Journal: Frontiers in Pharmacology

Article Title: Farnesyl Transferase Inhibitor Lonafarnib Enhances α7nAChR Expression Through Inhibiting DNA Methylation of CHRNA7 and Increases α7nAChR Membrane Trafficking

doi: 10.3389/fphar.2020.589780

Figure Lengend Snippet: Role of DNA methylation in the lonafarnib affected activity, total expression, membrane expression, and phosphorylation of a7nAChR. (A) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle, DNMT inhibitor RG108 or anisomycin. ** P < 0.01 vs. control mice, ## P < 0.01 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (B) Evoked I ACh by ACh (3 mM) in the slices of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin, ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (C) Levels of biotinylated a7nAChR (membrane surface) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of phospho-a7nAChR in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. The expression of protein and the amplitude of evoked I ACh were normalized by the values of control group with vehicle.

Article Snippet: CaMKII inhibitor KN93 and DNMT inhibitor RG108 were purchased from MCE.

Techniques: DNA Methylation Assay, Activity Assay, Expressing, Membrane, Phospho-proteomics, Control, Comparison

Journal: Frontiers in Pharmacology

Article Title: Farnesyl Transferase Inhibitor Lonafarnib Enhances α7nAChR Expression Through Inhibiting DNA Methylation of CHRNA7 and Increases α7nAChR Membrane Trafficking

doi: 10.3389/fphar.2020.589780

Figure Lengend Snippet: Lonafarnib administration affects CaMKII signaling pathways, partially modulating the membrane expression of a7nAChR. (A and B) Levels of phospho-PKC and phospho-PKA in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. (C) Levels of phospho-CaMKII in the hippocampus of control and lonafarnib-treated mice treated with vehicle, RG108, or anisomycin. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (D) Levels of biotinylated a7nAChR (membrane) protein in the hippocampus of control and lonafarnib-treated mice treated with vehicle or CaMKII pathway blocker KN93. Surface a7nAChR was normalized by surface GluR2 protein, which was again normalized by vehicle-treated control group. ** P < 0.01 vs. control mice; # P < 0.05 vs. lonafarnib-treated mice (two-way ANOVA, followed by Tukey’s multiple comparison test). (E) Levels of a7nAChR total proteins in the hippocampus of control and lonafarnib-treated mice treated with vehicle and KN93, and total a7nAChR was normalized by GAPDH, which was again normalized by vehicle-treated group. ** P < 0.01 vs. control mice (two-way ANOVA, followed by Tukey’s multiple comparison test). The expression of protein was normalized by the values of control group with vehicle.

Article Snippet: CaMKII inhibitor KN93 and DNMT inhibitor RG108 were purchased from MCE.

Techniques: Protein-Protein interactions, Membrane, Expressing, Control, Comparison

Journal: Nature Communications

Article Title: Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation

doi: 10.1038/s41467-024-50168-5

Figure Lengend Snippet: a Diagram of CaMKII inhibition by CN19o peptide (left) and experimental schedule (right). b Cumulative sleep loss (SD – Basal) in E11-CN19scr and E11-CN19o mice over 24 h ( n = 8 for each group). The averaged parameters from the three days prior to SD are shown as Basal. c , e , f Sleep duration ( c ), P WS ( e ), and P SW ( f ) during ZT12–24 on Basal and SD ( n = 8 for each group). Two-sided Student’s paired t -test was performed within the groups. d Sleep rebound ratio (SD/Basal during ZT12-24; n = 8 for each group). Two-sided Welch’s t -test was used. g Cumulative sleep loss (MK-801 – Saline) in E11-CN19scr and E11-CN19o mice over 24 h ( n = 10 for each group). Each mouse received saline or 2 mg/kg MK-801 injection at ZT8, allowing at least 2 days between injections. h , j , k Sleep duration ( h ), P WS ( j ), and P SW ( k ) during ZT12–24 on days with saline or MK-801 injection ( n = 10 for each group). Two-sided Student’s paired t -test was used within the groups. i Sleep rebound ratio (MK-801 / Saline during ZT12–24, n = 10 for each group). Two-sided Welch’s t -test was used. l , m Daily NREM sleep duration ( l ) and REM sleep duration ( m ) in E11-CN19scr ( n = 4) and E11-CN19o ( n = 6) mice. Two-sided Welch’s t -test was used. n The differences in transition probabilities between wake, NREM, and REM sleep states. The solid-red and dotted-gray lines represent a significant increase and decrease, respectively. o Power spectral density (PSD) of the EEG during NREM sleep. The extracted diagram in the 0–10 Hz range is also shown (top-right). p Normalized delta power (0.5–4 Hz) during NREM sleep in E11-CN19scr ( n = 4) and E11-CN19o ( n = 6) mice. Two-sided Welch’s t -test was used. Line and interval plots show mean ± SEM. In box plot, boxes show the median, 25th and 75th percentiles, and whiskers show minima to maxima excluding outliers. * P < 0.05, ** P < 0.01. Source data are provided as a Source Data file.

