje cells (C and E). Panels A and B depict representative cortical regions. Arrowheads indicate ISH-positive astrocytes, whereas arrows indicate GFAP-negative cells of unknown identity that express IP-10. In panels C and D, parts of the cerebellum from two consecutive sections are shown. Note the string-like distribution of IP-10 signals in the Purkinje cell layer. High-power magnifications of the Purkinje cell layer are shown in panels E and F. Original magnifications were ×20 (C and D), ×80 (B and F), and ×200 (A and E).
    Calbindin D, supplied by Millipore, used in various techniques. Bioz Stars score: 88/100, based on 101 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Boster Bio calbindin
    Dendritic SNPH Intrusion in PCs of Dysmyelinating Shi Mice In Vivo (A–F) Immunohistochemistry technique for capturing SNPH intrusion in PC dendrites. Shown is SNPH (green), Syt2 (red), and <t>Calbindin</t> (blue) labeling in 3.5-month-old WT (A, C, and E) and Shi (B, D, and F) mice. Scale bar, 10 μm. (G and H) High magnification of the maximum intensity projection image from the z stack through dendritic regions of WT (G) and Shi (H). (I and J) Orthogonal (slice) view of SNPH punctum (indicated by arrows in panels G and H) in the dendritic region from WT (I) and Shi (J) in x-z and y-z orientations, respectively. (K) Quantification of percentage area occupied by SNPH within the dendritic volume from 3 mice of each group. Data are shown as mean ± SEM. *p
    Calbindin, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Swant calbindin cabp
    Dendritic SNPH Intrusion in PCs of Dysmyelinating Shi Mice In Vivo (A–F) Immunohistochemistry technique for capturing SNPH intrusion in PC dendrites. Shown is SNPH (green), Syt2 (red), and <t>Calbindin</t> (blue) labeling in 3.5-month-old WT (A, C, and E) and Shi (B, D, and F) mice. Scale bar, 10 μm. (G and H) High magnification of the maximum intensity projection image from the z stack through dendritic regions of WT (G) and Shi (H). (I and J) Orthogonal (slice) view of SNPH punctum (indicated by arrows in panels G and H) in the dendritic region from WT (I) and Shi (J) in x-z and y-z orientations, respectively. (K) Quantification of percentage area occupied by SNPH within the dendritic volume from 3 mice of each group. Data are shown as mean ± SEM. *p
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    91
    Abcam α calbindin
    Dendritic SNPH Intrusion in PCs of Dysmyelinating Shi Mice In Vivo (A–F) Immunohistochemistry technique for capturing SNPH intrusion in PC dendrites. Shown is SNPH (green), Syt2 (red), and <t>Calbindin</t> (blue) labeling in 3.5-month-old WT (A, C, and E) and Shi (B, D, and F) mice. Scale bar, 10 μm. (G and H) High magnification of the maximum intensity projection image from the z stack through dendritic regions of WT (G) and Shi (H). (I and J) Orthogonal (slice) view of SNPH punctum (indicated by arrows in panels G and H) in the dendritic region from WT (I) and Shi (J) in x-z and y-z orientations, respectively. (K) Quantification of percentage area occupied by SNPH within the dendritic volume from 3 mice of each group. Data are shown as mean ± SEM. *p
    α Calbindin, supplied by Abcam, used in various techniques. Bioz Stars score: 91/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Santa Cruz Biotechnology anti calbindin
    Altered infrapyramidal bundle (IPB) in CRMP3 −/− mice. ( A – F ): Free-floating coronal ( A , B ) and sagittal ( C – F ) hippocampal sections (20µm) from 2.5 month old mice ( n = 5 for each genotype) immunostained with antibodies to <t>calbindin</t> (green) and DAPI (blue) ( A – D ) or with sulfide silver ( E , F ) from WT ( A , C , E ) or CRMP3 −/− ( B , D , F ) mice. In WT, the IPB stops before the beginning of the CA3 curvature ( A ) white arrows; and ( C ) black arrows, whereas it extends clearly beyond it in CRMP3 −/− mice ( D ), white arrows; and ( F ) black arrows. ( G ) Schematic drawing of mossy fibers (MF) showing their dentate origin and their characteristic trajectories (MB: main bundle). ( H ): Quantitation and analyses of IPB length. The IPB length “a” was measured from the tip of the inferior blade of the granular layer and the length of CA3, “b” was determined from the tip of the inferior blade to the apex of the curvature of the CA3 pyramidal cell layer. Quantitation of normalized IPBs defined as a/b confirms the abnormal IPB in the mutants. Statistical significance was assessed by two-tailed t test, *** p
    Anti Calbindin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Swant anti calbindin
    Cerebellar Purkinje cells persist in Gars Nmf249/+ mice. Cerebellar Purkinje cells were stained with <t>anti-calbindin</t> in control (A, C), Aars sti/sti (B), and Gars Nmf249/+ (D) mice. Purkinje cell loss is almost complete in Aars sti/sti by 2.5 months of age, but is not seen in Gars Nmf249/+ mice, even at 1.5 years of age. All images are from a similar region of the base of the rostral folia (3 and 4) of the cerebellum. Scale bar in D = 145 μm.
    Anti Calbindin, supplied by Swant, used in various techniques. Bioz Stars score: 91/100, based on 420 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Santa Cruz Biotechnology calbindin
    Immunocytological characterization of E13.5-derived cells. Images are derived from stage day in vitro 1 ( DIV 1 ) ( a , c , e ) or stage day in vitro 7 ( DIV 7 ) ( b , d , f , g – j ). They represent overlays of double staining for nestin ( red ) and DAPI ( blue ) ( a , b ), TUJ1 ( green ) and DAPI ( blue ), ( c , d ), tyrosine hydroxylase (TH) ( red ) and DAPI ( blue ) ( e , f ) and GFAP ( red ) and DAPI ( blue ) ( g ). h Triple labelling for TH ( red ), TUJ1 ( green ) and DAPI ( blue ), i , j Triple labelling for <t>calbindin</t> ( green ), TH ( red ) and DAPI ( blue ) and GIRK2 ( red ), TH ( green ) and DAPI ( blue ), respectively. Scale bars = 30 μm
    Calbindin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 115 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    The cerebella of HTRA2 KO and NesKO mice appeared grossly normal. ( A–D ) Calbindin D-28K staining of HTRA2 WT ( A ), KO ( B ), NesWT ( C ) and NesKO ( D ) cerebellum did not reveal any differences in Purkinje cell organization in P35 cerebellum ( n = 3). ( E–H ) Cerebellar neuronal populations did not appear altered in HTRA2 KO or NesKO mice compared to WT controls by Nissl staining at P30 ( n = 3). ( I–L ) PLP staining for myelinated axons appeared comparable between HTRA2 KO and WT controls, and NesKO and NesWT controls at P30 ( n = 3). ( M–P ) The cerebellar granule cell layer of P30 WT and HTRA2 KO, and NesKO and NesWT did not appear different upon staining for Pax6 ( n = 3). KO denotes HTRA2 KO, WT denotes HTRA2 WT, nKO denotes NesKO and nWT denotes NesWT. Scale bars: A–P: 500 µm.

    Journal: PLoS ONE

    Article Title: Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1

    doi: 10.1371/journal.pone.0115789

    Figure Lengend Snippet: The cerebella of HTRA2 KO and NesKO mice appeared grossly normal. ( A–D ) Calbindin D-28K staining of HTRA2 WT ( A ), KO ( B ), NesWT ( C ) and NesKO ( D ) cerebellum did not reveal any differences in Purkinje cell organization in P35 cerebellum ( n = 3). ( E–H ) Cerebellar neuronal populations did not appear altered in HTRA2 KO or NesKO mice compared to WT controls by Nissl staining at P30 ( n = 3). ( I–L ) PLP staining for myelinated axons appeared comparable between HTRA2 KO and WT controls, and NesKO and NesWT controls at P30 ( n = 3). ( M–P ) The cerebellar granule cell layer of P30 WT and HTRA2 KO, and NesKO and NesWT did not appear different upon staining for Pax6 ( n = 3). KO denotes HTRA2 KO, WT denotes HTRA2 WT, nKO denotes NesKO and nWT denotes NesWT. Scale bars: A–P: 500 µm.

    Article Snippet: Antibodies: Calbindin D-28K (Millipore), PAX6 (Developmental Studies Hybridoma Bank).

