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ai32 mice  (Jackson Laboratory)

 
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    Jackson Laboratory ai32 mice
    Ai32 Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ai32/ai32/pmc13052087-87-6-8
    Average 86 stars, based on 1 article reviews
    ai32 mice - by Bioz Stars, 2026-09
    86/100 stars

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    Related Articles

    other:

    Article Title: Alcohol attenuates CRF-induced excitatory effects from the extended amygdala to dorsostriatal cholinergic interneurons
    Article Snippet: ChAT-eGFP (stock 007902), ChAT-Cre (stock 031661), Drd1a-tdTomato (D1-tdT, stock 016204), Ai32 (stock 012569), CRH-ires-CRE (stock 012704), and C57BL/6J (stock 000664) mice were purchased from The Jackson Laboratory ( ; ; ; ; ).

    Article Title: Stress History Modulates Corticotropin-Releasing Factor Neurons to Establish Resilience
    Article Snippet: The study used male, wild-type, Crf-ires-Cre (Jackson Labs: 011087), ai14 (Cre-responsive tdTomato reporter mouse; Jackson Labs: 007915), ai32 (Cre-responsive ChR2 [channelrhodopsin-2]/fused with eYFP [enhanced yellow fluorescent protein]; Jackson Labs: 012569) mice on C57BL/6J background that were bred at the Icahn School of Medicine at Mount Sinai (ISMMS) and were used between 6 and 7 weeks at the start of experimental manipulations.

    Article Title: Rapid integration of somatosensory feedback in planning tongue movements
    Article Snippet: We obtained behavioral/neural data from 4 wild-type mice (1 female, 3 male; C57BL/6J, JAX #000664) and 19 double heterozygous VGAT-IRES-Cre/+; Ai32/+ (9 female, 10 male; obtained from crossing VGAT-IRES-Cre and Ai32; Jackson Labs: 028862; B6J.129S6(FVB)-Slc32a1 tm2(cre)Lowl /MwarJ; Jackson Labs: 012569; B6;129S-Gt(ROSA)26Sor tm32(CAG-COP4*H134R/EYFP)Hze /J) at 3-10 months of age.

    Transgenic Assay:

    Article Title: Neuroligin-2–dependent adhesion defines a molecular checkpoint for inhibitory synaptic plasticity
    Article Snippet: .. To enable targeted optogenetic stimulation of defined inhibitory 96 circuits, we also used several transgenic mouse lines obtained from Jackson Laboratory: Sst-IRES-Cre 97 (stock #013,044), Pvalb-IRES-Cre (stock #017,320), and Ai32 (B6.Cg-Gt(ROSA)26Sortm32(CAG-98 COP4*H134R/EYFP)Hze/J; stock #024,109). ..

    Knock-Out:

    Article Title: Neural Circuits between Nodose Ganglion and Pulmonary Neuroendocrine Cells Regulate Lung Inflammatory Responses
    Article Snippet: C57BL/6J mice were purchased from Charles River Laboratories. .. Tlr4 knockout ( Tlr4 −/− ) mice, Trpa1 knockout ( Trpa1 −/− ) mice Rosa26‐stop(flox)‐DTR and Ai9 strain Rosa26‐stop(flox)‐tdTomato reporter mice, as well as Ai32 (Rosa26‐LSL‐ChR2/EYFP) mice, were all obtained from The Jackson Laboratory. ..

    Article Title: Neural Circuits between Nodose Ganglion and Pulmonary Neuroendocrine Cells Regulate Lung Inflammatory Responses.
    Article Snippet: C57BL/6J mice were purchased from Charles River Laboratories. .. Tlr4 knockout ( Tlr4− / − ) mice, Trpa1 knockout ( Trpa1− / − ) mice Rosa26-stop(flox)-DTR and Ai9 strain Rosa26-stop(flox)-tdTomato reporter mice, as well as Ai32 (Rosa26-LSL-ChR2/EYFP) mice, were all obtained from The Jackson Laboratory. ..



