hippocampal ca1 region Search Results


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  • 91
    Freund-Vector hippocampal ca1 region
    NeuN immunohistochemistry and F-J B histofluorescence staining in the hippocampal <t>CA1</t> region of gerbils from the sham-operated (A, J), IPC + sham-operated (B, K), ischemia (C, E, G, L, N, P) and IPC + ischemia (D, F, H, M, O, Q) groups. NeuN-immunoreactive neurons were hardly observed in the SP (asterisk) of gerbils in the ischemia group 5 days after ischemia/reperfusion injury. NeuN-immunoreactive neurons in the SP of hippocampal CA1 region of animals in the IPC + ischemia group were still present 5 days after transient forebrain ischemia. Many F-J B-positive cells were detected in the gerbil hippocampal SP (asterisk) in the ischemia group only 5 days after transient forebrain ischemia; at this time, however, F-J B-positive cells in the IPC + ischemia group were rarely observed. Scale bars: 60 μm. (I, R) Relative analysis as percent in the mean number of NeuN-immunoreactive neurons and F-J B-positive cells in the SP of the gerbil hippocampal CA1 region ( n = 7 gerbils at each group); * P
    Hippocampal Ca1 Region, supplied by Freund-Vector, used in various techniques. Bioz Stars score: 91/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Olympus ca1 pyramidal cell layer
    Accurate decoding of self-location from unprocessed hippocampal recordings. A) Top, a typical ‘raw’ extracellular recording from a single <t>CA1</t> electrode. Bottom, wavelet decomposition of the same data, power shown for frequency bands from 2Hz to 15kHz (bottom to top row). B) At each timestep wavelet coefficients (64 time points, 26 frequency bands, 128 channels) were fed to a deep network consisting of 2D convolutional layers with shared weights, followed by a fully-connected layer with a regression head to decode self-location; schematic of architecture shown. C) Example trajectory from R2478, true position (black) and decoded position (blue) shown for 3s of data. Full test-set shown in Video 1 . D) Distribution of decoding errors from trial shown in (C), mean error (14.2cm ± 12.9cm, black), chance decoding of self-location from shuffled data (62.2cm ± 9.09cm, red). E) Across all five rats, the network (CNN) was more accurate than a machine learning baseline (SVM) and a Bayesian decoder (Bayesian) trained on action potentials. This was also true when the network was limited to high frequency components ( > 250Hz, CNN-Spikes). When only local frequencies were used (
    Ca1 Pyramidal Cell Layer, supplied by Olympus, used in various techniques. Bioz Stars score: 91/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher ca1 stratum pyramidale region
    Upregulation of gene expression for metabolic enzymes with aging. (a) Cumulative histograms for gene expression assays for selected enzymes in brain tissue samples collected from hippocampal <t>CA1</t> region (stratum pyramidale) of young (black circles) and aged animals (white circles). Note the right‐shift of the distribution of RT‐PCR scores with aging in majority of investigated genes. See Section 2 for details. Abbreviations: Pygb , glycogen phosphorylase; Hk1 , hexokinase 1; Pfkp , phosphofructokinase platelet form; Pkm , pyruvate kinase; Ldha/b , lactate dehydrogenase a/b; Glul , glutamine synthetase. (b) Quantification of the results shown in (a). Asterisks indicate a statistically significant difference (* p
    Ca1 Stratum Pyramidale Region, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Maixin-Bio rat hippocampal ca1 region immunohistochemistry
    Upregulation of gene expression for metabolic enzymes with aging. (a) Cumulative histograms for gene expression assays for selected enzymes in brain tissue samples collected from hippocampal <t>CA1</t> region (stratum pyramidale) of young (black circles) and aged animals (white circles). Note the right‐shift of the distribution of RT‐PCR scores with aging in majority of investigated genes. See Section 2 for details. Abbreviations: Pygb , glycogen phosphorylase; Hk1 , hexokinase 1; Pfkp , phosphofructokinase platelet form; Pkm , pyruvate kinase; Ldha/b , lactate dehydrogenase a/b; Glul , glutamine synthetase. (b) Quantification of the results shown in (a). Asterisks indicate a statistically significant difference (* p
    Rat Hippocampal Ca1 Region Immunohistochemistry, supplied by Maixin-Bio, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Zhongshan Golden Bridge Company rat hippocampal ca1 region tunel staining
    Cell apoptosis in the rat hippocampal <t>CA1</t> region <t>(TUNEL</t> staining, × 200). Apoptotic cells with brown or yellow nuclei are visible in the model and Dickkopf-1 groups at various time points (arrows). Fewer apoptotic cells with weak staining are observed in the Dickkopf-1 group, compared with the model group, at corresponding time points.
    Rat Hippocampal Ca1 Region Tunel Staining, supplied by Zhongshan Golden Bridge Company, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    adobe systems hippocampus ca1 field
    Cell apoptosis in the rat hippocampal <t>CA1</t> region <t>(TUNEL</t> staining, × 200). Apoptotic cells with brown or yellow nuclei are visible in the model and Dickkopf-1 groups at various time points (arrows). Fewer apoptotic cells with weak staining are observed in the Dickkopf-1 group, compared with the model group, at corresponding time points.
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    91
    Collaborative Drug Discovery Inc hippocampal ca1 region
    Simulations of diffusion in the ECS of the <t>CA1</t> hippocampus in WT and Has3 −/− mice. In these simulations, informed by our results on ECS parameters in individual layers, molecules were released for 1 ms from point sources in the center
    Hippocampal Ca1 Region, supplied by Collaborative Drug Discovery Inc, used in various techniques. Bioz Stars score: 91/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Hamilton Company hippocampal ca1 region
    Optogenetic activation of PV+ interneurons had no effect on impaired theta oscillation of AβO-injected PV-Cre mice (A) Schematic illustration of micro-injection of AβO and ChR2 virus into hippocampal <t>CA1</t> region of PV-Cre mice. (B) Fluorescence image of ChR2 expressed PV+ interneurons in hippocampal CA1 region. Individual neurons are pointed by white arrows. (C) Schematic illustration of in vivo recording. (D) Example traces of spontaneous theta-filtered LFP signals (top) and spectrogram (bottom) recorded in control PV-Cre mice (left) and AβO-injected PV-Cre mice (right). The 3 s-long blue light stimulation of PV+ interneuron s is represented by light blue shaded region. (E) Example traces of PSD curves obtained from the spontaneous theta oscillation recorded in control PV-Cre mice (black), AβO-injected PV-Cre mice (red) and AβO-injected PV-Cre mice with blue light (blue). (F-G) Mean peak frequency (F) and mean peak power (G) of spontaneous theta-filtered LFP signals of control PV-Cre mice (black, n = 5), AβO-injected PV-Cre mice (red, n = 5) and AβO-injected PV-Cre mice with blue light (blue, n = 5). All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ p
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    91
    MicroProbes for Life Science ca1 stratum radiatum
    GRAB Ado sensors reveal somatodendritic Ado release in hippocampal slices. (A1) Left panel: sparse expression of Ado1.0 in cultured hippocampal pyramidal neurons. Right panel: fluorescence images and pseudocolor images of Ado1.0 ΔF/F 0 in the somatodendritic (purple box) and axonal (blue box) compartments in response to field stimuli (30 Hz, 100 pulses), high K + , or Ado (100 nM); scale bar, 50 μm. Example traces and summary data are shown in (A2) and (A3) , respectively; n = 11-21 ROIs from 4 coverslips per group. (B) Schematic illustration depicting the strategy used to image acute hippocampal brain slices prepared from mice expressing Ado1.0med and tdTomato-ChrimsonR in the <t>CA1</t> region while using a 633-nm laser to activate the neurons. At the right is an image showing Ado1.0med fluorescence; the box shows the region magnified in (C) . (C) Magnified fluorescence images of the CA1 region showing Ado1.0med (green) and tdTomato-ChrimsonR (red) in CA1 regions (scale bar, 100 μm). The pyramidal cell layer (Str. py) is located between the stratum oriens (Str. ori) and stratum <t>radiatum</t> (Str. rad). (D) Pseudocolor images (left), averaged traces (middle), and group summary (right) of Ado1.0med ΔF/F 0 in response to 633-nm laser pulses applied at 20 Hz for the indicated duration (scale bar, 100 μm); the solid line shown in the right panel a linear fit to the data; n = 6 slices from 4 mice. (E) Blocking L-type VGCCs inhibits optogenetically induced Ado release. Where indicated, nimodipine (Nim, 20 μM) and Cd 2+ (100 μM) were applied (scale bar, 100 μm); n = 5 slices from 3 mice. (F) Blocking ENT transporters inhibits optogenetically induced Ado release. Where indicated, dipyridamole (DIPY, 20 μM) was used to block ENTs. Averaged traces (F1) and the group summary (F2) of Ado1.0med ΔF/F 0 are shown; n = 4 slices from 3 mice. (G) Model depicting the novel mode of neuronal activity–dependent Ado release from hippocampal neurons. Ado is released slowly from the postsynaptic membrane via a vesicle-independent, ENT-dependent mechanism, serving as a putative retrograde signal to regulate presynaptic activity. This activity-dependent release of Ado requires L-type voltage-gated Ca 2+ channels (VGCCs). In contrast, classic neurotransmitters such as glutamate (Glu) are released from presynaptic vesicles requires P/Q-type and N-type VGCCs. AdoR, adenosine receptor; ENTs, equilibrative nucleoside transporters; Syts, synaptotagmins.
    Ca1 Stratum Radiatum, supplied by MicroProbes for Life Science, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Novoprotein hippocampal ca1 region
    GRAB Ado sensors reveal somatodendritic Ado release in hippocampal slices. (A1) Left panel: sparse expression of Ado1.0 in cultured hippocampal pyramidal neurons. Right panel: fluorescence images and pseudocolor images of Ado1.0 ΔF/F 0 in the somatodendritic (purple box) and axonal (blue box) compartments in response to field stimuli (30 Hz, 100 pulses), high K + , or Ado (100 nM); scale bar, 50 μm. Example traces and summary data are shown in (A2) and (A3) , respectively; n = 11-21 ROIs from 4 coverslips per group. (B) Schematic illustration depicting the strategy used to image acute hippocampal brain slices prepared from mice expressing Ado1.0med and tdTomato-ChrimsonR in the <t>CA1</t> region while using a 633-nm laser to activate the neurons. At the right is an image showing Ado1.0med fluorescence; the box shows the region magnified in (C) . (C) Magnified fluorescence images of the CA1 region showing Ado1.0med (green) and tdTomato-ChrimsonR (red) in CA1 regions (scale bar, 100 μm). The pyramidal cell layer (Str. py) is located between the stratum oriens (Str. ori) and stratum <t>radiatum</t> (Str. rad). (D) Pseudocolor images (left), averaged traces (middle), and group summary (right) of Ado1.0med ΔF/F 0 in response to 633-nm laser pulses applied at 20 Hz for the indicated duration (scale bar, 100 μm); the solid line shown in the right panel a linear fit to the data; n = 6 slices from 4 mice. (E) Blocking L-type VGCCs inhibits optogenetically induced Ado release. Where indicated, nimodipine (Nim, 20 μM) and Cd 2+ (100 μM) were applied (scale bar, 100 μm); n = 5 slices from 3 mice. (F) Blocking ENT transporters inhibits optogenetically induced Ado release. Where indicated, dipyridamole (DIPY, 20 μM) was used to block ENTs. Averaged traces (F1) and the group summary (F2) of Ado1.0med ΔF/F 0 are shown; n = 4 slices from 3 mice. (G) Model depicting the novel mode of neuronal activity–dependent Ado release from hippocampal neurons. Ado is released slowly from the postsynaptic membrane via a vesicle-independent, ENT-dependent mechanism, serving as a putative retrograde signal to regulate presynaptic activity. This activity-dependent release of Ado requires L-type voltage-gated Ca 2+ channels (VGCCs). In contrast, classic neurotransmitters such as glutamate (Glu) are released from presynaptic vesicles requires P/Q-type and N-type VGCCs. AdoR, adenosine receptor; ENTs, equilibrative nucleoside transporters; Syts, synaptotagmins.
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    91
    VANGL2 LTD hippocampal ca1 region
    Ryk is required for oligomeric Aβ -mediated synapse loss in vivo . a, Timeline and schematic of intracerebroventricular infusion of the Ryk monoclonal antibody. Cannula and pre-infused osmotic minipumps were implanted at ∼2 months old. Minipumps were removed 2 weeks later. b-c, Staining and quantification of glutamatergic synapses in 5XFAD mice infused with the Ryk monoclonal antibody. d, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into <t>CA1</t> and CA3 regions of the hippocampus bilaterally. 2 weeks later, Aβ oligomers were injected into the lateral ventricular for 5 days. 5 days later, animals were fixed with perfusion and sectioning and stained with synaptic markers. e-f, Representative images and quantification of synaptic puncta detected by costaining for Bassoon (red)- and PSD95 (green)-immunoreactive (arrowheads) in stratum radiatum. n=4 for Ryk +/+ mice, n=3 for Ryk +/+ mice with oligomeric Aβ injection, n=3 for Ryk cKO mice and n=3 for Ryk cKO mice with oligomeric Aβ injection. * P
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    93
    Olympus ca1 hippocampal region
    The effect of Arc overexpression or knockdown on hippocampal neuronal densities in 2VO rats treated with 0.4 mg/kg DSS. The top part of the figure shows the Nissl staining of the DG per animal group. The bottom part shows the neuronal density quantifications in the <t>CA1</t> region per group. Bars represent mean ± SD for sample replications ( n = 10). ∗ p
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    Image Search Results