    Techniques: Mouse Assay, Staining, Plasmid Purification

    CD44 expression in neuron-lineage cells during postnatal development. A–C: Double immunostaining of CD44 and calbindin in the cerebellum at P7. D–L: Double immunostaining of CD44 and NeuN at P7 (D–H) and P42 (I–L). H: Negative controle. G L: High magnification of F K. Nucleus was counterstained with TO-PRO-3 (blue). J: Quantitative analysis of the number of CD44-positive neuron-lineage cells by FACS at P3, P7 and P10. *p

    Journal: PLoS ONE

    Article Title: Dynamic Changes of CD44 Expression from Progenitors to Subpopulations of Astrocytes and Neurons in Developing Cerebellum

    doi: 10.1371/journal.pone.0053109

    Figure Lengend Snippet: CD44 expression in neuron-lineage cells during postnatal development. A–C: Double immunostaining of CD44 and calbindin in the cerebellum at P7. D–L: Double immunostaining of CD44 and NeuN at P7 (D–H) and P42 (I–L). H: Negative controle. G L: High magnification of F K. Nucleus was counterstained with TO-PRO-3 (blue). J: Quantitative analysis of the number of CD44-positive neuron-lineage cells by FACS at P3, P7 and P10. *p

    Article Snippet: The primary antibodies used included antibodies directed against GLAST (1∶1000; Frontier Science, Hokkaido, Japan), GFAP (1∶400; Millipore-Chemicon), Sox2 (1∶100; Cell Signaling Technology, Danvers, MA), Olig2 (1∶20; IBL, Takasaki, Japan), CC1 (1∶400; Calbiochem, San Diego, CA), Calbindin (1∶100; Cell Signaling Technology) and NeuN (1∶100; Millipore-Chemicon).

    Techniques: Expressing, Double Immunostaining, FACS

    The transcriptome of cerebellar lobule X is distinct from other lobules, regardless of Npc1 expression. ( A – D ) Calbindin 1 staining of Purkinje neurons in representative sagittal cerebellar sections of a Npc1 +/+ mouse at nine weeks of age ( A ), and Npc1 −/− mice at 4.5 weeks ( B ), seven weeks ( C ), or nine weeks of age ( D ). The Purkinje neuron marker, Calbindin 1, is shown in red and a DAPI (4’,6-diamidino-2-phenylindole) counterstain in blue. Scale bar = 500 µm. ( E ) Principal component analysis of RNA-sequencing data sets from cerebellar lobules III, VI, and X from 4.5 weeks old Npc1 +/+ and Npc1 −/− transgenic mice.

    Journal: International Journal of Molecular Sciences

    Article Title: Identification of Novel Pathways Associated with Patterned Cerebellar Purkinje Neuron Degeneration in Niemann-Pick Disease, Type C1

    doi: 10.3390/ijms21010292

    Figure Lengend Snippet: The transcriptome of cerebellar lobule X is distinct from other lobules, regardless of Npc1 expression. ( A – D ) Calbindin 1 staining of Purkinje neurons in representative sagittal cerebellar sections of a Npc1 +/+ mouse at nine weeks of age ( A ), and Npc1 −/− mice at 4.5 weeks ( B ), seven weeks ( C ), or nine weeks of age ( D ). The Purkinje neuron marker, Calbindin 1, is shown in red and a DAPI (4’,6-diamidino-2-phenylindole) counterstain in blue. Scale bar = 500 µm. ( E ) Principal component analysis of RNA-sequencing data sets from cerebellar lobules III, VI, and X from 4.5 weeks old Npc1 +/+ and Npc1 −/− transgenic mice.

    Article Snippet: The primary antibody used was anti-calbindin (1:2000, Cell Signaling Technologies, Danvers, MA, USA), with the corresponding secondary antibody of Alexa Fluor 594 goat anti-rabbit (1:5000, Thermo Fisher Scientific, Waltham, MA, USA).

    Techniques: Expressing, Staining, Mouse Assay, Marker, RNA Sequencing Assay, Transgenic Assay

    Neuroanatomical and histological examination of the brain . A. Brain weight. Brain weight analysis was perform in 24 weeks GSK-3α KO (n = 19-10) and WT (n = 14-10) animals. Values are mean (± SEM). *p ≤ 0.05; **p ≤ 0.001. B. Rotarod. GSK-3α KO (n = 13) and WT (n = 11) mice were tested on an accelerating rotarod in 3-day trials. Significant differences between the groups (p.value = 0.013) were found on day1 in the balance and coordination; however no changes were found in motor learning. C-D. Decrease in Purkinje cell density and size in GSK-3α KO mice. C . Purkinje cells image. Immunohistochemistry against Calbindin antibody of WT and GSK-3α KO cerebellum (shown original magnification, ×4 (upper panel) and ×10 (lower panel)). D . Statistical analysis of Purkinje cell density. Average cell density was determined by taking the ratio of the number of Purkinje cells to the length of cerebellar cortex segments. Cell density is significantly decreased in the GSK-3α KO (p

    Journal: Molecular Brain

    Article Title: Abnormalities in brain structure and behavior in GSK-3alpha mutant mice

    doi: 10.1186/1756-6606-2-35

    Figure Lengend Snippet: Neuroanatomical and histological examination of the brain . A. Brain weight. Brain weight analysis was perform in 24 weeks GSK-3α KO (n = 19-10) and WT (n = 14-10) animals. Values are mean (± SEM). *p ≤ 0.05; **p ≤ 0.001. B. Rotarod. GSK-3α KO (n = 13) and WT (n = 11) mice were tested on an accelerating rotarod in 3-day trials. Significant differences between the groups (p.value = 0.013) were found on day1 in the balance and coordination; however no changes were found in motor learning. C-D. Decrease in Purkinje cell density and size in GSK-3α KO mice. C . Purkinje cells image. Immunohistochemistry against Calbindin antibody of WT and GSK-3α KO cerebellum (shown original magnification, ×4 (upper panel) and ×10 (lower panel)). D . Statistical analysis of Purkinje cell density. Average cell density was determined by taking the ratio of the number of Purkinje cells to the length of cerebellar cortex segments. Cell density is significantly decreased in the GSK-3α KO (p

    Article Snippet: Sections were blocked with Universal Blocking Buffer (Daco) for 10 min, following overnight incubation with specific antibodies against Calbindin antibody (1:200; Cell Signaling Technologies).

    Techniques: Mouse Assay, Significance Assay, Immunohistochemistry

    Neurodegeneration in the cerebellum of ATM −/− pigs. ( A ) Compared with controls (CTRL N = six), the cerebellum of ATM −/− pigs ( N = five) immunostained with anti-calbindin antibodies (bar 100 µm) had a reduced number of PC (black arrow) on 1 day (left graph, P = 0.02, Mann–Whitney test), and this change remained in adult pigs (right graph, P = 0.02, Mann–Whitney test). ( B ) PC loss (represented by red line length) was also evaluated by maximal inter-PC distance (left and right panels, H E stain, bar = 100 µm). The inter-PC distance was elevated by ∼14% in ATM −/− pigs compared with CTRL at 1d (left graph, P = 0.02, Mann–Whitney test), consistent with reduced PCs (black arrows). This difference increased during postnatal development to ∼36% in adults (right graph, P = 0.005, Mann–Whitney test). ( C ) The angle between the soma and the main dendrite of PCs was reduced in A–T pigs at 1 day (left graph, P = 0.057, Mann–Whitney test) and in adults (right graph, P = 0.02, Mann–Whitney test). ( D ) PC volume showed no significant differences between groups at day 1 (left graph) or in adults (right graph, n.s., Mann–Whitney test).

    Journal: Human Molecular Genetics

    Article Title: A novel porcine model of ataxia telangiectasia reproduces neurological features and motor deficits of human disease

    doi: 10.1093/hmg/ddv356

    Figure Lengend Snippet: Neurodegeneration in the cerebellum of ATM −/− pigs. ( A ) Compared with controls (CTRL N = six), the cerebellum of ATM −/− pigs ( N = five) immunostained with anti-calbindin antibodies (bar 100 µm) had a reduced number of PC (black arrow) on 1 day (left graph, P = 0.02, Mann–Whitney test), and this change remained in adult pigs (right graph, P = 0.02, Mann–Whitney test). ( B ) PC loss (represented by red line length) was also evaluated by maximal inter-PC distance (left and right panels, H E stain, bar = 100 µm). The inter-PC distance was elevated by ∼14% in ATM −/− pigs compared with CTRL at 1d (left graph, P = 0.02, Mann–Whitney test), consistent with reduced PCs (black arrows). This difference increased during postnatal development to ∼36% in adults (right graph, P = 0.005, Mann–Whitney test). ( C ) The angle between the soma and the main dendrite of PCs was reduced in A–T pigs at 1 day (left graph, P = 0.057, Mann–Whitney test) and in adults (right graph, P = 0.02, Mann–Whitney test). ( D ) PC volume showed no significant differences between groups at day 1 (left graph) or in adults (right graph, n.s., Mann–Whitney test).

    Article Snippet: Immunostaining was performed using anti-calbindin antibodies (Cell Signaling cat # 2136, 1:5000) and hematoxylin counterstain to assess PC number, morphology and nuclei.

    Techniques: MANN-WHITNEY, Staining

    Immunohistochemical analysis for calbindin expression using TMA technology. Immunohistochemical staining of the TMA representing the four major RCC subtypes along with corresponding tumor-adjacent renal epithelium was performed using a human anti-calbindin-specific

    Journal: Molecular & Cellular Proteomics : MCP

    Article Title: Systematic Comparative Protein Expression Profiling of Clear Cell Renal Cell Carcinoma

    doi: 10.1074/mcp.M900168-MCP200

    Figure Lengend Snippet: Immunohistochemical analysis for calbindin expression using TMA technology. Immunohistochemical staining of the TMA representing the four major RCC subtypes along with corresponding tumor-adjacent renal epithelium was performed using a human anti-calbindin-specific

    Article Snippet: Immunohistochemistry was performed as described previously ( ) by applying the mAbs directed against calbindin (1:100; ab9481, Abcam plc, Cambridge, UK) and gelsolin (1:50; 610412, BD Transduction Laboratories) or a polyclonal Ab directed against heart fatty acid-binding protein (H-FABP; 1:50; 18-003-42444, GenWay Biotech Inc., San Diego, CA) for 1 h at room temperature.

