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Gabazine

Gabazine is a potent and selective GABA(A) receptor antagonist.
It is commonly used in neuroscience research to investigate the role of GABA-mediated inhibition in various neurological processes and disorders.
Gabazine acts by binding to the GABA(A) receptor, blocking the inhibitory effects of GABA and altering neuronal excitability.
Researchers can use Gabazine to study the contribution of GABA-ergic signaling in areas such as synaptic transmission, neuronal network dynamics, and the pathophysiology of conditions like epilepsy, anxiety, and cogntiive dysfunction.
PubCompare.ai can help optimize Gabazine research by providing access to the latest protocols from literature, preprints, and patents, and enabling intelligent comparisons to identify the most robust and reliable experimental approaches.

Most cited protocols related to «Gabazine»

1
Lentiviral Expression of GCaMP Calcium Sensors
Cited 164 times
GCaMP variants were made in a modified SIV-based lentiviral construct, pGP-syn-GCaMP-nls-mCherry-WPRE, derived from pCL20cSLFR MSCV-GFP51 (link). The prolentiviral vector included a 476-bp human synapsin promoter, GCaMP, a nuclear localization sequence fused to mCherry, and the woodchuck hepatitis post-transcriptional regulatory element. Site-directed mutagenesis was conducted by PCR and mutated regions were incorporated into the lentiviral constructs by gene assembly52 (link).
Hippocampi were dissected and dissociated in papain. Cells were plated at a density of 225,000 viable cells/well in 24-well glass-bottom plates (Mattek, #1.5 glass coverslips), pre-coated with Matrigel (BD Biosciences). Cells were cultured in growth medium (28 mM glucose, 2.4 mM sodium bicarbonate, 100 μg/mL transferrin, B-27 supplement (1X, Invitrogen), 500 μM L-glutamine, 50 units/mL penicillin, 50 mg/mL streptomycin, 5% fetal bovine serum in MEM).
Lentiviral particles were made in a biosafety level 2 laboratory by transfecting a prolentiviral construct and packaging and coat pseudotyping DNA constructs (pCAG-SIVgprre, pCAG4-RTR-SIV, pCMV-VSV-G)51 (link),53 (link) into HEK293T/17 cells (ATCC) in 10-cm plates. After 72 h, supernatant was collected (6 mL) and filtered. Neuronal cultures were infected at 3 days in vitro. Each well of a 24-well plate was incubated overnight with 0.5 mL of lentivirus in conditioned growth medium. The growth medium was supplemented with 4 μM AraC to inhibit glial proliferation. In some experiments, OGB1-AM was loaded into cells by incubating neurons in 1 mL of 2 μM OGB1-AM (Invitrogen) for 30 min and rinsing 3 times with imaging buffer (145 mM NaCl, 2.5 mM KCl, 10 mM glucose, 10 mM HEPES pH 7.4, 2 mM CaCl2, 1 mM MgCl2).
Neurons were stimulated in imaging buffer containing a drug cocktail to inhibit synaptic receptors (10 μM CNQX, 10 μM (R)-CPP, 10 μM gabazine, 1 mM (S)-MCPG, Tocris). Under these conditions, intracellular calcium increases are presumably caused by the opening of voltage sensitive calcium channels.
Action potentials (APs) (83 Hz) were evoked by field stimulation with a Grass Technologies S48 stimulation unit and a custom-built 24-well cap stimulator with pairs of parallel platinum wires. The microscope was an Olympus IX81 with a 10× (0.4 NA) air objective lens and EMCCD camera (Andor 897, 512 × 512 pixels, 35 frames/s), Cairn OptoLED illumination system, and GFP (Excitation: 450-490 nm; Dichroic: 495 nm long-pass; Emission: 500-550 nm) and TxRed (Excitation: 540-580 nm; Dichroic: 585 nm long-pass; Emission: 593-668 nm) filter sets. The field of view was 800 μm × 800 μm. Images were background subtracted (mean of 5% lowest pixel values). Responses were quantified for each cell as change in fluorescence divided by baseline fluorescence measured one second prior to stimulation. Signal-to-noise ratio (SNR) was quantified as peak ΔF/F0 response over the standard deviation of the signal during a one second period prior to stimulation.