    NeuN immunohistochemistry and F-J B histofluorescence staining in the hippocampal CA1 region of gerbils from the sham-operated (A, J), IPC + sham-operated (B, K), ischemia (C, E, G, L, N, P) and IPC + ischemia (D, F, H, M, O, Q) groups. NeuN-immunoreactive neurons were hardly observed in the SP (asterisk) of gerbils in the ischemia group 5 days after ischemia/reperfusion injury. NeuN-immunoreactive neurons in the SP of hippocampal CA1 region of animals in the IPC + ischemia group were still present 5 days after transient forebrain ischemia. Many F-J B-positive cells were detected in the gerbil hippocampal SP (asterisk) in the ischemia group only 5 days after transient forebrain ischemia; at this time, however, F-J B-positive cells in the IPC + ischemia group were rarely observed. Scale bars: 60 μm. (I, R) Relative analysis as percent in the mean number of NeuN-immunoreactive neurons and F-J B-positive cells in the SP of the gerbil hippocampal CA1 region ( n = 7 gerbils at each group); * P

    Journal: Neural Regeneration Research

    Article Title: Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

    doi: 10.4103/1673-5374.187039

    Figure Lengend Snippet: NeuN immunohistochemistry and F-J B histofluorescence staining in the hippocampal CA1 region of gerbils from the sham-operated (A, J), IPC + sham-operated (B, K), ischemia (C, E, G, L, N, P) and IPC + ischemia (D, F, H, M, O, Q) groups. NeuN-immunoreactive neurons were hardly observed in the SP (asterisk) of gerbils in the ischemia group 5 days after ischemia/reperfusion injury. NeuN-immunoreactive neurons in the SP of hippocampal CA1 region of animals in the IPC + ischemia group were still present 5 days after transient forebrain ischemia. Many F-J B-positive cells were detected in the gerbil hippocampal SP (asterisk) in the ischemia group only 5 days after transient forebrain ischemia; at this time, however, F-J B-positive cells in the IPC + ischemia group were rarely observed. Scale bars: 60 μm. (I, R) Relative analysis as percent in the mean number of NeuN-immunoreactive neurons and F-J B-positive cells in the SP of the gerbil hippocampal CA1 region ( n = 7 gerbils at each group); * P

    Article Snippet: In particular, the vulnerability of neurons in the hippocampus varies with hippocampal subregions; the most vulnerable subregion to transient forebrain ischemia is the hippocampal CA1 region (Schmidt-Kastner and Freund, 1991).

    Techniques: Immunohistochemistry, Staining

    Western blot analysis of SOD1, SOD2, CAT and GPX in the hippocampal CA1 region of gerbils in all groups. (A–D) Protein expression levels of SOD1, SOD2, CAT and GPX. ROD as percent of the immunoblot band is presented (* P

    Journal: Neural Regeneration Research

    Article Title: Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

    doi: 10.4103/1673-5374.187039

    Figure Lengend Snippet: Western blot analysis of SOD1, SOD2, CAT and GPX in the hippocampal CA1 region of gerbils in all groups. (A–D) Protein expression levels of SOD1, SOD2, CAT and GPX. ROD as percent of the immunoblot band is presented (* P

    Article Snippet: In particular, the vulnerability of neurons in the hippocampus varies with hippocampal subregions; the most vulnerable subregion to transient forebrain ischemia is the hippocampal CA1 region (Schmidt-Kastner and Freund, 1991).

    Techniques: Western Blot, Expressing

    Cresyl violet (CV) staining in the hippocampus of gerbils from the sham-operated (A, a), IPC + sham-operated (B, b), ischemia (C, c, E, e, G, g) and IPC + ischemia (D, d, F, f, H, h) groups. In the ischemia group, a few CV-positive cells were found in the hippocampal CA1 stratum pyramidale (asterisk) only 5 days after transient forebrain ischemia. However, the distribution pattern of CV-positive cells in the IPC + ischemia group was similar to that in the sham-operated group. IPC: Ischemic preconditioning; CA: cornus ammonis; DG: dentate gyrus; SO: stratum oriens; SR: stratum radiatum. Scale bars: 200 μm (low magnification, A–H), 60 μm (a–h: high magnification of boxes in A–H).

    Journal: Neural Regeneration Research

    Article Title: Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

    doi: 10.4103/1673-5374.187039

    Figure Lengend Snippet: Cresyl violet (CV) staining in the hippocampus of gerbils from the sham-operated (A, a), IPC + sham-operated (B, b), ischemia (C, c, E, e, G, g) and IPC + ischemia (D, d, F, f, H, h) groups. In the ischemia group, a few CV-positive cells were found in the hippocampal CA1 stratum pyramidale (asterisk) only 5 days after transient forebrain ischemia. However, the distribution pattern of CV-positive cells in the IPC + ischemia group was similar to that in the sham-operated group. IPC: Ischemic preconditioning; CA: cornus ammonis; DG: dentate gyrus; SO: stratum oriens; SR: stratum radiatum. Scale bars: 200 μm (low magnification, A–H), 60 μm (a–h: high magnification of boxes in A–H).