    Techniques: Immunohistochemistry, Expressing, Staining

    Immunohistochemical analysis for calbindin expression in tumor-adjacent renal epithelium and distinct kidney tumor subtypes. Randomly selected sections of the TMA representing tumor-adjacent renal epithelium and various RCC subtypes were used to document

    Journal: Molecular & Cellular Proteomics : MCP

    Article Title: Systematic Comparative Protein Expression Profiling of Clear Cell Renal Cell Carcinoma

    doi: 10.1074/mcp.M900168-MCP200

    Figure Lengend Snippet: Immunohistochemical analysis for calbindin expression in tumor-adjacent renal epithelium and distinct kidney tumor subtypes. Randomly selected sections of the TMA representing tumor-adjacent renal epithelium and various RCC subtypes were used to document

    Article Snippet: Immunohistochemistry was performed as described previously ( ) by applying the mAbs directed against calbindin (1:100; ab9481, Abcam plc, Cambridge, UK) and gelsolin (1:50; 610412, BD Transduction Laboratories) or a polyclonal Ab directed against heart fatty acid-binding protein (H-FABP; 1:50; 18-003-42444, GenWay Biotech Inc., San Diego, CA) for 1 h at room temperature.

    Techniques: Immunohistochemistry, Expressing

    Normal postnatal cerebellar development in L7Dpl and wild-type mice. Normal foliation and thickness of the EGL in Tg15 L7Dpl and wild-type mice (P1 in A and B and P8 in G and H ). At P1, no loss of Purkinje cells as determined by Calbindin immunostaining ( C and D ) and regular thickness of the external (eEGL) and inner (iEGL) part of the EGL, as identified by p27 immunostaining, which identifies committed postmitotic EGL neurons, in contrast to the still-proliferating p27-negative eEGL ( E and F ). At P8, no loss of Purkinje cells (Calbindin, I and J ) and a normal EGL, split into proliferating eEGL and postmitotic iEGL ( K and L ); see labels. [Bar = 550 μm ( A and B ), 950μm ( G and H ), and 80 μm ( C - F and I - L ).]

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Transgene-driven expression of the Doppel protein in Purkinje cells causes Purkinje cell degeneration and motor impairment

    doi: 10.1073/pnas.0308681101

    Figure Lengend Snippet: Normal postnatal cerebellar development in L7Dpl and wild-type mice. Normal foliation and thickness of the EGL in Tg15 L7Dpl and wild-type mice (P1 in A and B and P8 in G and H ). At P1, no loss of Purkinje cells as determined by Calbindin immunostaining ( C and D ) and regular thickness of the external (eEGL) and inner (iEGL) part of the EGL, as identified by p27 immunostaining, which identifies committed postmitotic EGL neurons, in contrast to the still-proliferating p27-negative eEGL ( E and F ). At P8, no loss of Purkinje cells (Calbindin, I and J ) and a normal EGL, split into proliferating eEGL and postmitotic iEGL ( K and L ); see labels. [Bar = 550 μm ( A and B ), 950μm ( G and H ), and 80 μm ( C - F and I - L ).]

    Article Snippet: On selected sections, the following immunostains were carried out according to the manufacturer's instructions: glial fibrillary acidic protein; rabbit polyclonal antibody, 1:1,000; Dako, Carpenteria, CA), NeuN (antineuronal nuclei; mouse monoclonal antibody, 1:2,000; Chemicon), calbindin (Calbindin D-28K; rabbit polyclonal antiserum, 1:100; Chemicon), or the cyclin-dependent kinase inhibitor p27 (p27Kip1 ; rabbit polyclonal antiserum, 1:100, Santa Cruz Biotechnology).

    Techniques: Mouse Assay, Immunostaining

    Severe loss of Purkinje cells, secondary granule cell degeneration, and gliosis in Tg15 L7Dpl mice at 6 weeks of age. ( A-D ) Calbindin immunohistochemical staining reveals a subtotal loss of Purkinje cells in L7Dpl transgenic mice, leaving only a small population in Lob. XI and XII (blue arrowheads in B ). The red square indicates the area shown at high magnification in D , which is devoid of Purkinje cells. Shown is the control cerebellum with normal density of Purkinje cells at low ( A ) and high ( C ) magnification. Concomitant loss of granule cells is demonstrated by immunostaining for NeuN ( E-H ), which specifically stains cerebellar granule cells. Note the pronounced cell loss in the anterior part of the cerebellum (blue arrowheads). The red squares in E and F indicate the area shown magnified in G and H . In H , the depletion of granule cells (adjacent to a gyrus with more cells) is shown. The cell loss is accompanied by massive gliosis, as shown in I-L , again showing a caudal rostral gradient in its severity ( J ). Red boxes in I and J indicate the area shown at high magnification in K and L . [Bar = 1,000 μm( A, B, E, F, I , and J ) and 100 μm( C, D, G, H, K , and L ).]

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Transgene-driven expression of the Doppel protein in Purkinje cells causes Purkinje cell degeneration and motor impairment

    doi: 10.1073/pnas.0308681101

    Figure Lengend Snippet: Severe loss of Purkinje cells, secondary granule cell degeneration, and gliosis in Tg15 L7Dpl mice at 6 weeks of age. ( A-D ) Calbindin immunohistochemical staining reveals a subtotal loss of Purkinje cells in L7Dpl transgenic mice, leaving only a small population in Lob. XI and XII (blue arrowheads in B ). The red square indicates the area shown at high magnification in D , which is devoid of Purkinje cells. Shown is the control cerebellum with normal density of Purkinje cells at low ( A ) and high ( C ) magnification. Concomitant loss of granule cells is demonstrated by immunostaining for NeuN ( E-H ), which specifically stains cerebellar granule cells. Note the pronounced cell loss in the anterior part of the cerebellum (blue arrowheads). The red squares in E and F indicate the area shown magnified in G and H . In H , the depletion of granule cells (adjacent to a gyrus with more cells) is shown. The cell loss is accompanied by massive gliosis, as shown in I-L , again showing a caudal rostral gradient in its severity ( J ). Red boxes in I and J indicate the area shown at high magnification in K and L . [Bar = 1,000 μm( A, B, E, F, I , and J ) and 100 μm( C, D, G, H, K , and L ).]

    Article Snippet: On selected sections, the following immunostains were carried out according to the manufacturer's instructions: glial fibrillary acidic protein; rabbit polyclonal antibody, 1:1,000; Dako, Carpenteria, CA), NeuN (antineuronal nuclei; mouse monoclonal antibody, 1:2,000; Chemicon), calbindin (Calbindin D-28K; rabbit polyclonal antiserum, 1:100; Chemicon), or the cyclin-dependent kinase inhibitor p27 (p27Kip1 ; rabbit polyclonal antiserum, 1:100, Santa Cruz Biotechnology).

    Techniques: Mouse Assay, Immunohistochemistry, Staining, Transgenic Assay, Immunostaining

    Photomicrographs showing Lucifer yellow-labeled spiny cells identified in the accumbens core ( A ) and shell ( B ) region. In control rats, most injections of individual cells with Lucifer yellow resulted in single-cell labeling of spiny neurons. A, A single Lucifer yellow-labeled spiny neuron ( A1, arrow ) that was converted into a peroxidase stain using Lucifer yellow antibodies ( A2 ). This cell was subsequently identified in the accumbens core region ( A3, arrow ), as delineated by the calbindin-positive neuropil (presence of Texas Red fluorescence). Spiny neurons in the core region tended to have more widespread dendritic processes than those recovered in the shell region. B, A single Lucifer yellow-labeled spiny neuron ( B1, arrow ) in which the fluorescence was converted into a peroxidase stain ( B2, arrow ). This neuron was located in the accumbens shell region as outlined by the negative staining for calbindin immunoreactivity ( B3, absence of Texas Red fluorescence). The axon of this cell ( B1, asterisk ) was traced into the ventral pallidum where numerous collaterals were emitted ( B4 , low power; B5, high power). The three highlighted arrows with asterisks in B4 show collaterals of the primary axon. The solid arrows in B4 and B5 mark the same axonal collateral. bv, Blood vessel (in B4 and B5 indicating the same structure); VS, ventral striatum; VP, ventral pallidum; ac, anterior commissure; cc, corpus callosum. Scale bars, 30 μm. A2 and A3 are at the same scale as A1 ; B3 is at the same scale as B2 .