Control experiments varying stimulation voltage, frequency, and pulse width insured suprathreshold stimulation of neurons. Voltage imaging using the ArchWT-GFP archaerhodopsin-based voltage sensor54 (link) confirmed that individual pulses (1 ms, 40 V, 83 Hz) reliably triggered single APs. The imaging and stimulation system was controlled by custom scripts written in MetaMorph software (version 7.7.5, Molecular Devices) and Ephus software55 (link) (ephus.org). Detailed neuronal culture screening methods will be described elsewhere (T.J.W., T.W.C., E.R.S., R.A.K., V.J., L.L.L., K.S., and D.S.K., manuscript in preparation).
Chen T.W., Wardill T.J., Sun Y., Pulver S.R., Renninger S.L., Baohan A., Schreiter E.R., Kerr R.A., Orger M.B., Jayaraman V., Looger L.L., Svoboda K, & Kim D.S. (2013). Ultra-sensitive fluorescent proteins for imaging neuronal activity. Nature, 499(7458), 295-300.
Publication 2013
2
Characterization of Optogenetic Proton Pumps
Cited 14 times
In vitro methods were as described in Chow et al. (2010 (link)). Briefly, opsins were mammalian codon-optimized, and were synthesized by Genscript (Genscript Corp., NJ, USA). Opsins were fused in frame, without stop codons, ahead of GFP (using BamHI and AgeI) in a lentiviral vector containing the CaMKII promoter (FCK-ArchT-GFP). Codon-optimized sequences of ArchT and ArchT-GFP are stored in GENBANK (http://www.ncbi.nlm.nih.gov/) at accession numbers: HM367071, ArchT, HM367072, ArchT-GFP. Genes are available for request at the link http://syntheticneurobiology.org/protocols. The amino acid sequence of ArchT is: MDPIALQAGYDLLGDGRPETLWLGIGTLLMLIGTFYFIVKGWGVTDKEAREYYSITILVPGIASAAYLSMFFGIGLTEVTVAGEVLDIYYARYADWLFTTPLLLLDLALLAKVDRVSIGTLVGVDALMIVTGLIGALSHTPLARYSWWLFSTICMIVVLYFLATSLRAAAKERGPEVASTFNTLTALVLVLWTAYPILWIIGTEGAGVVGLGIETLLFMVLDVTAKVGFGFILLRSRAILGDTEAPEP.
Swiss Webster or C57 mice (Taconic or Jackson Labs) were used. Hippocampal and cortical cultures were prepared as described in Chow et al. (2010 (link)). Neurons were transfected at 3–5 days in vitro using calcium phosphate (Invitrogen). GFP fluorescence was used to identify successfully transfected neurons.
Whole-cell patch clamp recordings were made on neurons at 9–14 days in vitro, using a Multiclamp 700B amplifier, Digidata 1440 digitizer, and a PC running pClamp (Molecular Devices). During recording, neurons were bathed in Tyrode solution containing (in mM): 125 NaCl, 2 KCl, 3 CaCl2, 1 MgCl2, 10 HEPES, 30 glucose, 0.01 NBQX, and 0.01 gabazine, at pH 7.3 (NaOH adjusted), and with 305–310 mOsm (sucrose adjusted). Borosilicate glass (Warner) pipettes were filled with a solution containing (in mM): 125 K-Gluconate, 8 NaCl, 0.1 CaCl2, 0.6 MgCl2, 1 EGTA, 10 HEPES, 4 Mg–ATP, 0.4 Na–GTP, at pH 7.3 (KOH adjusted), and with 295–300 mOsm (sucrose adjusted). Pipette resistance was 5–10 MΩ; access resistance was 10–30 MΩ, monitored throughout the voltage-clamp recording; resting membrane potential was approximately −60 mV in current-clamp recording. To assess proton pumping by previously uncharacterized opsins, neurons were bathed in recording solution containing (in mM): 125 N-methyl-d-glucamine, 2 Cs-methanesulfonate, 3 CdSO4, 1 MgSO4, 10 HEPES, 30 glucose, 0.01 NBQX, 0.01 gabazine, pH 7.3 (H2SO4 adjusted), 305–310 mOsm (sucrose adjusted), and pipettes were also filled with analogous solutions containing (in mM): 125 Cs-methanesulfonate, 8 N-methyl-d-glucamine, 0.1 CdSO4, 0.6 MgSO4, 1 EGTA, 10 HEPES, 4 Mg–ATP, 0.4 Tris–GTP, pH 7.3 (CsOH adjusted), 295–300 mOsm (sucrose adjusted).
