Anti Cacna1g Cav3 1 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity"
Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity
Figure Legend Snippet: Activation of NmbR stimulates recombinant Cav3.2 channels heterologously expressed in HEK293 cells. A, western blot analysis of NmbR in HEK293 cells transiently transfected with NmbR cDNA. Blots depicted are representative of three independent experiments. B, membrane localization of NmbR in transfected HEK293 cells. Alphabets a through c in the diagram indicate the differential interference contrast (DIC, a ), the EGFP fluorescent signals of NmbR ( b ), and the merged image ( c ), respectively. C, exemplary current traces show the effect of Nmb (100 nM) on Cav3.1 (α1G), Cav3.2 (α1H) and Cav3.3 (α1I) channel currents. Currents were elicited by a 100 ms depolarizing step pulse from the holding potential of -110 mV to -30 mV. D, summary data show the effect of 100 nM Nmb on Cav3.1 ( n = 10), Cav3.2 ( n = 9) and Cav3.3 ( n = 7) channel currents. ** p
Techniques Used: Activation Assay, Recombinant, Western Blot, Transfection
2) Product Images from "Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei"
Article Title: Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei
Journal: Brain Structure & Function
Figure Legend Snippet: Low-voltage activated calcium channel family (Cav3) subunits in the abducens and trochlear nucleus. a Consecutive coronal paraffin sections through the abducens nucleus (nVI) ( a ) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (third panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (second panel) as reference. b, c Close-up of Cav subunit expression in nVI MIF (red arrowheads) and SIF motoneurons (MNs) (green arrows) and INTs (blue arrow). d Consecutive coronal paraffin sections through the trochlear nucleus (nVI) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (second panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (third panel) as reference. Thin dashed lines in d indicate the border of nIV and thick dashed lines indicate the boundary between the MIF and SIF MNs. e Close-up of Cav subunit expression in MIF (red arrowheads) and SIF MNs (green arrow) on different sections as those illustrated in d . Note the weak Cav3.1 expression along the membrane of some SIF MNs (left column, black star). Red dashed lines indicate the tentative position of the border delineating the dorsal cap of nIV. f Cerebellar Purkinje cells located on the same consecutive sections as nVI as controls for immunopositivity of the different Cav subunits. Scale bar indicates 100 μm in a, d, f and 50 μm in b, c, e
Techniques Used: Immunolabeling, Immunostaining, Expressing
3) Product Images from "Bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure"
Article Title: Bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure
Figure Legend Snippet: Knockdown of Cav3.1 in dmVMH decreased burst firing, and rescued anxiety-like behavior and metabolic alteration induced by chronic stress. (a) Schematic of Cav3.1 shRNA construct and injection of shRNA-expressing lenti-viral vector into dmVMH to interfere with Cav 3.1 expression. (b) Representative images of dmVMH Cav 3.1 immunostaining in chronic stress and RNAi (under chronic stress) animals (left). Proportion of burst firing neurons decreased in RNAi group (2/13, 15.38%) compared with stress group (7/17, 41.18%) (right). Scale bar is 100 μm. (c) Time spent in central area and number of entries into central area of open field in control, chronic stress, and RNAi groups. Residence time: control (n = 8) versus chronic stress group (n = 8), P = 0.0068; chronic stress versus RNAi group (n = 7), P = 0.0017. Number of entries: control versus chronic stress group, P = 0.4830; chronic stress versus RNAi group, P = 0.8437 (unpaired Student’s t -test). (d) Time spent in open arm and number of entries into open arm of elevated plus-maze in control, chronic stress, and RNAi groups. Residence time: control versus chronic stress group, P = 0.0009; chronic stress versus RNAi group, P = 0.0379. Number of entries: control versus chronic stress group, P
Techniques Used: shRNA, Construct, Injection, Expressing, Plasmid Preparation, Immunostaining