Article Snippet: The membranes were reacted to anti-CaMKIIα antibody (1:3,000, SMC-124D, StressMarq) after blocking with Blocking One (Nacalai), followed by the reaction to the secondary antibody: anti-mouse IgG peroxidase (HRP)-conjugated antibody (1:3,000, W402B, Promega).

Techniques: Inhibition, Saline, Injection

Journal: Nature Communications

Article Title: Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation

doi: 10.1038/s41467-024-50168-5

Figure Lengend Snippet: a Diagram of CN19o expression in E11 neurons for CaMKII inhibition. b Hourly normalized delta power (0.5–4 Hz) during NREM sleep in E11-CN19scr ( n = 22) and E11-CN19o mice ( n = 15) in SD experiments. Mice were allowed to behave freely for 1 day prior to SD, and the value is shown as Basal. SD was effectively performed during ZT0–6 with a high success rate (93.4 ± 5.3%). c Normalized delta power during NREM sleep on Basal and SD during ZT6–12 in E11-CN19scr ( n = 22) and E11-CN19o mice ( n = 15). Two-sided Welch’s t -test was performed between Basal and SD within the groups. d The percentage of delta power change upon SD during ZT6–12 in E11-CN19scr ( n = 22) and E11-CN19o mice ( n = 15). The groups were compared using two-sided Welch’s t -test. e Diagram of CN19o expression in cortical PV neurons with enhanced specificity using E11 enhancer and Pvalb −2A-Cre mice. f Hourly normalized delta power (0.5–4 Hz) during NREM sleep in Pvalb −2A-Cre:E11-DIO-CN19scr ( n = 16) and Pvalb −2A-Cre:E11-DIO-CN19o mice ( n = 13) in SD experiments. Mice were allowed to behave freely for 1 day prior to SD, and the value is shown as Basal. SD was effectively performed during ZT0–6 with a high success rate (95.0 ± 6.2%). g Normalized delta power during NREM sleep on Basal and SD during ZT6–12 in Pvalb −2A-Cre:E11-DIO-CN19scr ( n = 16) and Pvalb −2A-Cre:E11-DIO-CN19o mice ( n = 13). Two-sided Welch’s t -test was performed between Basal and SD within the groups. h The percentage of delta power change upon SD during ZT6–12 in Pvalb −2A-Cre:E11-DIO-CN19scr ( n = 16) and Pvalb −2A-Cre:E11-DIO-CN19o mice ( n = 13). The groups were compared using two-sided Welch’s t -test. Line plots show mean ± SEM. In box plot, boxes show the median, 25th and 75th percentiles, and whiskers show minima to maxima excluding outliers. Source data are provided as a Source Data file.

Article Snippet: The membranes were reacted to anti-CaMKIIα antibody (1:3,000, SMC-124D, StressMarq) after blocking with Blocking One (Nacalai), followed by the reaction to the secondary antibody: anti-mouse IgG peroxidase (HRP)-conjugated antibody (1:3,000, W402B, Promega).