    Journal: The Journal of Neuroscience

    Article Title: Amphetamine Withdrawal Alters Bistable States and Cellular Coupling in Rat Prefrontal Cortex and Nucleus Accumbens Neurons Recorded In Vivo

    doi: 10.1523/JNEUROSCI.20-06-02332.2000

    Figure Lengend Snippet: Photomicrographs showing Lucifer yellow-labeled spiny cells identified in the accumbens core ( A ) and shell ( B ) region. In control rats, most injections of individual cells with Lucifer yellow resulted in single-cell labeling of spiny neurons. A, A single Lucifer yellow-labeled spiny neuron ( A1, arrow ) that was converted into a peroxidase stain using Lucifer yellow antibodies ( A2 ). This cell was subsequently identified in the accumbens core region ( A3, arrow ), as delineated by the calbindin-positive neuropil (presence of Texas Red fluorescence). Spiny neurons in the core region tended to have more widespread dendritic processes than those recovered in the shell region. B, A single Lucifer yellow-labeled spiny neuron ( B1, arrow ) in which the fluorescence was converted into a peroxidase stain ( B2, arrow ). This neuron was located in the accumbens shell region as outlined by the negative staining for calbindin immunoreactivity ( B3, absence of Texas Red fluorescence). The axon of this cell ( B1, asterisk ) was traced into the ventral pallidum where numerous collaterals were emitted ( B4 , low power; B5, high power). The three highlighted arrows with asterisks in B4 show collaterals of the primary axon. The solid arrows in B4 and B5 mark the same axonal collateral. bv, Blood vessel (in B4 and B5 indicating the same structure); VS, ventral striatum; VP, ventral pallidum; ac, anterior commissure; cc, corpus callosum. Scale bars, 30 μm. A2 and A3 are at the same scale as A1 ; B3 is at the same scale as B2 .

    Article Snippet: Sections containing Lucifer yellow-labeled cells were further labeled for calbindin immunoreactivity (1000×; Sigma, St. Louis, MO) using the Texas Red indirect fluorescence method as described previously ( , , ; ).

    Techniques: Labeling, Staining, Fluorescence, Negative Staining

    Photomicrographs showing Lucifer yellow-labeled PFC pyramidal neurons injected during in vivo intracellular recording from the PFC of drug-naive rats. In addition to the presence of truncated apical dendrites, the labeled cortical cells are identified as corticostriatal projection neurons based on the following features: (1) the axon of the Lucifer yellow-stained cell had a trajectory ( arrows in D from a section adjacent to A ) that could be traced into the striatal complex, and (2) the cell ( A, open arrow , Lucifer yellow fluorescence) did not contain calbindin immunoreactivity that is known to stain cortical GABAergic interneurons ( B, arrowheads ; same section showing Texas Red fluorescence for calbindin-D 28k ). Open arrow in B marks the site of the Lucifer yellow-stained cell shown in A . C (high power of A ) shows numerous dendritic spines on basilar dendrites of this pyramidal projection neuron. Arrowhead indicates a pair of calbindin-positive interneurons stained by Texas Red fluorescence and examined using the Lucifer yellow filter cube. E, F, Another Lucifer yellow-filled PFC neuron that had a stellate-like somatodendritic morphology ( E ) with dense dendritic branching in which the apical dendrite ( E, open arrow ) was not immediately apparent. Nevertheless, the axon of this cell could also be traced into the striatal complex ( F, arrows ). The primary axon was found to branch into two equal-diameter axons before entering the corpus callosum ( asterisks ); only one branch is observed to enter the ipsilateral striatal complex. bv, Blood vessel (in A–D indicating the same structure); vs , ventral striatum; cc, corpus callosum. Scale bars: A , B, 80 μm; C–F, 40 μm.

    Journal: The Journal of Neuroscience

    Article Title: Amphetamine Withdrawal Alters Bistable States and Cellular Coupling in Rat Prefrontal Cortex and Nucleus Accumbens Neurons Recorded In Vivo

    doi: 10.1523/JNEUROSCI.20-06-02332.2000

    Figure Lengend Snippet: Photomicrographs showing Lucifer yellow-labeled PFC pyramidal neurons injected during in vivo intracellular recording from the PFC of drug-naive rats. In addition to the presence of truncated apical dendrites, the labeled cortical cells are identified as corticostriatal projection neurons based on the following features: (1) the axon of the Lucifer yellow-stained cell had a trajectory ( arrows in D from a section adjacent to A ) that could be traced into the striatal complex, and (2) the cell ( A, open arrow , Lucifer yellow fluorescence) did not contain calbindin immunoreactivity that is known to stain cortical GABAergic interneurons ( B, arrowheads ; same section showing Texas Red fluorescence for calbindin-D 28k ). Open arrow in B marks the site of the Lucifer yellow-stained cell shown in A . C (high power of A ) shows numerous dendritic spines on basilar dendrites of this pyramidal projection neuron. Arrowhead indicates a pair of calbindin-positive interneurons stained by Texas Red fluorescence and examined using the Lucifer yellow filter cube. E, F, Another Lucifer yellow-filled PFC neuron that had a stellate-like somatodendritic morphology ( E ) with dense dendritic branching in which the apical dendrite ( E, open arrow ) was not immediately apparent. Nevertheless, the axon of this cell could also be traced into the striatal complex ( F, arrows ). The primary axon was found to branch into two equal-diameter axons before entering the corpus callosum ( asterisks ); only one branch is observed to enter the ipsilateral striatal complex. bv, Blood vessel (in A–D indicating the same structure); vs , ventral striatum; cc, corpus callosum. Scale bars: A , B, 80 μm; C–F, 40 μm.

    Article Snippet: Sections containing Lucifer yellow-labeled cells were further labeled for calbindin immunoreactivity (1000×; Sigma, St. Louis, MO) using the Texas Red indirect fluorescence method as described previously ( , , ; ).

    Techniques: Labeling, Injection, In Vivo, Staining, Fluorescence

    Photomicrographs showing examples of dye-coupled cells in the deep layer of PFC ( A–C ) and in the ventral striatum ( D, E ) of rats recorded 21–28 d after withdrawal from amphetamine. In each case, a single cell was injected with the dye during in vivo intracellular recording from amphetamine-withdrawn rats. Coupled cells were recovered in the prelimbic ( A ), infralimbic ( B ), and orbital ( C ) cortices that exhibit properties consistent with PFC pyramidal neurons. Arrows with numbers indicate the number of cell bodies in each cluster of coupled cells, whereas the open arrows label their apical dendrites. Superficial layers in A–C are toward the top of the photomicrographs. D, A pair of spiny neurons ( arrows ) in the ventrolateral striatum of an amphetamine-treated rats after injecting a single neuron. Double staining of the coupled neurons for calbindin-D 28k immunoreactivity (marked by Texas Red fluorescence) reveals that the coupled cells lie at the border of a striosome (as marked by negative neuropil staining for calbindin immunoreactivity). The background level of Texas Red fluorescence does not appear as intense because of the use of the I3 filter cube to view the Lucifer yellow fluorescence, but nevertheless still reveals the border of this striosome. E, A cluster of Lucifer yellow-labeled spiny cells ( arrows ) in the ventromedial striatum (at the juncture of the accumbens core region) of an amphetamine-withdrawn rat. The Lucifer yellow was subsequently converted into a peroxidase stain ( brown ) using antibodies to Lucifer yellow to better reveal the dendrodendritic contacts between the coupled cells. In all cases, the coupling was restricted to cells of the same morphological cell class. Open arrows mark axonal collaterals in contact with dendritic processes. The cell marked by arrow 1 was located on the adjacent section to F (data not shown). Scale bars: A–C, 30 μm; D, 40 μm; E is at the same scale as D .

    Journal: The Journal of Neuroscience

    Article Title: Amphetamine Withdrawal Alters Bistable States and Cellular Coupling in Rat Prefrontal Cortex and Nucleus Accumbens Neurons Recorded In Vivo

    doi: 10.1523/JNEUROSCI.20-06-02332.2000

    Figure Lengend Snippet: Photomicrographs showing examples of dye-coupled cells in the deep layer of PFC ( A–C ) and in the ventral striatum ( D, E ) of rats recorded 21–28 d after withdrawal from amphetamine. In each case, a single cell was injected with the dye during in vivo intracellular recording from amphetamine-withdrawn rats. Coupled cells were recovered in the prelimbic ( A ), infralimbic ( B ), and orbital ( C ) cortices that exhibit properties consistent with PFC pyramidal neurons. Arrows with numbers indicate the number of cell bodies in each cluster of coupled cells, whereas the open arrows label their apical dendrites. Superficial layers in A–C are toward the top of the photomicrographs. D, A pair of spiny neurons ( arrows ) in the ventrolateral striatum of an amphetamine-treated rats after injecting a single neuron. Double staining of the coupled neurons for calbindin-D 28k immunoreactivity (marked by Texas Red fluorescence) reveals that the coupled cells lie at the border of a striosome (as marked by negative neuropil staining for calbindin immunoreactivity). The background level of Texas Red fluorescence does not appear as intense because of the use of the I3 filter cube to view the Lucifer yellow fluorescence, but nevertheless still reveals the border of this striosome. E, A cluster of Lucifer yellow-labeled spiny cells ( arrows ) in the ventromedial striatum (at the juncture of the accumbens core region) of an amphetamine-withdrawn rat. The Lucifer yellow was subsequently converted into a peroxidase stain ( brown ) using antibodies to Lucifer yellow to better reveal the dendrodendritic contacts between the coupled cells. In all cases, the coupling was restricted to cells of the same morphological cell class. Open arrows mark axonal collaterals in contact with dendritic processes. The cell marked by arrow 1 was located on the adjacent section to F (data not shown). Scale bars: A–C, 30 μm; D, 40 μm; E is at the same scale as D .