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    ( A ) Sample images of GFP-labeled CINs in the striatum of a ChAT-eGFP mouse. Scale bar: 0.5 mm, 50 μm (inset). ( B ) Bath application of CRF (100 nM) increased the spontaneous firing of dorsal striatal CINs in cell-attached electrophysiological recordings. This effect was prevented by pretreatment with the CRFR1 antagonist NBI 35695 (5 μM). n=7 cells from 3 mice (7/3) for CRF and 6/3 for CRF plus antagonist recordings. ( C ) Data showing that CRF significantly increases the firing from baseline, and the firing frequency in the presence of CRF following pretreatment with CRFR1 antagonist is significantly lower. ***p<0.001 by paired t-test, ***p<0.001 by Mann-Whitney test. n=7 cells from 3 mice. ( D ) Sample images of ACh sensor fluorescence in dorsal striatal slices before and during bath application of CRF (100 nM). AAV-hSyn-GRAB ACh4m was infused into the dorsal striatum of wild-type mice, and live-tissue confocal imaging was conducted 2 weeks post-infusion. Scale bar: 10 μm for left and right. ( E ) Sample trace of spontaneous ACh release events (indicated by red arrows, top). Bath application of CRF increased ACh sensor fluorescence (bottom). ( F ) Summary data showing a significant increase in ACh sensor fluorescence following CRF application. *p<0.05 by Mann-Whitney test. n=7 slices from 7 mice. ( G ) Schematic of cell-attached electrophysiological recordings from dorsal striatal CINs in <t>CRF-Cre;Ai32;ChAT-eGFP</t> mice, with simultaneous optogenetic stimulation of CRF + fibers using blue light (470 nm, 2 ms, 50 Hz, 60 s). ( H ) Sample trace showing the increase in CIN firing frequency during blue light stimulation of CRF + fibers. ( I ) Data demonstrating a significant and reversible increase in CIN firing frequency during optogenetic stimulation, *p<0.05, ***p<0.001 by one-way RM ANOVA. n=13 neurons from 8 animals. ( J ) Sample trace showing no change in CIN firing frequency during blue light stimulation of CRF + fibers when CRFR1 antagonist (antalarmin hydrochloride, 2 μM) was bath applied. (K) Data demonstrating no significant change in CIN firing frequency during optogenetic stimulation. n=9 neurons from 3 mice. Data are presented as mean ± SEM.
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    ( A ) Sample images of GFP-labeled CINs in the striatum of a ChAT-eGFP mouse. Scale bar: 0.5 mm, 50 μm (inset). ( B ) Bath application of CRF (100 nM) increased the spontaneous firing of dorsal striatal CINs in cell-attached electrophysiological recordings. This effect was prevented by pretreatment with the CRFR1 antagonist NBI 35695 (5 μM). n=7 cells from 3 mice (7/3) for CRF and 6/3 for CRF plus antagonist recordings. ( C ) Data showing that CRF significantly increases the firing from baseline, and the firing frequency in the presence of CRF following pretreatment with CRFR1 antagonist is significantly lower. ***p<0.001 by paired t-test, ***p<0.001 by Mann-Whitney test. n=7 cells from 3 mice. ( D ) Sample images of ACh sensor fluorescence in dorsal striatal slices before and during bath application of CRF (100 nM). AAV-hSyn-GRAB ACh4m was infused into the dorsal striatum of wild-type mice, and live-tissue confocal imaging was conducted 2 weeks post-infusion. Scale bar: 10 μm for left and right. ( E ) Sample trace of spontaneous ACh release events (indicated by red arrows, top). Bath application of CRF increased ACh sensor fluorescence (bottom). ( F ) Summary data showing a significant increase in ACh sensor fluorescence following CRF application. *p<0.05 by Mann-Whitney test. n=7 slices from 7 mice. ( G ) Schematic of cell-attached electrophysiological recordings from dorsal striatal CINs in <t>CRF-Cre;Ai32;ChAT-eGFP</t> mice, with simultaneous optogenetic stimulation of CRF + fibers using blue light (470 nm, 2 ms, 50 Hz, 60 s). ( H ) Sample trace showing the increase in CIN firing frequency during blue light stimulation of CRF + fibers. ( I ) Data demonstrating a significant and reversible increase in CIN firing frequency during optogenetic stimulation, *p<0.05, ***p<0.001 by one-way RM ANOVA. n=13 neurons from 8 animals. ( J ) Sample trace showing no change in CIN firing frequency during blue light stimulation of CRF + fibers when CRFR1 antagonist (antalarmin hydrochloride, 2 μM) was bath applied. (K) Data demonstrating no significant change in CIN firing frequency during optogenetic stimulation. n=9 neurons from 3 mice. Data are presented as mean ± SEM.
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    Image Search Results