Techniques: Expressing, Inhibition

Journal: Nature Communications

Article Title: Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation

doi: 10.1038/s41467-024-50168-5

Figure Lengend Snippet: a Illustration of CaMKIIα protein sequences (left) and endogenous CaMKIIα activation mechanism (right). The phosphorylation of T286 residue in the regulatory segment is critical for CaMKIIα activity regulation. b – d Daily sleep duration ( b ), P WS ( c ), and P SW ( d ) in E11-EGFP ( n = 11), E11-CaMKIIα (WT) ( n = 11), and E11-CaMKIIα (T286D) ( n = 12) mice. The groups were compared using two-sided Welch’s t -test with Bonferroni correction. e Diagram of CaMKII expression and experimental schedule in Per or Cry dKO mice under constant dark conditions. f – h Daily sleep duration ( f ), P WS ( g ), and P SW ( h ) in the Per (left) or Cry (right) dKO mice expressing E11-CaMKIIα (WT) ( n = 7 or 6) or E11-CaMKIIα (T286D) ( n = 6 or 5). The groups were compared using two-sided Welch’s t -test. i , j Daily NREM sleep duration ( i ) and REM sleep duration ( j ) in E11-CaMKIIα (WT) and E11-CaMKIIα (T286D) mice ( n = 8 for each group). The groups were compared using two-sided Welch’s t -test. k The difference in transition probabilities between wake, NREM, and REM sleep states in E11-CaMKIIα (T286D) mice versus E11-CaMKIIα (WT) mice. The solid red and dotted gray lines represent a significant increase and decrease, respectively. l Power spectral density (PSD) of the EEG during NREM sleep. The extracted diagram in the 0–10 Hz range is also shown in the top-right corner of the panel. m Normalized slow-oscillation power (SO, 0.5–1 Hz) during NREM sleep in E11-CaMKIIα (WT) and E11-CaMKIIα (T286D) mice ( n = 8 for each group). The groups were compared using two-sided Welch’s t -test. n Diagram of CaMKIIα expression in cortical PV neurons with enhanced specificity using E11 enhancer and Pvalb −2A-Cre mice. o – q Daily sleep duration ( o ), P WS ( p ), and P SW ( q ) in Pvalb −2A-Cre:E11-DIO- CaMKIIα (WT), and Pvalb −2A-Cre:E11-DIO-CaMKIIα (T286D) mice ( n = 12 for each group). The groups were compared using two-sided Welch’s t -test. Line and interval plots show mean ± SEM. * P < 0.05, ** P < 0.01. Source data are provided as a Source Data file.

Article Snippet: The membranes were reacted to anti-CaMKIIα antibody (1:3,000, SMC-124D, StressMarq) after blocking with Blocking One (Nacalai), followed by the reaction to the secondary antibody: anti-mouse IgG peroxidase (HRP)-conjugated antibody (1:3,000, W402B, Promega).

Techniques: Activation Assay, Residue, Activity Assay, Expressing

Journal: Nature Communications

Article Title: Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation

doi: 10.1038/s41467-024-50168-5

Figure Lengend Snippet: a Representative whole-brain views of dorsal and lateral double-positive (c-Fos+PV+) cell distribution. The brains of E11-CaMKIIα (WT) (left) and E11-CaMKIIα (T286D) (right) mice were collected. b Stacked percentage bar plots of c-Fos+PV+ cells in the E11-CaMKIIα (WT) and E11-CaMKIIα (T286D) brains ( n = 4 for each group). The plot depicts the demographics of c-Fos+PV+ cells in major brain regions. c A region-wise heat map of relative cell number showing changes in c-Fos+PV+ cell number in the isocortex. The E11-CaMKIIα (T286D) brains were compared to the E11-CaMKIIα (WT) brains, with red indicating an increase and blue indicating a decrease. d The rate of double-positive (c-Fos+PV + ) cells in c-Fos+ cells in each cortical region (left) or entire isocortex (right). The groups were compared using two-sided Welch’s t -test. e The cortical distribution of c-Fos signal intensity per c-Fos+PV+ cell in each group. f Experimental design for quantitative analysis of CaMKIIα T286 phosphorylation in E11 neurons. The cortical region of E11-CaMKIIα (T285D) mouse brain was dissected, and homogenates were used for LC-MS/MS analysis. g Signal intensities of peptides derived from CaMKIIα (T285D) with phosphorylated T286 residues ( n = 21 for each group). The intensities were normalized to the total CaMKIIα level, which was calculated using all quantifiable non-phosphorylated peptides derived from WT CaMKIIα. Two-sided two-samples Wilcoxon test was used to compare the groups. h CaMKII-dependent activity regulation of cortical PV neurons for homeostasis regulation. i Cortical feedback circuit model for sleep homeostasis regulation. Bar plots show mean ± SEM. In box plot, boxes show the median, 25th and 75th percentiles, and whiskers show minima to maxima excluding outliers. Brain region acronyms follow the ontology defined by the Allen Brain Atlas. Source data are provided as a Source Data file.