    Article Snippet: Sections containing Lucifer yellow-labeled cells were further labeled for calbindin immunoreactivity (1000×; Sigma, St. Louis, MO) using the Texas Red indirect fluorescence method as described previously ( , , ; ).

    Techniques: Injection, In Vivo, Double Staining, Fluorescence, Staining, Labeling

    Histology of explants cultured for six days. Representative images for 3–5 organs in each condition. All sections counterstained with hematoxylin (blue nuclei). A–D. Note lack of cysts in control ( Vehicle ) explants and the progressively greater size (a typical cyst is boxed in each image) and extent of cysts per organs exposed to 470 nM dexamethasone ( Dex )-alone, 100 µM 8-Br-cAMP ( cAMP )-only, or both chemicals. E–H. Brown color indicates immunoreactivity to megalin antibody. Note patchy reactivity of cyst epithelia in organs exposed to 470 nM dexamethasone-alone, 100 µM 8-Br-cAMP-alone or both chemicals. I–L. Uromodulin immunoreactivity (brown); note that cysts are not labeled. M–P. Immunostaining with antibody to calbindin-28. Most cyst epithelia are unreactive (M, O and P) but a small subset of cysts in cAMP-exposed organs were positive and one such is depicted in O′. Q–T. These sections were probed with Dolichos biflorus lectin. Note that the lectin prominently labeled non-dilated tubules between cysts; in addition, the great majority of cysts did not bind the lectin. In (R), an asterisk indicates a rare, labeled cyst. Bar in A–D is 500 µm, and bar for other frames is 50 µm.

    Journal: PLoS ONE

    Article Title: Ex Vivo Modeling of Chemical Synergy in Prenatal Kidney Cystogenesis

    doi: 10.1371/journal.pone.0057797

    Figure Lengend Snippet: Histology of explants cultured for six days. Representative images for 3–5 organs in each condition. All sections counterstained with hematoxylin (blue nuclei). A–D. Note lack of cysts in control ( Vehicle ) explants and the progressively greater size (a typical cyst is boxed in each image) and extent of cysts per organs exposed to 470 nM dexamethasone ( Dex )-alone, 100 µM 8-Br-cAMP ( cAMP )-only, or both chemicals. E–H. Brown color indicates immunoreactivity to megalin antibody. Note patchy reactivity of cyst epithelia in organs exposed to 470 nM dexamethasone-alone, 100 µM 8-Br-cAMP-alone or both chemicals. I–L. Uromodulin immunoreactivity (brown); note that cysts are not labeled. M–P. Immunostaining with antibody to calbindin-28. Most cyst epithelia are unreactive (M, O and P) but a small subset of cysts in cAMP-exposed organs were positive and one such is depicted in O′. Q–T. These sections were probed with Dolichos biflorus lectin. Note that the lectin prominently labeled non-dilated tubules between cysts; in addition, the great majority of cysts did not bind the lectin. In (R), an asterisk indicates a rare, labeled cyst. Bar in A–D is 500 µm, and bar for other frames is 50 µm.

    Article Snippet: In some sections, immunohistochemistry was performed for: aquaporin-1 (Abcam ab15080), calbindin-28 (Abcam ab25085), megalin (Acris Antibodies DM3613P), phospho-histone H3 (Abcam ab5176), uromodulin (Santa Cruz sc-20631), the macrophage marker F4/80 (Abcam ab6640) and the M2 macrophage marker, the mannose receptor/CD206 (Abcam ab8918 and Abdserotec MCA2235GA).

    Techniques: Cell Culture, Labeling, Immunostaining

    Expression of conventional markers in the cochlea of the common marmoset ( a ) Selected genes are evaluated in the cochlea of common marmosets. We selected 14 cochlear cell markers and nine genes causal for hereditary hearing loss. Antibodies specific to them were used in this study. ( b ) A cross-sectional view of the common marmoset cochlea duct under low magnification (left). The corresponding schema with anatomical landmarks is shown (right). ( c ) Schema for the subtypes of lateral wall fibrocytes. ( d–g ) The expression patterns of conventional markers in the lateral wall. CX26, CX30, CTGF, AQP1, CALDESMON, NKCC1, and Na + /K + ATPase α1 expression were all observed in the cochleae, as well as previously in rodent. High magnification images were shown in the most right panels of ( f,g ). ( h ) Expression patterns of conventional markers in OC. MYOSIN 7a and CALBINDIN expression was observed in three rows of outer hair cells and one row of inner hair cells. SOX2 expression was observed in inner pillar cells, outer pillar cells, Deiters’ cells, and Hensen’s cells. ( i ) Expression pattern of conventional markers in SGNs. Expression of βIII TUBULIN and PERIPHERIN was observed in marmoset SGNs. The nuclei were counterstained with Hoechst (blue). Scale bar: 200 μm in b, 100 μm in ( c–i ). Basal turns in ( d–g,i ), apical turn in h. SV: stria vascularis, SLF: spiral ligament fibrocytes (I-V: Type I-V), OC: organ of Corti, SL: spiral limbus, SGN: spiral ganglion neurons, MC: Marginal cells, SPC: Spiral prominence cells, ISC: Inner sulcus cells, OSC: Outer sulcus cells, CC: Claudius cells, HC: Hensen’s cells, DC: Deiters’ cells, IPC: inner pillar cells, OPC: outer pillar cells, PC: inner phalangeal cells, BC: border cells, OHC: Outer hair cells, IHC: Inner hair cells.

    Journal: Scientific Reports

    Article Title: Distinct Expression Patterns Of Causative Genes Responsible For Hereditary Progressive Hearing Loss In Non-Human Primate Cochlea

    doi: 10.1038/srep22250

    Figure Lengend Snippet: Expression of conventional markers in the cochlea of the common marmoset ( a ) Selected genes are evaluated in the cochlea of common marmosets. We selected 14 cochlear cell markers and nine genes causal for hereditary hearing loss. Antibodies specific to them were used in this study. ( b ) A cross-sectional view of the common marmoset cochlea duct under low magnification (left). The corresponding schema with anatomical landmarks is shown (right). ( c ) Schema for the subtypes of lateral wall fibrocytes. ( d–g ) The expression patterns of conventional markers in the lateral wall. CX26, CX30, CTGF, AQP1, CALDESMON, NKCC1, and Na + /K + ATPase α1 expression were all observed in the cochleae, as well as previously in rodent. High magnification images were shown in the most right panels of ( f,g ). ( h ) Expression patterns of conventional markers in OC. MYOSIN 7a and CALBINDIN expression was observed in three rows of outer hair cells and one row of inner hair cells. SOX2 expression was observed in inner pillar cells, outer pillar cells, Deiters’ cells, and Hensen’s cells. ( i ) Expression pattern of conventional markers in SGNs. Expression of βIII TUBULIN and PERIPHERIN was observed in marmoset SGNs. The nuclei were counterstained with Hoechst (blue). Scale bar: 200 μm in b, 100 μm in ( c–i ). Basal turns in ( d–g,i ), apical turn in h. SV: stria vascularis, SLF: spiral ligament fibrocytes (I-V: Type I-V), OC: organ of Corti, SL: spiral limbus, SGN: spiral ganglion neurons, MC: Marginal cells, SPC: Spiral prominence cells, ISC: Inner sulcus cells, OSC: Outer sulcus cells, CC: Claudius cells, HC: Hensen’s cells, DC: Deiters’ cells, IPC: inner pillar cells, OPC: outer pillar cells, PC: inner phalangeal cells, BC: border cells, OHC: Outer hair cells, IHC: Inner hair cells.