Photocurrents were measured with 1- or 15-s duration light pulses in neurons voltage clamped at −60 mV. Light-induced membrane hyperpolarizations were measured with 1-s light pulses, in neurons current clamped at their resting membrane potential. For all experiments except for the action spectrum characterization experiments, a DG-4 optical switch with 300 W xenon lamp (Sutter Instruments) was used to deliver light pulses. The DG-4 was controlled via TTL pulses generated through a Digidata signal generator. A 575 ± 25 nm bandpass filter (Chroma) was used to deliver yellow light. In order to extend our power characterization of Arch and ArchT beyond the power of the yellow light available on our microscope using the configuration that we utilized, we extrapolated to higher effective yellow powers by equating various powers of unfiltered white light illumination from the DG4, to approximate effective yellow power equivalents, as done in Chow et al. (2010 (link)). For action spectrum characterization, a Till Photonics PolyChrome V, 150 W xenon, 15 nm monochromator bandwidth, was used. Data was analyzed using Clampfit (Molecular Devices) and MATLAB (Mathworks, Inc.). Statistical analysis and curve fitting was done with Statview (SAS Institute), MATLAB, GraphPad, and Origin (OriginLab).
Han X., Chow B.Y., Zhou H., Klapoetke N.C., Chuong A., Rajimehr R., Yang A., Baratta M.V., Winkle J., Desimone R, & Boyden E.S. (2011). A High-Light Sensitivity Optical Neural Silencer: Development and Application to Optogenetic Control of Non-Human Primate Cortex. Frontiers in Systems Neuroscience, 5, 18.
Publication 2010
3
Characterization of Optogenetic Tools in Neurons
Cited 13 times
Recordings in cultured neurons were performed 4–6 d after transfection in Tyrode’s solution (320 mOsm): 125 mM NaCl, 2 mM KCl, 2 mM CaCl2, 2 mM MgCl2, 30 mM glucose and 25 mM HEPES, titrated to pH 7.3–7.4 with NaOH. Tyrode was perfused at a rate of 1–2 ml min−1 and was kept at room temperature (20–22 °C). Intracellular solution (300 mOsm) contained 130 mM K-gluconate, 10 mM KCl, 10 mM HEPES, 10 mM EGTA and 2 mM MgCl2, titrated to pH 7.3 with KOH. Characterization of excitatory tools was done with bath-applied tetrodotoxin (TTX) (1 µM; Sigma-Aldrich) and intracellular QX-314 chloride (1 mM; Tocris Bioscience). In vitro patching of hyperpolarizing tools and current clamp recordings for depolarizing tools were performed in the presence of synaptic transmission blockers 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 µM; Sigma-Aldrich) and d(-)-2-amino-5-phosphonovaleric acid (APV; 25 µM, Sigma-Aldrich) as well as gabazine for the current clamp experiments (10 µM; Sigma-Aldrich). Recordings were performed on an upright Leica DM-LFSA microscope.
Recordings of ChETAA, ChETATR and ChIEF-expressing fast-spiking cells were performed in acute slices from Pvalb::cre transgenic mice, 6 weeks (ChETAA versus ChETATR comparison) or 4 weeks (ChETAA versus ChIEF comparison) after virus injections. Artificial cerebrospinal fluid (ACSF) (300 mOsm) was composed of 123 mM NaCl, 26 mM NaHCO3, 3 mM KCl, 1.25 mM NaH2PO4·H2O, 1 mM MgCl2·6H2O, 2 mM CaCl2·2H2O and 11 mM glucose. ACSF was bubbled with 95% O2 and 5% CO2 (Praxair) to an equilibrium pH of 7.3. ACSF was perfused at a rate of 7 ml min−1 and heated to 32 °C. The intracellular solution was adjusted to 280 mOsm using water. Fast-spiking cells were identified by eYFP expression and characteristic electrophysiological properties. Recordings were performed on an upright Leica DM-LFSA microscope.