Article Snippet: The membranes were reacted to anti-CaMKIIα antibody (1:3,000, SMC-124D, StressMarq) after blocking with Blocking One (Nacalai), followed by the reaction to the secondary antibody: anti-mouse IgG peroxidase (HRP)-conjugated antibody (1:3,000, W402B, Promega).

Techniques: Liquid Chromatography with Mass Spectroscopy, Derivative Assay, Activity Assay

Journal: Nature communications

Article Title: Enhanced TARP-γ8-PSD-95 coupling in excitatory neurons contributes to the rapid antidepressant-like action of ketamine in male mice.

doi: 10.1038/s41467-023-42780-8

Figure Lengend Snippet: Fig. 5 | CaMKIIα-dependent TARP-γ8-PSD-95 coupling is necessary for the rapid antidepressant effects of ketamine. a The representative image of western blot. b The quantification of protein expression of p-CaMKIIα and CaMKIIα (n = 9 per group). c Preference for sucrose in the SPT (n = 9, 8, 9, and 10 in Vehicle-ACSF, Vehicle-KN93, Ketamine-ACSF, and Ketamine-KN93, respectively). d, e Immobility time in the FST (d) and total distance in the OFT (e) (n = 9, 9, 10, and 8 in Vehicle- ACSF, Vehicle-KN93, Ketamine-ACSF and Ketamine-KN93, respectively). f Representative western blot image of Co-IP assay. g Quantification of association between PSD-95 and TARP-γ8 (n = 8, 7, 7, and 9 in Vehicle-ACSF, Vehicle-KN93, Ketamine-ACSF and Ketamine-KN93, respectively). h, i Total protein expression of PSD-95 (h) and TARP-γ8 (i) (n = 8 samples per group). j Representative traces of AMPARs-mediated mEPSC recordings in ventral hippocampal CA1 neurons from different groups. k, l Quantification of cumulative probability and amplitude (k)

Article Snippet: Primary antibodies used to recognize specific protein, including: TARP-γ8 (1:1000; sc-514421, Santa Cruz Biotechnology, Santa Cruz, CA), GluA1 (1:1000; ab31232, Abcam, Cambridge, UK), GluA2 (1:1000; ab52932, Abcam, Cambridge, UK), βactin (1:3000; sc-47778, Santa Cruz Biotechnology, Santa Cruz, CA), PSD-95 (1:1000; ab18258, Abcam, Cambridge, UK), CaMKIIα (1:800; 50049, Cell Signaling, USA), Phospho-CaMKII (1:800; 12716, Cell Signaling, USA).

Techniques: Western Blot, Expressing, Co-Immunoprecipitation Assay

Journal: Nature communications

Article Title: Enhanced TARP-γ8-PSD-95 coupling in excitatory neurons contributes to the rapid antidepressant-like action of ketamine in male mice.

doi: 10.1038/s41467-023-42780-8

Figure Lengend Snippet: Fig. 6 | Knockdown of TARP-γ8 in excitatory neurons in the ventral hippo- campus blocks the antidepressant effects of ketamine. a Immunofluorescence results showing TARP-γ8 (green) was mainly expressed in CaMKIIα (purple)- expressing neurons rather than GAD67 (purple)-expressing neurons. Scale bar = 30 μm (two bars on the left), 50 μm (two bars on the right). DAPI (blue). Experi- ments were repeated independently 3 times with similar results. b AAV-expressing constructs with CaMKIIα promoter encoding GFP and shRNAs targeting TARP-γ8. c Timeline of experimental procedure. d Preference for sucrose in the SPT (n = 8 samples per group). e Immobility time in the FST (n = 8, 8, 9, and 10 in Vehicle-Scr-shRNA, Vehicle-Cacng8-shRNA, Ketamine-Scr-shRNA and Ketamine- Cacng8-shRNA, respectively). f Total distance in the OFT (n = 8, 9, 10 and 10 in