    Article Snippet: Antibodies The primary antibodies used in this study are as follows: anti-SOX2 (goat IgG, Santa Cruz Biotechnology, Dallas, TX, USA, sc17320, 1:100), anti-CX26 (mouse IgG, Zymed, San Francisco, CA, USA, 13–8100, 1:300), anti-CX30 (rabbit IgG, Sigma-Aldrich, St. Louis, MO, USA, HPA014846, 1:200), anti-CX31 (rabbit IgG, Proteintech, Manchester, UK, 12880–1-AP, 1:100), anti-CTGF (goat IgG, Santa Cruz Biotechnology, sc14939, 1:100), anti-AQP1 (rabbit IgG, Millipore, Billerica, MA, USA, AB3272, 1:300), anti-CALDESMON (Sigma-Aldrich, C0297, 1:100), anti-CA II (rabbit IgG, Santa Cruz Biotechnology, sc25596, 1:100), anti-NKCC1 (goat IgG, Santa Cruz Biotechnology, sc21545, 1:300), anti-Na+/K+-ATPase α1 (rabbit IgG, Novus Biologicals, Littleton, CO, USA, EP1845Y, 1:500), anti-CALBINDIN (rabbit IgG, Abcam, Cambridge, UK, ab11426, 1:1000), anti-ZO-1 (goat IgG, Abcam, ab190085, 1:100), anti-CRYM (mouse IgG, GeneTex, Irvine, CA, USA, GTX84654, 1:100), anti-MYOSIN 7a (mouse IgG, DSHB, Iowa City, IA,USA, 138–1-s, 1:30; rabbit IgG, Proteus, 25–6790), anti-GRHL2 (rabbit IgG, Sigma-Aldrich, HPA004820, 1:200, rabbit IgG, LSBio, LS-B3983, 1:150), anti-DFNA5 (rabbit IgG, Sigma-Aldrich, HPA011326, 1:400), anti-COCH (rabbit IgG, Sigma-Aldrich, HPA050122, 1:100), anti-β-TUBULIN III (mouse IgG, Sigma-Aldrich, T8660, 1:250), anti-ATP6B1 (goat IgG, Santa Cruz Biotechnology, sc21206, 1:50), and anti-PERIPHERIN (rabbit IgG, Millipore, AB1530, 1:100).

    Techniques: Expressing, Immunohistochemistry

    MtDNA loss in astrocytes depletes Calbindin-positive interneurons in cortex, upper neuronal layers. Immunofluorescnece staining of mid-sagittal sections of 7–8 months old mice, brain graph shows sampling site. a Neuronal nuclei (NeuN, green), Calbindin-positive neurons (red) and nucleus (DAPI, blue). b Quantification of NeuN-and Calbindin-positive neurons in somatosensory cortex, cortical layers I and II are boxed. Scale bars: 20 μm. The data are presented as mean and error bars indicate standard deviation. Statistical significance: *** p

    Journal: Nature Communications

    Article Title: Loss of mtDNA activates astrocytes and leads to spongiotic encephalopathy

    doi: 10.1038/s41467-017-01859-9

    Figure Lengend Snippet: MtDNA loss in astrocytes depletes Calbindin-positive interneurons in cortex, upper neuronal layers. Immunofluorescnece staining of mid-sagittal sections of 7–8 months old mice, brain graph shows sampling site. a Neuronal nuclei (NeuN, green), Calbindin-positive neurons (red) and nucleus (DAPI, blue). b Quantification of NeuN-and Calbindin-positive neurons in somatosensory cortex, cortical layers I and II are boxed. Scale bars: 20 μm. The data are presented as mean and error bars indicate standard deviation. Statistical significance: *** p

    Article Snippet: Primary antibodies were rabbit Calbindin (Abcam), GFAP (Millipore), ALDH1L1 (Abcam), cleaved Caspase 3 (Cell Signaling Technology), IBA1 (Wako), Olig2 (Merck Millipore), KI67 (Merck Millipore); mouse Nestin (Merck Millipore), SDHA (CII) (Abcam), NeuN (Chemion), GAD67 (Merck Millipore); Neurofilament Marker pan axonal cocktail (BioLegend); chicken MAP2 (Thermo Scientific); rat MBP (Nordic BioSite).

    Techniques: Staining, Mouse Assay, Sampling, Standard Deviation

    Astrocytic IP-10 gene expression in the CNS of BDV-infected rats. Rats were infected as adults (A) or neonates (B to F) and euthanatized 11 days (A), 33 days (C to F), or 75 days (B) later. Following perfusion of rats using either 4% buffered paraformaldehyde (A) or Bouin's fixative (B to F), brains were removed and processed for analysis by ISH. ISH with a 33 P-radiolabeled IP-10 antisense probe was combined with IHC for GFAP as a marker for astrocytes (A, B, D, and F) or Calbindin-D as a marker for Purkinje cells (C and E). Panels A and B depict representative cortical regions. Arrowheads indicate ISH-positive astrocytes, whereas arrows indicate GFAP-negative cells of unknown identity that express IP-10. In panels C and D, parts of the cerebellum from two consecutive sections are shown. Note the string-like distribution of IP-10 signals in the Purkinje cell layer. High-power magnifications of the Purkinje cell layer are shown in panels E and F. Original magnifications were ×20 (C and D), ×80 (B and F), and ×200 (A and E).

    Journal: Journal of Virology

    Article Title: Chemokine Gene Expression in Astrocytes of Borna Disease Virus-Infected Rats and Mice in the Absence of Inflammation

    doi:

    Figure Lengend Snippet: Astrocytic IP-10 gene expression in the CNS of BDV-infected rats. Rats were infected as adults (A) or neonates (B to F) and euthanatized 11 days (A), 33 days (C to F), or 75 days (B) later. Following perfusion of rats using either 4% buffered paraformaldehyde (A) or Bouin's fixative (B to F), brains were removed and processed for analysis by ISH. ISH with a 33 P-radiolabeled IP-10 antisense probe was combined with IHC for GFAP as a marker for astrocytes (A, B, D, and F) or Calbindin-D as a marker for Purkinje cells (C and E). Panels A and B depict representative cortical regions. Arrowheads indicate ISH-positive astrocytes, whereas arrows indicate GFAP-negative cells of unknown identity that express IP-10. In panels C and D, parts of the cerebellum from two consecutive sections are shown. Note the string-like distribution of IP-10 signals in the Purkinje cell layer. High-power magnifications of the Purkinje cell layer are shown in panels E and F. Original magnifications were ×20 (C and D), ×80 (B and F), and ×200 (A and E).

    Article Snippet: Staining of sections with a mouse MAb to Calbindin-D (Sigma) at a 1:200 dilution was done as described for MAb W3/13.

    Techniques: Expressing, Infection, In Situ Hybridization, Immunohistochemistry, Marker

    Dendritic SNPH Intrusion in PCs of Dysmyelinating Shi Mice In Vivo (A–F) Immunohistochemistry technique for capturing SNPH intrusion in PC dendrites. Shown is SNPH (green), Syt2 (red), and Calbindin (blue) labeling in 3.5-month-old WT (A, C, and E) and Shi (B, D, and F) mice. Scale bar, 10 μm. (G and H) High magnification of the maximum intensity projection image from the z stack through dendritic regions of WT (G) and Shi (H). (I and J) Orthogonal (slice) view of SNPH punctum (indicated by arrows in panels G and H) in the dendritic region from WT (I) and Shi (J) in x-z and y-z orientations, respectively. (K) Quantification of percentage area occupied by SNPH within the dendritic volume from 3 mice of each group. Data are shown as mean ± SEM. *p

    Journal: Cell reports

    Article Title: Inappropriate Intrusion of an Axonal Mitochondrial Anchor into Dendrites Causes Neurodegeneration

    doi: 10.1016/j.celrep.2019.09.012

    Figure Lengend Snippet: Dendritic SNPH Intrusion in PCs of Dysmyelinating Shi Mice In Vivo (A–F) Immunohistochemistry technique for capturing SNPH intrusion in PC dendrites. Shown is SNPH (green), Syt2 (red), and Calbindin (blue) labeling in 3.5-month-old WT (A, C, and E) and Shi (B, D, and F) mice. Scale bar, 10 μm. (G and H) High magnification of the maximum intensity projection image from the z stack through dendritic regions of WT (G) and Shi (H). (I and J) Orthogonal (slice) view of SNPH punctum (indicated by arrows in panels G and H) in the dendritic region from WT (I) and Shi (J) in x-z and y-z orientations, respectively. (K) Quantification of percentage area occupied by SNPH within the dendritic volume from 3 mice of each group. Data are shown as mean ± SEM. *p

    Article Snippet: Sections were then incubated with primary antibodies against SNPH (1:250; Abcam), Synaptotagmin2 (1:250; Developmental Studies Hybridoma Bank) and Calbindin (1:250; BosterBio) overnight in PBS containing 0.3% Triton X-100 and 5% normal goat serum.