    Article Snippet: In particular, the vulnerability of neurons in the hippocampus varies with hippocampal subregions; the most vulnerable subregion to transient forebrain ischemia is the hippocampal CA1 region (Schmidt-Kastner and Freund, 1991).

    Techniques: Staining

    SOD1 and SOD2 immunohistochemistry in the hippocampal CA1 region of gerbils in the sham-operated (A and J), IPC + sham-operated (B and K), ischemia (C, E, G, L, N and P) and IPC + ischemia (D, F, H, M, O and Q) groups. SOD1 immunoreactivity was well detected in the SP. In the ischemia group, SOD1 immunoreactivity was significantly decreased in the SP (asterisk) 5 days after transient ischemia. However, SOD1 immunoreactivity in the IPC + ischemia group was similar to that in the sham-operated group. SOD2 immunoreactivity was also detected in the SP and the change of SOD2 immunoreactivity in all groups was similar to that of SOD1 immunoreactivity. Scale bars: 60 μm. (I, R) ROD as percent values of SOD1 and SOD2 immunoreactivity in the SP of animals in all groups ( n = 7 animals in each group; * P

    Journal: Neural Regeneration Research

    Article Title: Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

    doi: 10.4103/1673-5374.187039

    Figure Lengend Snippet: SOD1 and SOD2 immunohistochemistry in the hippocampal CA1 region of gerbils in the sham-operated (A and J), IPC + sham-operated (B and K), ischemia (C, E, G, L, N and P) and IPC + ischemia (D, F, H, M, O and Q) groups. SOD1 immunoreactivity was well detected in the SP. In the ischemia group, SOD1 immunoreactivity was significantly decreased in the SP (asterisk) 5 days after transient ischemia. However, SOD1 immunoreactivity in the IPC + ischemia group was similar to that in the sham-operated group. SOD2 immunoreactivity was also detected in the SP and the change of SOD2 immunoreactivity in all groups was similar to that of SOD1 immunoreactivity. Scale bars: 60 μm. (I, R) ROD as percent values of SOD1 and SOD2 immunoreactivity in the SP of animals in all groups ( n = 7 animals in each group; * P

    Article Snippet: In particular, the vulnerability of neurons in the hippocampus varies with hippocampal subregions; the most vulnerable subregion to transient forebrain ischemia is the hippocampal CA1 region (Schmidt-Kastner and Freund, 1991).

    Techniques: Immunohistochemistry

    CAT and GPX immunohistochemistry in the hippocampal CA1 region of gerbils in the sham-operated (A and J), IPC + sham-operated (B and K), ischemia (C, E, G, L, N and P) and IPC + ischemia (D, F, H, M, O and Q) groups. CAT immunoreactivity was easily observed in the SP of animals in the sham-operated group. CAT immunoreactivity was markedly decreased in the SP (asterisk) 5 days after transient ischemia. In the IPC + ischemia group, CAT immunoreactivity in the SP was steadily maintained without change. GPX immunoreactivity was also detected in the SP and its change pattern after transient ischemia was similar to the change pattern of CAT immunoreactivity. However, GPX immunoreactivity in the IPC + sham-operated and IPC + ischemia groups was significantly increased than in the sham-operated-group. Scale bars: 60 μm. (I, R) ROD as percent values of CAT and GPX immunoreactivity in the SP in all of the groups ( n = 7 animals in each group; * P

    Journal: Neural Regeneration Research

    Article Title: Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

    doi: 10.4103/1673-5374.187039

    Figure Lengend Snippet: CAT and GPX immunohistochemistry in the hippocampal CA1 region of gerbils in the sham-operated (A and J), IPC + sham-operated (B and K), ischemia (C, E, G, L, N and P) and IPC + ischemia (D, F, H, M, O and Q) groups. CAT immunoreactivity was easily observed in the SP of animals in the sham-operated group. CAT immunoreactivity was markedly decreased in the SP (asterisk) 5 days after transient ischemia. In the IPC + ischemia group, CAT immunoreactivity in the SP was steadily maintained without change. GPX immunoreactivity was also detected in the SP and its change pattern after transient ischemia was similar to the change pattern of CAT immunoreactivity. However, GPX immunoreactivity in the IPC + sham-operated and IPC + ischemia groups was significantly increased than in the sham-operated-group. Scale bars: 60 μm. (I, R) ROD as percent values of CAT and GPX immunoreactivity in the SP in all of the groups ( n = 7 animals in each group; * P

    Article Snippet: In particular, the vulnerability of neurons in the hippocampus varies with hippocampal subregions; the most vulnerable subregion to transient forebrain ischemia is the hippocampal CA1 region (Schmidt-Kastner and Freund, 1991).

    Techniques: Immunohistochemistry

    Accurate decoding of self-location from unprocessed hippocampal recordings. A) Top, a typical ‘raw’ extracellular recording from a single CA1 electrode. Bottom, wavelet decomposition of the same data, power shown for frequency bands from 2Hz to 15kHz (bottom to top row). B) At each timestep wavelet coefficients (64 time points, 26 frequency bands, 128 channels) were fed to a deep network consisting of 2D convolutional layers with shared weights, followed by a fully-connected layer with a regression head to decode self-location; schematic of architecture shown. C) Example trajectory from R2478, true position (black) and decoded position (blue) shown for 3s of data. Full test-set shown in Video 1 . D) Distribution of decoding errors from trial shown in (C), mean error (14.2cm ± 12.9cm, black), chance decoding of self-location from shuffled data (62.2cm ± 9.09cm, red). E) Across all five rats, the network (CNN) was more accurate than a machine learning baseline (SVM) and a Bayesian decoder (Bayesian) trained on action potentials. This was also true when the network was limited to high frequency components ( > 250Hz, CNN-Spikes). When only local frequencies were used (

    Journal: bioRxiv

    Article Title: Deepinsight: a general framework for interpreting wide-band neural activity

    doi: 10.1101/871848

    Figure Lengend Snippet: Accurate decoding of self-location from unprocessed hippocampal recordings. A) Top, a typical ‘raw’ extracellular recording from a single CA1 electrode. Bottom, wavelet decomposition of the same data, power shown for frequency bands from 2Hz to 15kHz (bottom to top row). B) At each timestep wavelet coefficients (64 time points, 26 frequency bands, 128 channels) were fed to a deep network consisting of 2D convolutional layers with shared weights, followed by a fully-connected layer with a regression head to decode self-location; schematic of architecture shown. C) Example trajectory from R2478, true position (black) and decoded position (blue) shown for 3s of data. Full test-set shown in Video 1 . D) Distribution of decoding errors from trial shown in (C), mean error (14.2cm ± 12.9cm, black), chance decoding of self-location from shuffled data (62.2cm ± 9.09cm, red). E) Across all five rats, the network (CNN) was more accurate than a machine learning baseline (SVM) and a Bayesian decoder (Bayesian) trained on action potentials. This was also true when the network was limited to high frequency components ( > 250Hz, CNN-Spikes). When only local frequencies were used (

    Article Snippet: Sections were then inspected using Olympus microscope and tetrode tracks reaching into CA1 pyramidal cell layer were verified.

    Techniques:

    Model generalizes across recording techniques and brain regions (A) Overview of auditory recording. We recorded electrophysiological signals while the mouse is freely moving inside a small enclosure and is presented with pure tone stimuli ranging from 4kHz to 64kHz. (B) R 2 -score for decoding of frequency tone from auditory cortex (0.73 ± 0.08), chance level is indicated by the red line. (C) An example section for decoding of auditory tone frequencies from auditory electrophysiological recordings, real tone colored in black, decoded tone in green, the line between real and decoded indicates magnitude of error. (D) Influence plots for decoding of auditory tone stimuli, same method as used for CA1 recordings. (E) Calcium recordings from rat running on a linear track in VR. We record from 685 cells and use Suite2p to preprocess the raw images and extract calcium traces which we feed through the model to decode linear position. (F) R 2 -score for decoding of linear position from two-photon CA1 recordings (0.90 ± 0.03), chance level is indicated by the red line. (G) Example trajectory through the virtual linear track (linearized to [− π, π ] with real position (black) and decoded position (orange)). (H) Influence plots for decoding of position from two-photon calcium imaging. Note that the range of frequencies is between 0Hz and 15Hz as the sampling rate of the calcium traces is 30Hz.