Figure Legend Snippet: T-VGCC mediated enhancement of burst firing in dmVMH neurons under chronic stress. (a) Schematic of structure of T-VGCC located on cell membrane (left top). Representative immunofluorescence showing Cav 3.1 (left bottom), Cav 3.2 (right top), and Cav 3.3 (right bottom) expression in dmVMH, respectively, with stronger Cav3.1 expression observed. Scale bar is 200 μm. (b) Quantification of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH tissue between control (n = 5 mice) and chronic stress groups (n = 6 mice). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0232). (c) Single-cell qRT-PCR analysis of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH neurons between control (n = 16 cells) and chronic stress groups (n = 14 cells). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0390). (d) Evoked burst firing trace of dmVMH neurons without and with T-VGCC antagonist (mibefradil, 10 μM), 10 pA current injection was given in cosine waveform. (e) Effects of mibefradil on onset time and RMP of dmVMH neurons from wild-type (n = 15) and chronic stress groups (n = 13). Significant differences were observed in both onset time and RMP (paired Student’s t- test, P = 0.0388 and P = 0.0395) in the stress group, whereas the control group demonstrated obvious changes in RMP but not onset time (paired Student’s t -test, P = 0.0275 and P = 0.3125). (f) Single-cell qRT-PCR analysis of Cav 3.1 expression among three neuronal subtypes in dmVMH. Upper: burst firing neurons (n = 11) showed higher Cav 3.1 expression than other two subtypes (unpaired Student’s t -test, P = 0.0133 compared with silent neurons (n = 7), P = 0.0139 compared with tonic-firing neurons (n = 12)); bottom: Cav 3.1 expression in burst firing subtype showed significant differences between control and chronic-stress groups (unpaired Student’s t -test, silent: control, n = 3, stress, n = 3, P = 0.5574; tonic-firing: control, n = 7, stress, n = 5, P = 0.9339; bursting: control, n = 5, stress, n = 6, P = 0.0165). (g) Effects of mibefradil on suprathreshold and subthreshold activity in dmVMH burst firing neurons in control (n = 5) and chronic stress groups (n = 7). Mibefradil inhibited T-VGCC and caused a right frequency-current curve shift (two-way ANOVA, control, P = 0.2140, F (1, 8) = 1.854; stress, P = 0.0077, F (1, 12) = 10.22); lower, mibefradil application exerted no obvious influence on current-voltage curve of burst neurons (two-way ANOVA, control, P = 0.8188, F (1, 10) = 0.0573; stress, P = 0.4487, F (1, 10) = 0.6218). (h) Obvious differences were observed in suprathreshold activity (two-way ANOVA, P = 0.0047, F (1, 110) = 20.53), but not in subthreshold (two-way ANOVA, P = 0.9913, F (1, 33) = 4.958) membrane potential of dmVMH burst firing neurons between control (n = 5) and chronic stress groups (n = 7) after application of mibefradil. Data are means ± SEM. * P
Techniques Used: Immunofluorescence, Expressing, Mouse Assay, Quantitative RT-PCR, Injection, Activity Assay
4) Product Images from "Developmentally Regulated Rebound Depolarization Enhances Spike Timing Precision in Auditory Midbrain Neurons"
Article Title: Developmentally Regulated Rebound Depolarization Enhances Spike Timing Precision in Auditory Midbrain Neurons
Journal: Frontiers in Cellular Neuroscience
Figure Legend Snippet: Developmental regulation of rebound depolarization in inferior colliculus (IC) neurons. (A) Distribution of rebound (red circle) and non-rebound (blue triangle) neurons in the IC. The IC was divided into the ICX (lateral region), ICC (middle region), and ICD (mediodorsal region). (B) Responses of a rebound neuron (top traces) and a non-rebound neuron (bottom traces) to a positive (60 pA) and a negative (−100 pA) current pulse. Arrowhead points to the rebound. (C) The rebound and anode break spikes (arrow) were blocked by 5 μm mibefradil. (D) Proportions of rebound neurons before (P9–11), during (P12–13), and after (P14–21) the onset of hearing. (E–G) Double-labeling immunocytochemistry with T-type calcium channel isoforms CaV3.1 ( E , green), CaV3.2 ( F , green), and CaV3.3 ( G , green) and the microtubule-associated protein 2 (MAP2; E – G , red) in the IC from P10 and P21 rats demonstrates a developmental increase in the expression of CaV3.1, CaV3.2, and CaV3.3, with the highest changes in the CaV3.2 expression in IC neurons. Scale bars 20 μm.
Techniques Used: Immunocytochemistry, Labeling, Expressing