    Techniques: Mouse Assay, In Vivo, Immunohistochemistry, Labeling

    SNPH Intrusion Sensitizes PC Dendrites to Glutamatergic Excitotoxicity In Vivo (A and B) Representative images of lentivirally transduced GFP-SNPH (1–469) (A) and GFP-SNPH (B) in PCs of SNPH-KO mice injected with saline (no harmaline, vehicle only). (C-H) Effect of harmaline on GFP-SNPH (1–469)-transduced (C) and GFP-SNPH-transduced (F) PC dendrites. Degenerating dendrites in GFP-SNPH-transduced PCs can be seen in (F). Also shown is Calbindin labeling of GFP SNPH (1–469) (D) and GFP-SNPH (G) from (C) and (F). Merged images of GFP SNPH (1–469) and GFP-SNPH with Calbindin are shown in (E) and (H), respectively. (I–K) Representative image of a harmaline-induced degenerating PC (white arrow in I) transduced with GFP-SNPH. Calbindin staining from the same section is shown in (J), whereas a merged image is shown in (K). Scale bars, 20 μm. (L) Quantification of dendritic shrinkage in GFP-SNPH (1–469)- and GFP-SNPH-transduced PCs in the absence (n = 3 mice, vehicle only) or presence of harmaline (n = 5 mice). Data are shown as mean ± SEM. ***p

    Journal: Cell reports

    Article Title: Inappropriate Intrusion of an Axonal Mitochondrial Anchor into Dendrites Causes Neurodegeneration

    doi: 10.1016/j.celrep.2019.09.012

    Figure Lengend Snippet: SNPH Intrusion Sensitizes PC Dendrites to Glutamatergic Excitotoxicity In Vivo (A and B) Representative images of lentivirally transduced GFP-SNPH (1–469) (A) and GFP-SNPH (B) in PCs of SNPH-KO mice injected with saline (no harmaline, vehicle only). (C-H) Effect of harmaline on GFP-SNPH (1–469)-transduced (C) and GFP-SNPH-transduced (F) PC dendrites. Degenerating dendrites in GFP-SNPH-transduced PCs can be seen in (F). Also shown is Calbindin labeling of GFP SNPH (1–469) (D) and GFP-SNPH (G) from (C) and (F). Merged images of GFP SNPH (1–469) and GFP-SNPH with Calbindin are shown in (E) and (H), respectively. (I–K) Representative image of a harmaline-induced degenerating PC (white arrow in I) transduced with GFP-SNPH. Calbindin staining from the same section is shown in (J), whereas a merged image is shown in (K). Scale bars, 20 μm. (L) Quantification of dendritic shrinkage in GFP-SNPH (1–469)- and GFP-SNPH-transduced PCs in the absence (n = 3 mice, vehicle only) or presence of harmaline (n = 5 mice). Data are shown as mean ± SEM. ***p

    Article Snippet: Sections were then incubated with primary antibodies against SNPH (1:250; Abcam), Synaptotagmin2 (1:250; Developmental Studies Hybridoma Bank) and Calbindin (1:250; BosterBio) overnight in PBS containing 0.3% Triton X-100 and 5% normal goat serum.

    Techniques: In Vivo, Mouse Assay, Injection, Labeling, Transduction, Staining

    Altered infrapyramidal bundle (IPB) in CRMP3 −/− mice. ( A – F ): Free-floating coronal ( A , B ) and sagittal ( C – F ) hippocampal sections (20µm) from 2.5 month old mice ( n = 5 for each genotype) immunostained with antibodies to calbindin (green) and DAPI (blue) ( A – D ) or with sulfide silver ( E , F ) from WT ( A , C , E ) or CRMP3 −/− ( B , D , F ) mice. In WT, the IPB stops before the beginning of the CA3 curvature ( A ) white arrows; and ( C ) black arrows, whereas it extends clearly beyond it in CRMP3 −/− mice ( D ), white arrows; and ( F ) black arrows. ( G ) Schematic drawing of mossy fibers (MF) showing their dentate origin and their characteristic trajectories (MB: main bundle). ( H ): Quantitation and analyses of IPB length. The IPB length “a” was measured from the tip of the inferior blade of the granular layer and the length of CA3, “b” was determined from the tip of the inferior blade to the apex of the curvature of the CA3 pyramidal cell layer. Quantitation of normalized IPBs defined as a/b confirms the abnormal IPB in the mutants. Statistical significance was assessed by two-tailed t test, *** p

    Journal: Brain Sciences

    Article Title: Opposing Morphogenetic Defects on Dendrites and Mossy Fibers of Dentate Granular Neurons in CRMP3-Deficient Mice

    doi: 10.3390/brainsci8110196

    Figure Lengend Snippet: Altered infrapyramidal bundle (IPB) in CRMP3 −/− mice. ( A – F ): Free-floating coronal ( A , B ) and sagittal ( C – F ) hippocampal sections (20µm) from 2.5 month old mice ( n = 5 for each genotype) immunostained with antibodies to calbindin (green) and DAPI (blue) ( A – D ) or with sulfide silver ( E , F ) from WT ( A , C , E ) or CRMP3 −/− ( B , D , F ) mice. In WT, the IPB stops before the beginning of the CA3 curvature ( A ) white arrows; and ( C ) black arrows, whereas it extends clearly beyond it in CRMP3 −/− mice ( D ), white arrows; and ( F ) black arrows. ( G ) Schematic drawing of mossy fibers (MF) showing their dentate origin and their characteristic trajectories (MB: main bundle). ( H ): Quantitation and analyses of IPB length. The IPB length “a” was measured from the tip of the inferior blade of the granular layer and the length of CA3, “b” was determined from the tip of the inferior blade to the apex of the curvature of the CA3 pyramidal cell layer. Quantitation of normalized IPBs defined as a/b confirms the abnormal IPB in the mutants. Statistical significance was assessed by two-tailed t test, *** p

    Article Snippet: Immunohistochemistry Cryostat sections (10–20 µm) were collected on Superfrost Plus slides, permeabilized with 0.1% Triton X-100 in PBS containing 1% gelatin, and stained with the following antibodies: mouse monoclonal against MAP2 (Chemicon International, Temecula, CA, USA), rabbit polyclonal against MAP2 (Sigma, St. Louis, MO, USA), β-galactosidase ( Promega Madison, WI, USA), anti-neuropilin 1 (NP1; Abcam, Cambridge, MA, USA) and anti-neuropilin 2 (NP2; Sigma, St. Louis, MO, USA), neurofilament 200 (Biorad, Hercules, CA, USA), or anti-calbindin (Santa Cruz, Santa Cruz, CA, USA, ) antibodies.

    Techniques: Mouse Assay, Quantitation Assay, Two Tailed Test

    Cerebellar Purkinje cells persist in Gars Nmf249/+ mice. Cerebellar Purkinje cells were stained with anti-calbindin in control (A, C), Aars sti/sti (B), and Gars Nmf249/+ (D) mice. Purkinje cell loss is almost complete in Aars sti/sti by 2.5 months of age, but is not seen in Gars Nmf249/+ mice, even at 1.5 years of age. All images are from a similar region of the base of the rostral folia (3 and 4) of the cerebellum. Scale bar in D = 145 μm.

    Journal: Molecular and cellular neurosciences

    Article Title: An assessment of mechanisms underlying peripheral axonal degeneration caused by aminoacyl-tRNA synthetase mutations

    doi: 10.1016/j.mcn.2010.11.006

    Figure Lengend Snippet: Cerebellar Purkinje cells persist in Gars Nmf249/+ mice. Cerebellar Purkinje cells were stained with anti-calbindin in control (A, C), Aars sti/sti (B), and Gars Nmf249/+ (D) mice. Purkinje cell loss is almost complete in Aars sti/sti by 2.5 months of age, but is not seen in Gars Nmf249/+ mice, even at 1.5 years of age. All images are from a similar region of the base of the rostral folia (3 and 4) of the cerebellum. Scale bar in D = 145 μm.

    Article Snippet: Using a microtome, 4 μm sagittal sections of cerebellum or horizontal sections of lumbar spinal cord were cut and stained using anti-calbindin (D-280, Swant) with secondary antibody and signal detection using the ABC kit (Vector) and diaminobenzidine (Zymed).

    Techniques: Mouse Assay, Staining

    Plotting the distribution of myenteric neurons within the ventral stomach wall that were co-reactive for alpha-synuclein and either NOS, calbindin, or calretinin revealed regional specificity for the different chemical phenotypes. Neurons double labeled for alpha-synuclein and NOS (blue) were located primarily within the boundaries of the forestomach, whereas neurons double labeled for alpha-synuclein and either calbindin (green) or calretinin (red) were localized to the corpus and the antrum. The orientation of the stomach wall is mucosa side up, so for the x-axis 0 mm represents the edge of the forestomach and for the y-axis 0 mm and 35 mm represents the greater and lesser curvatures, respectively.

    Journal: Neuroscience

    Article Title: ALPHA-SYNUCLEIN-IMMUNOPOSITIVE MYENTERIC NEURONS AND VAGAL PREGANGLIONIC TERMINALS: AUTONOMIC PATHWAY IMPLICATED IN PARKINSON'S DISEASE?

    doi: 10.1016/j.neuroscience.2008.02.074

    Figure Lengend Snippet: Plotting the distribution of myenteric neurons within the ventral stomach wall that were co-reactive for alpha-synuclein and either NOS, calbindin, or calretinin revealed regional specificity for the different chemical phenotypes. Neurons double labeled for alpha-synuclein and NOS (blue) were located primarily within the boundaries of the forestomach, whereas neurons double labeled for alpha-synuclein and either calbindin (green) or calretinin (red) were localized to the corpus and the antrum. The orientation of the stomach wall is mucosa side up, so for the x-axis 0 mm represents the edge of the forestomach and for the y-axis 0 mm and 35 mm represents the greater and lesser curvatures, respectively.

    Article Snippet: The primary antibodies used were mouse alpha-synuclein (1:2,500; 610787; BD Biosciences, San Jose, CA) and one of the following three rabbit antibodies: NOS (1:2,500; SC-648; Santa Cruz Biotechnology, Inc., Santa Cruz, CA), calbindin (1:8,000; CB-38; SWant, Bellinzona, Switzerland), or calretinin (1:16,000; 7699/4; SWant).