    Journal: bioRxiv

    Article Title: Deepinsight: a general framework for interpreting wide-band neural activity

    doi: 10.1101/871848

    Figure Lengend Snippet: Model generalizes across recording techniques and brain regions (A) Overview of auditory recording. We recorded electrophysiological signals while the mouse is freely moving inside a small enclosure and is presented with pure tone stimuli ranging from 4kHz to 64kHz. (B) R 2 -score for decoding of frequency tone from auditory cortex (0.73 ± 0.08), chance level is indicated by the red line. (C) An example section for decoding of auditory tone frequencies from auditory electrophysiological recordings, real tone colored in black, decoded tone in green, the line between real and decoded indicates magnitude of error. (D) Influence plots for decoding of auditory tone stimuli, same method as used for CA1 recordings. (E) Calcium recordings from rat running on a linear track in VR. We record from 685 cells and use Suite2p to preprocess the raw images and extract calcium traces which we feed through the model to decode linear position. (F) R 2 -score for decoding of linear position from two-photon CA1 recordings (0.90 ± 0.03), chance level is indicated by the red line. (G) Example trajectory through the virtual linear track (linearized to [− π, π ] with real position (black) and decoded position (orange)). (H) Influence plots for decoding of position from two-photon calcium imaging. Note that the range of frequencies is between 0Hz and 15Hz as the sampling rate of the calcium traces is 30Hz.

    Article Snippet: Sections were then inspected using Olympus microscope and tetrode tracks reaching into CA1 pyramidal cell layer were verified.

    Techniques: Imaging, Sampling

    Upregulation of gene expression for metabolic enzymes with aging. (a) Cumulative histograms for gene expression assays for selected enzymes in brain tissue samples collected from hippocampal CA1 region (stratum pyramidale) of young (black circles) and aged animals (white circles). Note the right‐shift of the distribution of RT‐PCR scores with aging in majority of investigated genes. See Section 2 for details. Abbreviations: Pygb , glycogen phosphorylase; Hk1 , hexokinase 1; Pfkp , phosphofructokinase platelet form; Pkm , pyruvate kinase; Ldha/b , lactate dehydrogenase a/b; Glul , glutamine synthetase. (b) Quantification of the results shown in (a). Asterisks indicate a statistically significant difference (* p

    Journal: Glia

    Article Title: Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle. Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle

    doi: 10.1002/glia.23319

    Figure Lengend Snippet: Upregulation of gene expression for metabolic enzymes with aging. (a) Cumulative histograms for gene expression assays for selected enzymes in brain tissue samples collected from hippocampal CA1 region (stratum pyramidale) of young (black circles) and aged animals (white circles). Note the right‐shift of the distribution of RT‐PCR scores with aging in majority of investigated genes. See Section 2 for details. Abbreviations: Pygb , glycogen phosphorylase; Hk1 , hexokinase 1; Pfkp , phosphofructokinase platelet form; Pkm , pyruvate kinase; Ldha/b , lactate dehydrogenase a/b; Glul , glutamine synthetase. (b) Quantification of the results shown in (a). Asterisks indicate a statistically significant difference (* p

    Article Snippet: 2.8 RNA isolation and cDNA synthesis From every individual hippocampal slice, the total mRNA within CA1 stratum pyramidale region was prepared separately according to the manual (Applied Biosystems, Waltham, Massachusetts, USA).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

    Cellular distribution of phosphofructokinase platelet form (Pfkp) and lactate dehydrogenase (Ldha) in the hippocampus of young and middle‐aged (“Old”) animals. (a and b) Exemplary confocal images of Pfkp immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pfkp immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note, that aging promotes an increase in Pfkp immunofluorescence in neuronal somata (SP), unlike region of dendritic trees (SR). (d and e) Exemplary confocal images of Ldha immunofluorescence (magenta) distribution within hippocampal CA1 region in young (d) and aged (e) animals acquired in conditions described in a and b. (f) Quantification of Ldha immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). All immunofluorescence was normalized to values obtained within stratum radiatum of young animals. Note, that aging is associated with a shift in Ldha cellular distribution from SP towards SR. Asterisks indicate a statistically significant difference ( p

    Journal: Glia

    Article Title: Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle. Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle

    doi: 10.1002/glia.23319

    Figure Lengend Snippet: Cellular distribution of phosphofructokinase platelet form (Pfkp) and lactate dehydrogenase (Ldha) in the hippocampus of young and middle‐aged (“Old”) animals. (a and b) Exemplary confocal images of Pfkp immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pfkp immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note, that aging promotes an increase in Pfkp immunofluorescence in neuronal somata (SP), unlike region of dendritic trees (SR). (d and e) Exemplary confocal images of Ldha immunofluorescence (magenta) distribution within hippocampal CA1 region in young (d) and aged (e) animals acquired in conditions described in a and b. (f) Quantification of Ldha immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). All immunofluorescence was normalized to values obtained within stratum radiatum of young animals. Note, that aging is associated with a shift in Ldha cellular distribution from SP towards SR. Asterisks indicate a statistically significant difference ( p

    Article Snippet: 2.8 RNA isolation and cDNA synthesis From every individual hippocampal slice, the total mRNA within CA1 stratum pyramidale region was prepared separately according to the manual (Applied Biosystems, Waltham, Massachusetts, USA).

    Techniques: Immunofluorescence

    Cellular distribution of pyruvate kinase (Pkm) in the hippocampus of young and middle‐aged (“Old”) animals. (a and b) Exemplary confocal images of Pkm immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pkm immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note that with age, Pkm immunofluorescence is significantly upregulated in both SR and SP layers. Asterisks indicate a statistically significant difference (* p

    Journal: Glia

    Article Title: Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle. Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle

    doi: 10.1002/glia.23319

    Figure Lengend Snippet: Cellular distribution of pyruvate kinase (Pkm) in the hippocampus of young and middle‐aged (“Old”) animals. (a and b) Exemplary confocal images of Pkm immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pkm immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note that with age, Pkm immunofluorescence is significantly upregulated in both SR and SP layers. Asterisks indicate a statistically significant difference (* p

    Article Snippet: 2.8 RNA isolation and cDNA synthesis From every individual hippocampal slice, the total mRNA within CA1 stratum pyramidale region was prepared separately according to the manual (Applied Biosystems, Waltham, Massachusetts, USA).

    Techniques: Immunofluorescence

    Cellular localization of glycogen phosphorylase (Pygb) and phosphoglucomutase 1 (Pgm) in hippocampus is altered with aging. (a–b) Exemplary confocal images of Pygb immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pygb immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note, that aging promotes an increase in Pygb immunofluorescence in both hippocampal layers. (d and e) Exemplary confocal images of Pgm immunofluorescence (magenta) distribution within hippocampal CA1 region in young (d) and aged (e) animals acquired in conditions described in a and b. (f) Quantification of Pgm immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). All immunofluorescence was normalized to values obtained within stratum radiatum of young animals. Note that with age, Pgm immunofluorescence declines in dendritic region of hippocampal CA1 region, but rises within neuronal somata. Asterisks indicate a statistically significant difference ( p

    Journal: Glia

    Article Title: Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle. Aging‐associated changes in hippocampal glycogen metabolism in mice. Evidence for and against astrocyte‐to‐neuron lactate shuttle

    doi: 10.1002/glia.23319

    Figure Lengend Snippet: Cellular localization of glycogen phosphorylase (Pygb) and phosphoglucomutase 1 (Pgm) in hippocampus is altered with aging. (a–b) Exemplary confocal images of Pygb immunofluorescence (magenta) distribution within hippocampal CA1 region in young (a) and aged (b) animals acquired at low (obj. 20×, upper panel) and high magnification (obj. 60×, bottom panels). Localization of neuronal somata, dendrites and nuclei was revealed with antibodies against microtubule‐associated protein 2 (Map2, green) and DAPI (blue), respectively. Abbreviations: SP, stratum pyramidale; SR, stratum radiatum. (c) Quantification of Pygb immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). Note, that aging promotes an increase in Pygb immunofluorescence in both hippocampal layers. (d and e) Exemplary confocal images of Pgm immunofluorescence (magenta) distribution within hippocampal CA1 region in young (d) and aged (e) animals acquired in conditions described in a and b. (f) Quantification of Pgm immunofluorescence in hippocampal slices of young (black bars) and old animals (gray bars). All immunofluorescence was normalized to values obtained within stratum radiatum of young animals. Note that with age, Pgm immunofluorescence declines in dendritic region of hippocampal CA1 region, but rises within neuronal somata. Asterisks indicate a statistically significant difference ( p

    Article Snippet: 2.8 RNA isolation and cDNA synthesis From every individual hippocampal slice, the total mRNA within CA1 stratum pyramidale region was prepared separately according to the manual (Applied Biosystems, Waltham, Massachusetts, USA).

    Techniques: Immunofluorescence

    Cell apoptosis in the rat hippocampal CA1 region (TUNEL staining, × 200). Apoptotic cells with brown or yellow nuclei are visible in the model and Dickkopf-1 groups at various time points (arrows). Fewer apoptotic cells with weak staining are observed in the Dickkopf-1 group, compared with the model group, at corresponding time points.

    Journal: Neural Regeneration Research

    Article Title: Involvement of the Wnt signaling pathway and cell apoptosis in the rat hippocampus following cerebral ischemia/reperfusion injury ★

    doi: 10.3969/j.issn.1673-5374.2013.01.009

    Figure Lengend Snippet: Cell apoptosis in the rat hippocampal CA1 region (TUNEL staining, × 200). Apoptotic cells with brown or yellow nuclei are visible in the model and Dickkopf-1 groups at various time points (arrows). Fewer apoptotic cells with weak staining are observed in the Dickkopf-1 group, compared with the model group, at corresponding time points.