Article Snippet: Primary antibodies used to recognize specific protein, including: TARP-γ8 (1:1000; sc-514421, Santa Cruz Biotechnology, Santa Cruz, CA), GluA1 (1:1000; ab31232, Abcam, Cambridge, UK), GluA2 (1:1000; ab52932, Abcam, Cambridge, UK), βactin (1:3000; sc-47778, Santa Cruz Biotechnology, Santa Cruz, CA), PSD-95 (1:1000; ab18258, Abcam, Cambridge, UK), CaMKIIα (1:800; 50049, Cell Signaling, USA), Phospho-CaMKII (1:800; 12716, Cell Signaling, USA).

Techniques: Knockdown, Expressing, Construct, shRNA

Journal: Brain Pathology

Article Title: Antenatal low‐intensity pulsed ultrasound reduces neurobehavioral deficits and brain injury following dexamethasone‐induced intrauterine growth restriction

doi: 10.1111/bpa.12968

Figure Lengend Snippet: Maternal LIPUS treatment enhanced the activation of CaMKII and downstream Akt signaling in IUGR brains . Representative immunoblots and quantitative data of ( A ) CaMKII, ( B ) Akt, and ( C ) ERK phosphorylation and total protein expression at PND 1 after IUGR. Representative images of double immunostaining and quantitative data of ( D ) neuron number (NeuN + ) and pAkt S473‐positive neurons, and ( E ) pCaMKII‐positive neurons at PND 1 after IUGR. Sections were stained with DAPI (blue) to visualize the nuclei. Scale bar = 50 μm. Values are mean ±standard error of mean; * p < 0.05, ** p < 0.01, and *** p < 0.001 versus saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus DEX group (n = 7–8/group; one‐way ANOVA). DAPI, 4'‐6‐Diamidino‐2‐phenylindole; DEX, dexamethasone; IUGR, intrauterine growth restriction; L, low‐intensity pulsed ultrasound; PND, postnatal day

Article Snippet: Protein samples obtained from brain or placenta tissue homogenates were separated on 8%–12% sodium dodecyl sulfate‐polyacrylamide gels, transferred to Immobilon‐P membranes (Millipore), and probed overnight at 4°C with primary antibodies including anti‐BDNF (1:1000; GTX132621), anti‐GDNF (1:1000; GTX17447), and anti‐VEGF (1:1000; GTX102643) from GeneTex (Irvine, CA, USA); anti‐pCaMKII (1:1000; #12716), anti‐total CaMKII (1:1000; #11945), anti‐pAkt S473 (1:1000; #9271), anti‐pAktT308 (1:1000; #4056), anti‐total Akt (1:1000; #9272), anti‐pERK (1:1000; #9101), and anti‐total ERK (1:1000; #9102) from Cell Signaling; anti‐PlGF (1:1000; ab196666), anti‐glucose transporter (GLUT) 3 (ab41525), anti‐GLUT1 (ab115730), anti‐SLC38A1 (ab134268), anti‐SNAT2 (ab90677), and anti‐SLC38A4 (ab58785) from Abcam; and anti‐β‐actin (1:10000; A5441, Sigma‐Aldrich).

Techniques: Activation Assay, Western Blot, Phospho-proteomics, Expressing, Double Immunostaining, Staining, Saline

Journal: Brain Pathology

Article Title: Antenatal low‐intensity pulsed ultrasound reduces neurobehavioral deficits and brain injury following dexamethasone‐induced intrauterine growth restriction

doi: 10.1111/bpa.12968

Figure Lengend Snippet: The schematic diagram indicates the potential mechanisms of LIPUS treatment‐induced neuroprotection in IUGR offspring brain . Our results demonstrate that antenatal LIPUS treatment promotes neuronal survival and myelination, and reduces neurodevelopmental deficits in the postnatal IUGR rats. These effects are related to increasing BDNF and PlGF expression, and subsequently enhancing neuronal CaMKII‐Akt signaling activation in the newborn IUGR brain. Meanwhile, LIPUS treatment promotes GLUT1 production and BDNF expression in the placenta. Antenatal LIPUS treatment also increases fetal weight, fetal liver weight, and placental weight after IUGR. Our findings suggest that the enhancement of cerebral BDNF‐CaMKII‐Akt signaling, and placental GLUT1 and BDNF expression by LIPUS could be a potential strategy for the management of IUGR. BDNF, brain‐derived neurotrophic factor; GLUT, glucose transporter; IUGR, intrauterine growth restriction; L, low‐intensity pulsed ultrasound; PlGF, placental growth factor.