    Techniques: Labeling

    Vagal efferent varicosities positive for alpha-synuclein were in close proximity to myenteric neurons co-reactive for alpha-synuclein and either NOS (A), calbindin (B) or calretinin (C). Dextran-Texas Red tracing of vagal efferents (red) was combined with alpha-synuclein (green) and either NOS, calbindin, or calretinin (blue) double immunohistochemical labeling of myenteric neurons in the stomach. A subpopulation of alpha-synuclein-positive neurons were co-reactive for NOS (green nucleus with a light blue cytoplasm), calbindin or calretinin (light blue nucleus and cytoplasm). Yellow varicosities indicate co-localization of Dextran-Texas Red and alpha-synuclein. Scale bar in C = 25 µm for A–C.

    Journal: Neuroscience

    Article Title: ALPHA-SYNUCLEIN-IMMUNOPOSITIVE MYENTERIC NEURONS AND VAGAL PREGANGLIONIC TERMINALS: AUTONOMIC PATHWAY IMPLICATED IN PARKINSON'S DISEASE?

    doi: 10.1016/j.neuroscience.2008.02.074

    Figure Lengend Snippet: Vagal efferent varicosities positive for alpha-synuclein were in close proximity to myenteric neurons co-reactive for alpha-synuclein and either NOS (A), calbindin (B) or calretinin (C). Dextran-Texas Red tracing of vagal efferents (red) was combined with alpha-synuclein (green) and either NOS, calbindin, or calretinin (blue) double immunohistochemical labeling of myenteric neurons in the stomach. A subpopulation of alpha-synuclein-positive neurons were co-reactive for NOS (green nucleus with a light blue cytoplasm), calbindin or calretinin (light blue nucleus and cytoplasm). Yellow varicosities indicate co-localization of Dextran-Texas Red and alpha-synuclein. Scale bar in C = 25 µm for A–C.

    Article Snippet: The primary antibodies used were mouse alpha-synuclein (1:2,500; 610787; BD Biosciences, San Jose, CA) and one of the following three rabbit antibodies: NOS (1:2,500; SC-648; Santa Cruz Biotechnology, Inc., Santa Cruz, CA), calbindin (1:8,000; CB-38; SWant, Bellinzona, Switzerland), or calretinin (1:16,000; 7699/4; SWant).

    Techniques: Immunohistochemistry, Labeling

    Müller cells first branch at stereotyped depths within the IPL Retinal cross sections of different developmental ages double-stained for mGFP-labeled MG and Calbindin to mark S2 and S4 (black arrows). A ) At P6, most cells are unbranched, but occasional MG branches (white arrows) are seen in S1 and S5. B ) At P7, branches in S1 and S5 become more abundant and the first branches in central IPL emerge. C,D ) Between P8 (C) and P9 (D), branching in all layers continues to increase. Most cells branch in S1 and S5 by P9, but central layer branches continue to emerge after this time. E ) Percentage of cells per retina that have branches in each IPL sublamina, measured at P6–9. Scale bars: 20 µm.

    Journal: The Journal of comparative neurology

    Article Title: Anatomy and spatial organization of Müller glia in mouse retina

    doi: 10.1002/cne.24153

    Figure Lengend Snippet: Müller cells first branch at stereotyped depths within the IPL Retinal cross sections of different developmental ages double-stained for mGFP-labeled MG and Calbindin to mark S2 and S4 (black arrows). A ) At P6, most cells are unbranched, but occasional MG branches (white arrows) are seen in S1 and S5. B ) At P7, branches in S1 and S5 become more abundant and the first branches in central IPL emerge. C,D ) Between P8 (C) and P9 (D), branching in all layers continues to increase. Most cells branch in S1 and S5 by P9, but central layer branches continue to emerge after this time. E ) Percentage of cells per retina that have branches in each IPL sublamina, measured at P6–9. Scale bars: 20 µm.

    Article Snippet: Calbindin antibody (Swant CB38, RRID: AB_10000340) immunolabeled three IPL sublayers, including the two cholinergic sublayers, as previously reported ( ). (TH antibody (Millipore AB1542, RRID: AB_90755) labeled amacrine cells with large somata and projections to a single stratum of the IPL, a pattern consistent with this and other TH antibodies ( ).

    Techniques: Staining, Labeling

    Immunocytological characterization of E13.5-derived cells. Images are derived from stage day in vitro 1 ( DIV 1 ) ( a , c , e ) or stage day in vitro 7 ( DIV 7 ) ( b , d , f , g – j ). They represent overlays of double staining for nestin ( red ) and DAPI ( blue ) ( a , b ), TUJ1 ( green ) and DAPI ( blue ), ( c , d ), tyrosine hydroxylase (TH) ( red ) and DAPI ( blue ) ( e , f ) and GFAP ( red ) and DAPI ( blue ) ( g ). h Triple labelling for TH ( red ), TUJ1 ( green ) and DAPI ( blue ), i , j Triple labelling for calbindin ( green ), TH ( red ) and DAPI ( blue ) and GIRK2 ( red ), TH ( green ) and DAPI ( blue ), respectively. Scale bars = 30 μm

    Journal: Purinergic Signalling

    Article Title: Nucleotides affect neurogenesis and dopaminergic differentiation of mouse fetal midbrain-derived neural precursor cells

    doi: 10.1007/s11302-010-9206-7

    Figure Lengend Snippet: Immunocytological characterization of E13.5-derived cells. Images are derived from stage day in vitro 1 ( DIV 1 ) ( a , c , e ) or stage day in vitro 7 ( DIV 7 ) ( b , d , f , g – j ). They represent overlays of double staining for nestin ( red ) and DAPI ( blue ) ( a , b ), TUJ1 ( green ) and DAPI ( blue ), ( c , d ), tyrosine hydroxylase (TH) ( red ) and DAPI ( blue ) ( e , f ) and GFAP ( red ) and DAPI ( blue ) ( g ). h Triple labelling for TH ( red ), TUJ1 ( green ) and DAPI ( blue ), i , j Triple labelling for calbindin ( green ), TH ( red ) and DAPI ( blue ) and GIRK2 ( red ), TH ( green ) and DAPI ( blue ), respectively. Scale bars = 30 μm

    Article Snippet: Immunolabeling was performed with monoclonal antibodies against nestin, the glial glutamate transporter GLAST, O4 (all Chemicon International, Hofheim, Germany), glial fibrillary acidic protein (GFAP), neuron-specific tubulin TUJ1 (both Sigma-Aldrich), calbindin, tyrosine hydroxylase (TH), dopamine active transporter (DAT) (all Santa Cruz Biotechnology, Heidelberg, Germany) and polyclonal antibodies against TH, nuclear receptor related 1 (nurr1) protein, doublecortin, G-protein regulated inward-rectifier potassium channel 2 (GIRK2), corin and LMX1A (all Santa Cruz Biotechnology).

    Techniques: Derivative Assay, In Vitro, Double Staining

    Immunocytological analysis of proteins expressed in midbrain dopaminergic neurons in E10.5-derived cells. All images are derived from stage day in vitro 7 ( DIV 7 ). They represent overlays of triple labelling for calbindin ( green ), doublecortin ( DCX ) ( red ) and DAPI ( blue ) ( a ), calbindin ( green ), TH ( red ) and DAPI ( blue ) ( b ), TH ( green ) GIRK2 ( red ) and DAPI ( blue ) ( c ), TH ( green ), nurr1 ( red ) and DAPI ( blue ) ( d ), and DAT ( green ), TH ( red ) and DAPI ( blue ) ( e , f ). Scale bars = 30 μm

    Journal: Purinergic Signalling

    Article Title: Nucleotides affect neurogenesis and dopaminergic differentiation of mouse fetal midbrain-derived neural precursor cells

    doi: 10.1007/s11302-010-9206-7

    Figure Lengend Snippet: Immunocytological analysis of proteins expressed in midbrain dopaminergic neurons in E10.5-derived cells. All images are derived from stage day in vitro 7 ( DIV 7 ). They represent overlays of triple labelling for calbindin ( green ), doublecortin ( DCX ) ( red ) and DAPI ( blue ) ( a ), calbindin ( green ), TH ( red ) and DAPI ( blue ) ( b ), TH ( green ) GIRK2 ( red ) and DAPI ( blue ) ( c ), TH ( green ), nurr1 ( red ) and DAPI ( blue ) ( d ), and DAT ( green ), TH ( red ) and DAPI ( blue ) ( e , f ). Scale bars = 30 μm

    Article Snippet: Immunolabeling was performed with monoclonal antibodies against nestin, the glial glutamate transporter GLAST, O4 (all Chemicon International, Hofheim, Germany), glial fibrillary acidic protein (GFAP), neuron-specific tubulin TUJ1 (both Sigma-Aldrich), calbindin, tyrosine hydroxylase (TH), dopamine active transporter (DAT) (all Santa Cruz Biotechnology, Heidelberg, Germany) and polyclonal antibodies against TH, nuclear receptor related 1 (nurr1) protein, doublecortin, G-protein regulated inward-rectifier potassium channel 2 (GIRK2), corin and LMX1A (all Santa Cruz Biotechnology).

    Techniques: Derivative Assay, In Vitro