    Article Snippet: TUNEL staining to determine cell apoptosis in the rat hippocampal CA1 region TUNEL staining was performed in accordance with a kit (Beijing Zhong Shan-Golden Bridge Biological Technology Co., Ltd., Beijing, China), with sections developed using 3,3’-diaminobenzidine (Maixin-Bio, Fuzhou, Fujian Province, China), and counterstained in hematoxylin.

    Techniques: TUNEL Assay, Staining

    Simulations of diffusion in the ECS of the CA1 hippocampus in WT and Has3 −/− mice. In these simulations, informed by our results on ECS parameters in individual layers, molecules were released for 1 ms from point sources in the center

    Journal: The Journal of Neuroscience

    Article Title: Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space

    doi: 10.1523/JNEUROSCI.3458-13.2014

    Figure Lengend Snippet: Simulations of diffusion in the ECS of the CA1 hippocampus in WT and Has3 −/− mice. In these simulations, informed by our results on ECS parameters in individual layers, molecules were released for 1 ms from point sources in the center

    Article Snippet: Dex3 distribution in the hippocampal CA1 region was imaged with a CCD camera (QuantEM 512SC, Photometrics).

    Techniques: Diffusion-based Assay, Mouse Assay, Mass Spectrometry

    ECS is reduced in the CA1 stratum pyramidale in Has3 −/− mice. A , Transit of extracellular marker molecules through the CA1 stratum pyramidale. Fluorescently labeled extracellular marker dex3 was released by a short puff from a glass micropipette

    Journal: The Journal of Neuroscience

    Article Title: Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space

    doi: 10.1523/JNEUROSCI.3458-13.2014

    Figure Lengend Snippet: ECS is reduced in the CA1 stratum pyramidale in Has3 −/− mice. A , Transit of extracellular marker molecules through the CA1 stratum pyramidale. Fluorescently labeled extracellular marker dex3 was released by a short puff from a glass micropipette

    Article Snippet: Dex3 distribution in the hippocampal CA1 region was imaged with a CCD camera (QuantEM 512SC, Photometrics).

    Techniques: Mouse Assay, Marker, Labeling

    Increased cell packing in the CA1 stratum pyramidale of Has3 −/− mice. A , NeuN immunostaining of the hippocampus of Has3 −/− mice and WT littermates. Low-magnification views of hippocampus (left). Scale bar, 200 μm.

    Journal: The Journal of Neuroscience

    Article Title: Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space

    doi: 10.1523/JNEUROSCI.3458-13.2014

    Figure Lengend Snippet: Increased cell packing in the CA1 stratum pyramidale of Has3 −/− mice. A , NeuN immunostaining of the hippocampus of Has3 −/− mice and WT littermates. Low-magnification views of hippocampus (left). Scale bar, 200 μm.

    Article Snippet: Dex3 distribution in the hippocampal CA1 region was imaged with a CCD camera (QuantEM 512SC, Photometrics).

    Techniques: Mouse Assay, Immunostaining

    Spontaneous epileptiform activity in the CA1 region of Has3 −/− hippocampus. A , Extracellular field potential recordings in the stratum pyramidale of CA1 hippocampus in brain slices from WT and Has3 −/− mice. No activity

    Journal: The Journal of Neuroscience

    Article Title: Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space

    doi: 10.1523/JNEUROSCI.3458-13.2014

    Figure Lengend Snippet: Spontaneous epileptiform activity in the CA1 region of Has3 −/− hippocampus. A , Extracellular field potential recordings in the stratum pyramidale of CA1 hippocampus in brain slices from WT and Has3 −/− mice. No activity

    Article Snippet: Dex3 distribution in the hippocampal CA1 region was imaged with a CCD camera (QuantEM 512SC, Photometrics).

    Techniques: Activity Assay, Mouse Assay

    Simultaneous intracellular and field potential recordings in the CA1 region of the Has3 −/− hippocampus. A – C , Tracings illustrate the range of excitatory activity seen in CA1 stratum pyramidale neurons coincident with the spontaneous

    Journal: The Journal of Neuroscience

    Article Title: Hyaluronan Deficiency Due to Has3 Knock-Out Causes Altered Neuronal Activity and Seizures via Reduction in Brain Extracellular Space

    doi: 10.1523/JNEUROSCI.3458-13.2014

    Figure Lengend Snippet: Simultaneous intracellular and field potential recordings in the CA1 region of the Has3 −/− hippocampus. A – C , Tracings illustrate the range of excitatory activity seen in CA1 stratum pyramidale neurons coincident with the spontaneous

    Article Snippet: Dex3 distribution in the hippocampal CA1 region was imaged with a CCD camera (QuantEM 512SC, Photometrics).

    Techniques: Activity Assay

    Optogenetic activation of PV+ interneurons had no effect on impaired theta oscillation of AβO-injected PV-Cre mice (A) Schematic illustration of micro-injection of AβO and ChR2 virus into hippocampal CA1 region of PV-Cre mice. (B) Fluorescence image of ChR2 expressed PV+ interneurons in hippocampal CA1 region. Individual neurons are pointed by white arrows. (C) Schematic illustration of in vivo recording. (D) Example traces of spontaneous theta-filtered LFP signals (top) and spectrogram (bottom) recorded in control PV-Cre mice (left) and AβO-injected PV-Cre mice (right). The 3 s-long blue light stimulation of PV+ interneuron s is represented by light blue shaded region. (E) Example traces of PSD curves obtained from the spontaneous theta oscillation recorded in control PV-Cre mice (black), AβO-injected PV-Cre mice (red) and AβO-injected PV-Cre mice with blue light (blue). (F-G) Mean peak frequency (F) and mean peak power (G) of spontaneous theta-filtered LFP signals of control PV-Cre mice (black, n = 5), AβO-injected PV-Cre mice (red, n = 5) and AβO-injected PV-Cre mice with blue light (blue, n = 5). All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ p

    Journal: bioRxiv

    Article Title: Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomers in vivo

    doi: 10.1101/465112

    Figure Lengend Snippet: Optogenetic activation of PV+ interneurons had no effect on impaired theta oscillation of AβO-injected PV-Cre mice (A) Schematic illustration of micro-injection of AβO and ChR2 virus into hippocampal CA1 region of PV-Cre mice. (B) Fluorescence image of ChR2 expressed PV+ interneurons in hippocampal CA1 region. Individual neurons are pointed by white arrows. (C) Schematic illustration of in vivo recording. (D) Example traces of spontaneous theta-filtered LFP signals (top) and spectrogram (bottom) recorded in control PV-Cre mice (left) and AβO-injected PV-Cre mice (right). The 3 s-long blue light stimulation of PV+ interneuron s is represented by light blue shaded region. (E) Example traces of PSD curves obtained from the spontaneous theta oscillation recorded in control PV-Cre mice (black), AβO-injected PV-Cre mice (red) and AβO-injected PV-Cre mice with blue light (blue). (F-G) Mean peak frequency (F) and mean peak power (G) of spontaneous theta-filtered LFP signals of control PV-Cre mice (black, n = 5), AβO-injected PV-Cre mice (red, n = 5) and AβO-injected PV-Cre mice with blue light (blue, n = 5). All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ p

    Article Snippet: 3 μL of AβO1-42 (10 μM) ( ) and 1 μL of AAV5-EF1a-DIO-hChR2-mCherry were delivered into the hippocampal CA1 region through 5 μL micro-needle (Hamilton Company) connected to a motorized stereotaxic injector (Stoelting Co.) at the rate of 0.3 μL/min and 0.1 μL/min, respectively.

    Techniques: Activation Assay, Injection, Mouse Assay, Fluorescence, In Vivo

    AβO causes selective synaptic dysfunction of SST+ interneuron inputs to CA1 pyramidal neuron at theta-frequency (A) Schematic illustration of voltage-clamp recording of inhibitory postsynaptic current (IPSC) evoked by optical stimulation of SST+ interneuron (IPSC SST ) in CA1 pyramidal neuron using blue light. (B) Example traces of IPSC SST evoked by blue light stimulation at 5 Hz in DMSO-treated slice (control, top, black) and AβO-treated slice (AβO, bottom, red). (C) Short-term plasticity of IPSC SST in control (black) and AβO slices (red, two-way ANOVA, control: n = 13, AβO: n = 8). (D) Schematic illustration of voltage-clamp recording of PV+ interneuron-driven IPSC (IPSC PV ) onto CA1 pyramidal neuron using blue light stimulation. (E) Example traces of IPSC PV by blue light stimulation at 5 Hz in the control (top, black) and AβO slice (bottom, red). (F) Short-term plasticity of IPSC PV in control (black) and AβO slices (red, two-way ANOVA, control: n = 4, AβO: n = 7). All data represent mean ± SEM. Inset: ### p

    Journal: bioRxiv

    Article Title: Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomers in vivo

    doi: 10.1101/465112

    Figure Lengend Snippet: AβO causes selective synaptic dysfunction of SST+ interneuron inputs to CA1 pyramidal neuron at theta-frequency (A) Schematic illustration of voltage-clamp recording of inhibitory postsynaptic current (IPSC) evoked by optical stimulation of SST+ interneuron (IPSC SST ) in CA1 pyramidal neuron using blue light. (B) Example traces of IPSC SST evoked by blue light stimulation at 5 Hz in DMSO-treated slice (control, top, black) and AβO-treated slice (AβO, bottom, red). (C) Short-term plasticity of IPSC SST in control (black) and AβO slices (red, two-way ANOVA, control: n = 13, AβO: n = 8). (D) Schematic illustration of voltage-clamp recording of PV+ interneuron-driven IPSC (IPSC PV ) onto CA1 pyramidal neuron using blue light stimulation. (E) Example traces of IPSC PV by blue light stimulation at 5 Hz in the control (top, black) and AβO slice (bottom, red). (F) Short-term plasticity of IPSC PV in control (black) and AβO slices (red, two-way ANOVA, control: n = 4, AβO: n = 7). All data represent mean ± SEM. Inset: ### p

    Article Snippet: 3 μL of AβO1-42 (10 μM) ( ) and 1 μL of AAV5-EF1a-DIO-hChR2-mCherry were delivered into the hippocampal CA1 region through 5 μL micro-needle (Hamilton Company) connected to a motorized stereotaxic injector (Stoelting Co.) at the rate of 0.3 μL/min and 0.1 μL/min, respectively.