Article Snippet: Protein samples obtained from brain or placenta tissue homogenates were separated on 8%–12% sodium dodecyl sulfate‐polyacrylamide gels, transferred to Immobilon‐P membranes (Millipore), and probed overnight at 4°C with primary antibodies including anti‐BDNF (1:1000; GTX132621), anti‐GDNF (1:1000; GTX17447), and anti‐VEGF (1:1000; GTX102643) from GeneTex (Irvine, CA, USA); anti‐pCaMKII (1:1000; #12716), anti‐total CaMKII (1:1000; #11945), anti‐pAkt S473 (1:1000; #9271), anti‐pAktT308 (1:1000; #4056), anti‐total Akt (1:1000; #9272), anti‐pERK (1:1000; #9101), and anti‐total ERK (1:1000; #9102) from Cell Signaling; anti‐PlGF (1:1000; ab196666), anti‐glucose transporter (GLUT) 3 (ab41525), anti‐GLUT1 (ab115730), anti‐SLC38A1 (ab134268), anti‐SNAT2 (ab90677), and anti‐SLC38A4 (ab58785) from Abcam; and anti‐β‐actin (1:10000; A5441, Sigma‐Aldrich).

Techniques: Expressing, Activation Assay, Derivative Assay

Journal: Neurochemical Research

Article Title: Morin Improves Cognitive Deficits in an in Vivo Model of Vascular Dementia by Modulating the N-methyl-D-aspartate Receptor Signaling Pathways

doi: 10.1007/s11064-026-04717-7

Figure Lengend Snippet: Morin modulated the expression of NMDA receptors in the hippocampus of VaD rats. a the expression levels of NR1 ; b the expression levels of NR2A ; c the expression levels of NR2B ; d the expression levels of NR1 protein; e the expression levels of NR2A protein; f the expression levels of NR2B protein; g protein levels of p-CREB; h protein levels of p-CAMK2A; i protein levels of p-CAMK2D. Protein levels of NR1, NR2A, and NR2B were quantified by ELISA. Data are presented as mean ± SD ( n = 8 per group). Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test (data met assumptions of normality and homoscedasticity)/Kruskal-Wallis with Dunn’s test (data did not meet assumptions). * indicates a significant difference from the Sham group; # indicates a significant difference 2VO group; *# indicates a significant difference from both the Sham and 2VO groups, with a p-value of less than 0.05 considered statistically significant

Article Snippet: Moreover, phosphorylation levels of calcium/calmodulin-dependent protein kinase II isoforms CAMK2A and CAMK2D at Thr286 (p-CAMK2A, p-CAMK2D) were quantified using the Colorimetric Cell-Based ELISA Kit (CAMK2A/CAMK2D (Phospho-Thr286), Boster Bio, #EKC2366).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: Neurophotonics

Article Title: Hybrid fiber optic-fMRI for multimodal cell-specific recording and manipulation of neural activity in rodents

doi: 10.1117/1.NPh.9.3.032206

Figure Lengend Snippet: Literature overview of opto-fMRI experiments. All optogenetic constructs are excitatory and have rapid kinetics, unless otherwise noted. Cre-LoxP selection for expression is prepended in parentheses to the promoter, when applicable. If the experiment uses vector injection as opposed to constitutive optogenetic construct expression and the injection site differs from the stimulation site, the injection site is prepended in parentheses. Paradigms detail in parentheses the characteristics of the smallest structured stimulation train, and original sources should be consulted, as ON periods may contain additional pauses between stimulation trains. Step function opsins do not possess canonical within-stimulation-period parameters.

Article Snippet: Albaugh et al. 2016 , hChR2(H134R) , CBV , CaMKII α , NAcc , Block (10 ms, 40 hz) , iso.-med. , Rat.

Techniques: Construct, Selection, Expressing, Plasmid Preparation, Injection, Blocking Assay