    ( A ) Sample images of GFP-labeled CINs in the striatum of a ChAT-eGFP mouse. Scale bar: 0.5 mm, 50 μm (inset). ( B ) Bath application of CRF (100 nM) increased the spontaneous firing of dorsal striatal CINs in cell-attached electrophysiological recordings. This effect was prevented by pretreatment with the CRFR1 antagonist NBI 35695 (5 μM). n=7 cells from 3 mice (7/3) for CRF and 6/3 for CRF plus antagonist recordings. ( C ) Data showing that CRF significantly increases the firing from baseline, and the firing frequency in the presence of CRF following pretreatment with CRFR1 antagonist is significantly lower. ***p<0.001 by paired t-test, ***p<0.001 by Mann-Whitney test. n=7 cells from 3 mice. ( D ) Sample images of ACh sensor fluorescence in dorsal striatal slices before and during bath application of CRF (100 nM). AAV-hSyn-GRAB ACh4m was infused into the dorsal striatum of wild-type mice, and live-tissue confocal imaging was conducted 2 weeks post-infusion. Scale bar: 10 μm for left and right. ( E ) Sample trace of spontaneous ACh release events (indicated by red arrows, top). Bath application of CRF increased ACh sensor fluorescence (bottom). ( F ) Summary data showing a significant increase in ACh sensor fluorescence following CRF application. *p<0.05 by Mann-Whitney test. n=7 slices from 7 mice. ( G ) Schematic of cell-attached electrophysiological recordings from dorsal striatal CINs in CRF-Cre;Ai32;ChAT-eGFP mice, with simultaneous optogenetic stimulation of CRF + fibers using blue light (470 nm, 2 ms, 50 Hz, 60 s). ( H ) Sample trace showing the increase in CIN firing frequency during blue light stimulation of CRF + fibers. ( I ) Data demonstrating a significant and reversible increase in CIN firing frequency during optogenetic stimulation, *p<0.05, ***p<0.001 by one-way RM ANOVA. n=13 neurons from 8 animals. ( J ) Sample trace showing no change in CIN firing frequency during blue light stimulation of CRF + fibers when CRFR1 antagonist (antalarmin hydrochloride, 2 μM) was bath applied. (K) Data demonstrating no significant change in CIN firing frequency during optogenetic stimulation. n=9 neurons from 3 mice. Data are presented as mean ± SEM.

    Journal: eLife

    Article Title: Alcohol attenuates CRF-induced excitatory effects from the extended amygdala to dorsostriatal cholinergic interneurons

    doi: 10.7554/eLife.107145

    Figure Lengend Snippet: ( A ) Sample images of GFP-labeled CINs in the striatum of a ChAT-eGFP mouse. Scale bar: 0.5 mm, 50 μm (inset). ( B ) Bath application of CRF (100 nM) increased the spontaneous firing of dorsal striatal CINs in cell-attached electrophysiological recordings. This effect was prevented by pretreatment with the CRFR1 antagonist NBI 35695 (5 μM). n=7 cells from 3 mice (7/3) for CRF and 6/3 for CRF plus antagonist recordings. ( C ) Data showing that CRF significantly increases the firing from baseline, and the firing frequency in the presence of CRF following pretreatment with CRFR1 antagonist is significantly lower. ***p<0.001 by paired t-test, ***p<0.001 by Mann-Whitney test. n=7 cells from 3 mice. ( D ) Sample images of ACh sensor fluorescence in dorsal striatal slices before and during bath application of CRF (100 nM). AAV-hSyn-GRAB ACh4m was infused into the dorsal striatum of wild-type mice, and live-tissue confocal imaging was conducted 2 weeks post-infusion. Scale bar: 10 μm for left and right. ( E ) Sample trace of spontaneous ACh release events (indicated by red arrows, top). Bath application of CRF increased ACh sensor fluorescence (bottom). ( F ) Summary data showing a significant increase in ACh sensor fluorescence following CRF application. *p<0.05 by Mann-Whitney test. n=7 slices from 7 mice. ( G ) Schematic of cell-attached electrophysiological recordings from dorsal striatal CINs in CRF-Cre;Ai32;ChAT-eGFP mice, with simultaneous optogenetic stimulation of CRF + fibers using blue light (470 nm, 2 ms, 50 Hz, 60 s). ( H ) Sample trace showing the increase in CIN firing frequency during blue light stimulation of CRF + fibers. ( I ) Data demonstrating a significant and reversible increase in CIN firing frequency during optogenetic stimulation, *p<0.05, ***p<0.001 by one-way RM ANOVA. n=13 neurons from 8 animals. ( J ) Sample trace showing no change in CIN firing frequency during blue light stimulation of CRF + fibers when CRFR1 antagonist (antalarmin hydrochloride, 2 μM) was bath applied. (K) Data demonstrating no significant change in CIN firing frequency during optogenetic stimulation. n=9 neurons from 3 mice. Data are presented as mean ± SEM.

    Article Snippet: ChAT-eGFP (stock 007902), ChAT-Cre (stock 031661), Drd1a-tdTomato (D1-tdT, stock 016204), Ai32 (stock 012569), CRH-ires-CRE (stock 012704), and C57BL/6J (stock 000664) mice were purchased from The Jackson Laboratory ( ; ; ; ; ).

    Techniques: Labeling, MANN-WHITNEY, Fluorescence, Imaging