    Techniques:

    Optogenetic activation of SST+ interneurons restores phase-locking of CA1 pyramidal neurons relative to theta oscillation in AβO-injected PV-Cre mice (A) Classification (left) of putative CA1 pyramidal neurons (black) and putative CA1 interneurons (gray) based on spike waveform asymmetry ([(b-a)/(b+a)]) to the trough-to-peak latency (c), and an example spike waveform of CA1 pyramidal neuron (right). (B) Peri-stimulus histogram (PSTH, top) and raster plot (bottom) of SST+ interneuron (left) and PV+ interneuron (right) during blue light stimulation (+blue light). (C) Probability distribution of spike time to theta phase (spike phase, top), raster plot (middle), and polar plot showing spike phases and vector lengths in control SST-Cre mice (black), AβO-injected SST-Cre mice (red), and AβO-injected SST-Cre mice with blue light (blue). (D-E) Circular average of spike phases (D) and mean vector length of spike phase probability (E) in control SST-Cre mice (black), AβO-injected SST-Cre mice (red), and AβO-injected SST-Cre mice with blue light (blue). (G-I) Same as (D-F) but in PV-Cre mice. All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ , # p

    Journal: bioRxiv

    Article Title: Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomers in vivo

    doi: 10.1101/465112

    Figure Lengend Snippet: Optogenetic activation of SST+ interneurons restores phase-locking of CA1 pyramidal neurons relative to theta oscillation in AβO-injected PV-Cre mice (A) Classification (left) of putative CA1 pyramidal neurons (black) and putative CA1 interneurons (gray) based on spike waveform asymmetry ([(b-a)/(b+a)]) to the trough-to-peak latency (c), and an example spike waveform of CA1 pyramidal neuron (right). (B) Peri-stimulus histogram (PSTH, top) and raster plot (bottom) of SST+ interneuron (left) and PV+ interneuron (right) during blue light stimulation (+blue light). (C) Probability distribution of spike time to theta phase (spike phase, top), raster plot (middle), and polar plot showing spike phases and vector lengths in control SST-Cre mice (black), AβO-injected SST-Cre mice (red), and AβO-injected SST-Cre mice with blue light (blue). (D-E) Circular average of spike phases (D) and mean vector length of spike phase probability (E) in control SST-Cre mice (black), AβO-injected SST-Cre mice (red), and AβO-injected SST-Cre mice with blue light (blue). (G-I) Same as (D-F) but in PV-Cre mice. All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ , # p

    Article Snippet: 3 μL of AβO1-42 (10 μM) ( ) and 1 μL of AAV5-EF1a-DIO-hChR2-mCherry were delivered into the hippocampal CA1 region through 5 μL micro-needle (Hamilton Company) connected to a motorized stereotaxic injector (Stoelting Co.) at the rate of 0.3 μL/min and 0.1 μL/min, respectively.

    Techniques: Activation Assay, Injection, Mouse Assay, Plasmid Preparation

    Optogenetic activation of SST+ interneurons in AβO-injected SST-Cre mice restored impaired hippocampal theta oscillation (A) Schematic illustration of micro-injection of AβO and ChR2 virus into hippocampal CA1 region of SST-Cre mice. (B) Schematic illustration of hippocampal structure (left) and immunofluorescence image of AβO pointed by white arrows (right). (C) Fluorescence image of ChR2 expressed SST+ interneuron s in hippocampal CA1 region. Individual neurons are pointed by white arrows. (D) Schematic illustration of in vivo recording. (E) The recording location marked with Alexa 594 fluorescent dye and channel mapping of 32-channel silicon probe aligning with the Alexa 594 staining. The electrode crossed through stratum oriens (SO), stratum pyramidale (SP), stratum radiatum (SR) and stratum lacunosum-moleculare (SL-M) in CA1 area. (F) Example traces of spontaneous theta-filtered LFP signals (top) and spectrogram (bottom) recorded in control SST-Cre mice (left) and AβO-injected SST-Cre mice (right). The 3 s-long blue light stimulation of SST+ interneurons is represented by shaded region (light blue). (G) Example traces of power spectrum density (PSD) curves obtained from the spontaneous theta-filtered LFP signals recorded in control SST-Cre mice (black), AβO-injected SST-Cre mice (red) and AβO-injected SST-Cre mice with blue light (blue). (H-I) Mean peak frequency (H) and mean peak power (I) of spontaneous theta-filtered LFP signals of control SST-Cre mice (black, n = 5), AβO-injected SST-Cre mice (red, n = 9) and AβO-injected SST-Cre mice with blue light (blue, n = 9). All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ p

    Journal: bioRxiv

    Article Title: Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomers in vivo

    doi: 10.1101/465112

    Figure Lengend Snippet: Optogenetic activation of SST+ interneurons in AβO-injected SST-Cre mice restored impaired hippocampal theta oscillation (A) Schematic illustration of micro-injection of AβO and ChR2 virus into hippocampal CA1 region of SST-Cre mice. (B) Schematic illustration of hippocampal structure (left) and immunofluorescence image of AβO pointed by white arrows (right). (C) Fluorescence image of ChR2 expressed SST+ interneuron s in hippocampal CA1 region. Individual neurons are pointed by white arrows. (D) Schematic illustration of in vivo recording. (E) The recording location marked with Alexa 594 fluorescent dye and channel mapping of 32-channel silicon probe aligning with the Alexa 594 staining. The electrode crossed through stratum oriens (SO), stratum pyramidale (SP), stratum radiatum (SR) and stratum lacunosum-moleculare (SL-M) in CA1 area. (F) Example traces of spontaneous theta-filtered LFP signals (top) and spectrogram (bottom) recorded in control SST-Cre mice (left) and AβO-injected SST-Cre mice (right). The 3 s-long blue light stimulation of SST+ interneurons is represented by shaded region (light blue). (G) Example traces of power spectrum density (PSD) curves obtained from the spontaneous theta-filtered LFP signals recorded in control SST-Cre mice (black), AβO-injected SST-Cre mice (red) and AβO-injected SST-Cre mice with blue light (blue). (H-I) Mean peak frequency (H) and mean peak power (I) of spontaneous theta-filtered LFP signals of control SST-Cre mice (black, n = 5), AβO-injected SST-Cre mice (red, n = 9) and AβO-injected SST-Cre mice with blue light (blue, n = 9). All data represent mean ± SEM. Inset: N.S. p > 0.05, ∗ p

    Article Snippet: 3 μL of AβO1-42 (10 μM) ( ) and 1 μL of AAV5-EF1a-DIO-hChR2-mCherry were delivered into the hippocampal CA1 region through 5 μL micro-needle (Hamilton Company) connected to a motorized stereotaxic injector (Stoelting Co.) at the rate of 0.3 μL/min and 0.1 μL/min, respectively.

    Techniques: Activation Assay, Injection, Mouse Assay, Immunofluorescence, Fluorescence, In Vivo, Staining

    GRAB Ado sensors reveal somatodendritic Ado release in hippocampal slices. (A1) Left panel: sparse expression of Ado1.0 in cultured hippocampal pyramidal neurons. Right panel: fluorescence images and pseudocolor images of Ado1.0 ΔF/F 0 in the somatodendritic (purple box) and axonal (blue box) compartments in response to field stimuli (30 Hz, 100 pulses), high K + , or Ado (100 nM); scale bar, 50 μm. Example traces and summary data are shown in (A2) and (A3) , respectively; n = 11-21 ROIs from 4 coverslips per group. (B) Schematic illustration depicting the strategy used to image acute hippocampal brain slices prepared from mice expressing Ado1.0med and tdTomato-ChrimsonR in the CA1 region while using a 633-nm laser to activate the neurons. At the right is an image showing Ado1.0med fluorescence; the box shows the region magnified in (C) . (C) Magnified fluorescence images of the CA1 region showing Ado1.0med (green) and tdTomato-ChrimsonR (red) in CA1 regions (scale bar, 100 μm). The pyramidal cell layer (Str. py) is located between the stratum oriens (Str. ori) and stratum radiatum (Str. rad). (D) Pseudocolor images (left), averaged traces (middle), and group summary (right) of Ado1.0med ΔF/F 0 in response to 633-nm laser pulses applied at 20 Hz for the indicated duration (scale bar, 100 μm); the solid line shown in the right panel a linear fit to the data; n = 6 slices from 4 mice. (E) Blocking L-type VGCCs inhibits optogenetically induced Ado release. Where indicated, nimodipine (Nim, 20 μM) and Cd 2+ (100 μM) were applied (scale bar, 100 μm); n = 5 slices from 3 mice. (F) Blocking ENT transporters inhibits optogenetically induced Ado release. Where indicated, dipyridamole (DIPY, 20 μM) was used to block ENTs. Averaged traces (F1) and the group summary (F2) of Ado1.0med ΔF/F 0 are shown; n = 4 slices from 3 mice. (G) Model depicting the novel mode of neuronal activity–dependent Ado release from hippocampal neurons. Ado is released slowly from the postsynaptic membrane via a vesicle-independent, ENT-dependent mechanism, serving as a putative retrograde signal to regulate presynaptic activity. This activity-dependent release of Ado requires L-type voltage-gated Ca 2+ channels (VGCCs). In contrast, classic neurotransmitters such as glutamate (Glu) are released from presynaptic vesicles requires P/Q-type and N-type VGCCs. AdoR, adenosine receptor; ENTs, equilibrative nucleoside transporters; Syts, synaptotagmins.

    Journal: bioRxiv

    Article Title: A GRAB sensor reveals activity-dependent non-vesicular somatodendritic adenosine release

    doi: 10.1101/2020.05.04.075564

    Figure Lengend Snippet: GRAB Ado sensors reveal somatodendritic Ado release in hippocampal slices. (A1) Left panel: sparse expression of Ado1.0 in cultured hippocampal pyramidal neurons. Right panel: fluorescence images and pseudocolor images of Ado1.0 ΔF/F 0 in the somatodendritic (purple box) and axonal (blue box) compartments in response to field stimuli (30 Hz, 100 pulses), high K + , or Ado (100 nM); scale bar, 50 μm. Example traces and summary data are shown in (A2) and (A3) , respectively; n = 11-21 ROIs from 4 coverslips per group. (B) Schematic illustration depicting the strategy used to image acute hippocampal brain slices prepared from mice expressing Ado1.0med and tdTomato-ChrimsonR in the CA1 region while using a 633-nm laser to activate the neurons. At the right is an image showing Ado1.0med fluorescence; the box shows the region magnified in (C) . (C) Magnified fluorescence images of the CA1 region showing Ado1.0med (green) and tdTomato-ChrimsonR (red) in CA1 regions (scale bar, 100 μm). The pyramidal cell layer (Str. py) is located between the stratum oriens (Str. ori) and stratum radiatum (Str. rad). (D) Pseudocolor images (left), averaged traces (middle), and group summary (right) of Ado1.0med ΔF/F 0 in response to 633-nm laser pulses applied at 20 Hz for the indicated duration (scale bar, 100 μm); the solid line shown in the right panel a linear fit to the data; n = 6 slices from 4 mice. (E) Blocking L-type VGCCs inhibits optogenetically induced Ado release. Where indicated, nimodipine (Nim, 20 μM) and Cd 2+ (100 μM) were applied (scale bar, 100 μm); n = 5 slices from 3 mice. (F) Blocking ENT transporters inhibits optogenetically induced Ado release. Where indicated, dipyridamole (DIPY, 20 μM) was used to block ENTs. Averaged traces (F1) and the group summary (F2) of Ado1.0med ΔF/F 0 are shown; n = 4 slices from 3 mice. (G) Model depicting the novel mode of neuronal activity–dependent Ado release from hippocampal neurons. Ado is released slowly from the postsynaptic membrane via a vesicle-independent, ENT-dependent mechanism, serving as a putative retrograde signal to regulate presynaptic activity. This activity-dependent release of Ado requires L-type voltage-gated Ca 2+ channels (VGCCs). In contrast, classic neurotransmitters such as glutamate (Glu) are released from presynaptic vesicles requires P/Q-type and N-type VGCCs. AdoR, adenosine receptor; ENTs, equilibrative nucleoside transporters; Syts, synaptotagmins.

    Article Snippet: For electrical stimulation, a bipolar electrode (cat. number WE30031.0A3, MicroProbes for Life Science) was positioned near the CA1 stratum radiatum using fluorescence guidance.

    Techniques: Expressing, Cell Culture, Fluorescence, Mouse Assay, Blocking Assay, Activity Assay

    Ryk is required for oligomeric Aβ -mediated synapse loss in vivo . a, Timeline and schematic of intracerebroventricular infusion of the Ryk monoclonal antibody. Cannula and pre-infused osmotic minipumps were implanted at ∼2 months old. Minipumps were removed 2 weeks later. b-c, Staining and quantification of glutamatergic synapses in 5XFAD mice infused with the Ryk monoclonal antibody. d, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 and CA3 regions of the hippocampus bilaterally. 2 weeks later, Aβ oligomers were injected into the lateral ventricular for 5 days. 5 days later, animals were fixed with perfusion and sectioning and stained with synaptic markers. e-f, Representative images and quantification of synaptic puncta detected by costaining for Bassoon (red)- and PSD95 (green)-immunoreactive (arrowheads) in stratum radiatum. n=4 for Ryk +/+ mice, n=3 for Ryk +/+ mice with oligomeric Aβ injection, n=3 for Ryk cKO mice and n=3 for Ryk cKO mice with oligomeric Aβ injection. * P

    Journal: bioRxiv

    Article Title: Protecting synapses from amyloid β-associated degeneration by manipulations of Wnt/planar cell polarity signaling

    doi: 10.1101/2020.09.09.273011

    Figure Lengend Snippet: Ryk is required for oligomeric Aβ -mediated synapse loss in vivo . a, Timeline and schematic of intracerebroventricular infusion of the Ryk monoclonal antibody. Cannula and pre-infused osmotic minipumps were implanted at ∼2 months old. Minipumps were removed 2 weeks later. b-c, Staining and quantification of glutamatergic synapses in 5XFAD mice infused with the Ryk monoclonal antibody. d, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 and CA3 regions of the hippocampus bilaterally. 2 weeks later, Aβ oligomers were injected into the lateral ventricular for 5 days. 5 days later, animals were fixed with perfusion and sectioning and stained with synaptic markers. e-f, Representative images and quantification of synaptic puncta detected by costaining for Bassoon (red)- and PSD95 (green)-immunoreactive (arrowheads) in stratum radiatum. n=4 for Ryk +/+ mice, n=3 for Ryk +/+ mice with oligomeric Aβ injection, n=3 for Ryk cKO mice and n=3 for Ryk cKO mice with oligomeric Aβ injection. * P

    Article Snippet: To test whether Vangl2 is required for Aβ oligomers-induced synapse loss in vivo and in adulthood, we first injected AAV1-hSyn-eGFP-Cre into the hippocampal CA1 region of Vangl2 +/+ (Control) and Vangl2 fl/fl mice at the age of 2 months.

    Techniques: In Vivo, Staining, Mouse Assay, Injection

    Function blocking Ryk antibody and Ryk cKO can prevent synapse loss and preserve cognitive function in 5XFAD mice a , Schematics for timeline and experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 and CA3 region of the hippocampus bilaterally. Animals were fixed with perfusion and sectioning and stained with synaptic markers at 4 months of age. A separate set of animals were injected and subjected to NOR at 6 months of age. b-c, Representative images and quantification of synapse numbers. d, Quantification of Celsr3-positive glutamatergic synapse (Celsr3 colocalized with PSD95 and bassoon). e, Schematic showing the design of novel object recognition (NOR). Mice were subjected to an open arena for three trails to evaluate the memory of objects. f, Trajectories of mice in the NOR test session. g, Quantification of locomotion. h, Quantification of NOR. Student t -test. i, Schematic diagram showing the balance of Wnt/PCP signaling in synapse maintenance and the binding site of oligomeric Aβ. * P

    Journal: bioRxiv

    Article Title: Protecting synapses from amyloid β-associated degeneration by manipulations of Wnt/planar cell polarity signaling

    doi: 10.1101/2020.09.09.273011

    Figure Lengend Snippet: Function blocking Ryk antibody and Ryk cKO can prevent synapse loss and preserve cognitive function in 5XFAD mice a , Schematics for timeline and experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 and CA3 region of the hippocampus bilaterally. Animals were fixed with perfusion and sectioning and stained with synaptic markers at 4 months of age. A separate set of animals were injected and subjected to NOR at 6 months of age. b-c, Representative images and quantification of synapse numbers. d, Quantification of Celsr3-positive glutamatergic synapse (Celsr3 colocalized with PSD95 and bassoon). e, Schematic showing the design of novel object recognition (NOR). Mice were subjected to an open arena for three trails to evaluate the memory of objects. f, Trajectories of mice in the NOR test session. g, Quantification of locomotion. h, Quantification of NOR. Student t -test. i, Schematic diagram showing the balance of Wnt/PCP signaling in synapse maintenance and the binding site of oligomeric Aβ. * P

    Article Snippet: To test whether Vangl2 is required for Aβ oligomers-induced synapse loss in vivo and in adulthood, we first injected AAV1-hSyn-eGFP-Cre into the hippocampal CA1 region of Vangl2 +/+ (Control) and Vangl2 fl/fl mice at the age of 2 months.

    Techniques: Blocking Assay, Mouse Assay, Injection, Staining, Binding Assay

    Localization of Wnt/PCP signaling components in glutamatergic synapses in adult hippocampus and requirement of Vangl2 for synapse loss in the 5XFAD mice. a , Costaining of Vangl2 (Green) and Celsr3 (Green) with postsynaptic markers, PSD-95 (Red) and presynaptic mater bassoon (Red). Arrows indicate colocalized puncta. SR, stratum radiatum; SP, stratum pyramidale. b, Schematic diagram showing the distribution of the Wnt/PCP signaling components in glutamatergic synapses. c-f, Expression levels of Celsr3, Ryk and Vangl2 in the P2 synaptosome fraction for adult hippocampus in control and 5XFAD transgenic mice. Student t -test. g, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 region of the hippocampus bilaterally. 2 months later, animals were fixed with perfusion and sectioning and stained with synaptic markers. h, Vangl2 protein level in total protein extracts from hippocampi injected with AAV1-hSyn-eGFP-Cre virus. i, Representative images of costaining for Bassoon (red)- and PSD95 (green)- (arrowheads indicate colocalization) in the stratum radiatum. j, quantification of (I). n=5 for control mice, n=3 for Vangl2 cKO mice, n=4 for 5XFAD mice and n=8 for 5XFAD ; Vangl2 cKO mice. One-way ANOVA. * P

    Journal: bioRxiv

    Article Title: Protecting synapses from amyloid β-associated degeneration by manipulations of Wnt/planar cell polarity signaling

    doi: 10.1101/2020.09.09.273011

    Figure Lengend Snippet: Localization of Wnt/PCP signaling components in glutamatergic synapses in adult hippocampus and requirement of Vangl2 for synapse loss in the 5XFAD mice. a , Costaining of Vangl2 (Green) and Celsr3 (Green) with postsynaptic markers, PSD-95 (Red) and presynaptic mater bassoon (Red). Arrows indicate colocalized puncta. SR, stratum radiatum; SP, stratum pyramidale. b, Schematic diagram showing the distribution of the Wnt/PCP signaling components in glutamatergic synapses. c-f, Expression levels of Celsr3, Ryk and Vangl2 in the P2 synaptosome fraction for adult hippocampus in control and 5XFAD transgenic mice. Student t -test. g, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 region of the hippocampus bilaterally. 2 months later, animals were fixed with perfusion and sectioning and stained with synaptic markers. h, Vangl2 protein level in total protein extracts from hippocampi injected with AAV1-hSyn-eGFP-Cre virus. i, Representative images of costaining for Bassoon (red)- and PSD95 (green)- (arrowheads indicate colocalization) in the stratum radiatum. j, quantification of (I). n=5 for control mice, n=3 for Vangl2 cKO mice, n=4 for 5XFAD mice and n=8 for 5XFAD ; Vangl2 cKO mice. One-way ANOVA. * P

    Article Snippet: To test whether Vangl2 is required for Aβ oligomers-induced synapse loss in vivo and in adulthood, we first injected AAV1-hSyn-eGFP-Cre into the hippocampal CA1 region of Vangl2 +/+ (Control) and Vangl2 fl/fl mice at the age of 2 months.

    Techniques: Mouse Assay, Expressing, Transgenic Assay, Injection, Staining

    Vangl2 is required for Aβ oligomer-induced synapse loss in vitro and in vivo . a, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was added to hippocampal neuron cultures on DIV7 for 7 days and then oligomeric Aβ42 was added. 12 hours later after adding oligomeric Aβ42, cultures were fixed for staining synaptic markers. b, Western blot showing the level of Celsr3 and Vangl2 proteins in cultures infected with the AAV1-hSyn-eGFP-Cre virus. c, Immunostaining for pre-(green) and postsynaptic (red) puncta of glutamatergic synapses (arrowheads) in 14-DIV hippocampal cultures from littermate Vangl2 +/+ or Vangl2 fl/fl with or without oligomeric Aβ42. d, Quantification of ( c ). n=3 for Vangl2 +/+ mice, n=4 for Vangl2 fl/fl from 3 independent experiments. e, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 region of the hippocampus bilaterally. 2 weeks later, oligomeric Aβ was injected into cerebroventricular. 5 days after Aβ oligomer injection, animals were fixed with perfusion and sectioning and stained with synaptic markers. f, Vangl2 protein level in the total hippocampus extract from animals injected with the AAV1- hSyn-eGFP-Cre virus. g, Representative images of Bassoon (red)- and PSD95 (green)- immunoreactive puncta (arrowheads) in stratum radiatum of Vangl2 +/+ and Vangl2 fl/fl hippocampus (CA1) with or without oligomeric Aβ injection and quantification of synapse numbers. h, Quantification of ( g ). One-way ANOVA. n=8 of Vangl2 +/+ mice, n=3 of Vangl2 +/+ mice with oligomeric Aβ injection, n=6 of Vangl2 fl/fl mice and n=5 of Vangl2 fl/fl mice with oligomeric Aβ injection. * P

    Journal: bioRxiv

    Article Title: Protecting synapses from amyloid β-associated degeneration by manipulations of Wnt/planar cell polarity signaling

    doi: 10.1101/2020.09.09.273011

    Figure Lengend Snippet: Vangl2 is required for Aβ oligomer-induced synapse loss in vitro and in vivo . a, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was added to hippocampal neuron cultures on DIV7 for 7 days and then oligomeric Aβ42 was added. 12 hours later after adding oligomeric Aβ42, cultures were fixed for staining synaptic markers. b, Western blot showing the level of Celsr3 and Vangl2 proteins in cultures infected with the AAV1-hSyn-eGFP-Cre virus. c, Immunostaining for pre-(green) and postsynaptic (red) puncta of glutamatergic synapses (arrowheads) in 14-DIV hippocampal cultures from littermate Vangl2 +/+ or Vangl2 fl/fl with or without oligomeric Aβ42. d, Quantification of ( c ). n=3 for Vangl2 +/+ mice, n=4 for Vangl2 fl/fl from 3 independent experiments. e, Schematics illustrating the experimental design. AAV1-hSyn-eGFP-Cre virus was injected into CA1 region of the hippocampus bilaterally. 2 weeks later, oligomeric Aβ was injected into cerebroventricular. 5 days after Aβ oligomer injection, animals were fixed with perfusion and sectioning and stained with synaptic markers. f, Vangl2 protein level in the total hippocampus extract from animals injected with the AAV1- hSyn-eGFP-Cre virus. g, Representative images of Bassoon (red)- and PSD95 (green)- immunoreactive puncta (arrowheads) in stratum radiatum of Vangl2 +/+ and Vangl2 fl/fl hippocampus (CA1) with or without oligomeric Aβ injection and quantification of synapse numbers. h, Quantification of ( g ). One-way ANOVA. n=8 of Vangl2 +/+ mice, n=3 of Vangl2 +/+ mice with oligomeric Aβ injection, n=6 of Vangl2 fl/fl mice and n=5 of Vangl2 fl/fl mice with oligomeric Aβ injection. * P

    Article Snippet: To test whether Vangl2 is required for Aβ oligomers-induced synapse loss in vivo and in adulthood, we first injected AAV1-hSyn-eGFP-Cre into the hippocampal CA1 region of Vangl2 +/+ (Control) and Vangl2 fl/fl mice at the age of 2 months.

    Techniques: In Vitro, In Vivo, Staining, Western Blot, Infection, Immunostaining, Mouse Assay, Injection

    The effect of Arc overexpression or knockdown on hippocampal neuronal densities in 2VO rats treated with 0.4 mg/kg DSS. The top part of the figure shows the Nissl staining of the DG per animal group. The bottom part shows the neuronal density quantifications in the CA1 region per group. Bars represent mean ± SD for sample replications ( n = 10). ∗ p

    Journal: Frontiers in Neuroscience

    Article Title: 3′-Daidzein Sulfonate Sodium Protects Against Chronic Cerebral Hypoperfusion-Mediated Cognitive Impairment and Hippocampal Damage via Activity-Regulated Cytoskeleton-Associated Protein Upregulation

    doi: 10.3389/fnins.2019.00104

    Figure Lengend Snippet: The effect of Arc overexpression or knockdown on hippocampal neuronal densities in 2VO rats treated with 0.4 mg/kg DSS. The top part of the figure shows the Nissl staining of the DG per animal group. The bottom part shows the neuronal density quantifications in the CA1 region per group. Bars represent mean ± SD for sample replications ( n = 10). ∗ p

    Article Snippet: Arc expression in the CA1 hippocampal region was visualized at 400× magnification with an Olympus light microscope (Tokyo, Japan).

    Techniques: Over Expression, Staining