Recordings of eYFP-, eNpHR3.0- and eArch3.0-expressing pyramidal cells were performed in acute slices from wild-type C57BL/6 mice 6–7 weeks after virus injection. ACSF contained CNQX, APV and gabazine. Intracellular solution (280 mOsm) contained 135 mM K-gluconate, 5 mM KCl, 10 mM HEPES, 0.1 mM EGTA, 2 mM MgCl2, 2 mM Mg-ATP and 0.2 mM Na2-GTP, titrated to pH 7.4 with KOH. Pyramidal cells were identified by morphology and characteristic electrophysiological properties. Recordings were performed on an upright Olympus BX51 microscope. For all patching experiments, borosilicate glass (Sutter Instruments) pipette resistances were 3–6 MΩ. For cell-attached electrophysiology recordings, upon obtaining GΩ seals, holding potential was set so that no net current flowed across the membrane; the same stimulation protocols were used as for whole-cell spiking experiments. After the cell-attached recording was performed, we applied suction to the pipette to break into the cell and repeated the same experiments in whole-cell configuration to provide a direct within-cell comparison. No exogenous retinal cofactor was added to neurons in any preparation.
Data collection across opsins was randomized and distributed to minimize across-group differences in expression time, room temperature and so on.
Mattis J., Tye K.M., Ferenczi E.A., Ramakrishnan C., O’Shea D.J., Prakash R., Gunaydin L.A., Hyun M., Fenno L.E., Gradinaru V., Yizhar O, & Deisseroth K. (2011). Principles for applying optogenetic tools derived from direct comparative analysis of microbial opsins. Nature methods, 9(2), 159-172.
Publication 2011
4
Chemogenetic Modulation of Cocaine Seeking
Cited 11 times
Behavioral training and testing took place in standard Med Associates operant chambers described elsewhere23 (link). Rats underwent 10 daily 2 h self-administration sessions (>10 cocaine infusions/day, 0.2 mg/50 μl infusion). Pressing one lever yielded a 3.6 s cocaine infusion, tone, and light above the active lever (FR1 schedule), followed by a 20 s timeout, when pressing was recorded but did not yield cocaine or cues (Figure 2a). Inactive lever presses were recorded, but had no consequences. Animals then received 7+ d of extinction training (until criterion: <25 presses for 2 consecutive days), where lever presses yielded neither cocaine nor cues.
During 2 h cue-induced reinstatement tests, active lever presses yielded cocaine cues, but no cocaine. For cocaine priming tests, 10 mg/kg i.p. cocaine was administered immediately prior to the 2 h test, where lever presses yielded neither cocaine nor cues. For the CTb/Fos experiment, animals were perfused immediately after one of the following 2 h test sessions: CS+ reinstatement, an additional extinction session, exposure to a novel environment, or exposure to a discrete CS− (details in23 (link)). Behavior during the first 30 min of tests (which most influences Fos protein measured 90 min later) was compared to neuronal activation (Fig. 3).
Animals that received systemic CNO had 3 cued, and 3 cocaine primed reinstatement tests each. 30 min prior to each test, RVP (n=16) or CVP (n=17) Syn-hM4Di-HA-GFP animals, VP Syn-GFP animals (n=5), and animals with no virus expression (n=9) received counterbalanced i.p. injections of vehicle, and 2 doses of CNO [0.1 mg/kg: n=25; 1.0 mg/kg: n=25; 10 mg/kg: n=26; 20 mg/kg: n=30). Other animals received counterbalanced intra-VTA (after RVP or CVP Syn-hM4Di-HA-GFP) or intra-SN (after RVP Syn-hM4Di-HA-GFP) microinjections of vehicle (aCSF) and CNO (1 mM/0.3 μl) 5 min prior to each of 2 cued, and 2 primed reinstatement tests. Some of these animals were later habituated to an open field for 2 d, then locomotor activity after vehicle and CNO was tested over 2 d, 48 h+ apart (intra-VTA CNO: 0&1 mM/0.3 μl, n=23). TH::Cre animals (RVP Syn-hM4Di-HA-GFP +VTA DIO-Syn-hM4Di-mCherry: Cre+ n=9, Cre- n=10; RVP Syn-hM4Di-HA-GFP+SN DIO-Syn-hM4Di-mCherry: Cre+ n=8; VTA DIO-Syn-hM4Di-mCherry only n=6) received i.p. vehicle or CNO (10 mg/kg) 30 min before each of two cue-induced reinstatement tests. Animals with unilateral RVP Syn-hM4Di-HA-GFP +contralateral VTA cannulae underwent 3 cued reinstatement tests after unilateral VTA vehicle+i.p. CNO (10 mg/kg), and two of the following: intra-VTA baclofen/muscimol+ i.p. CNO (n=12 rats), intra-VTA CNQX/AP5+ i.p. CNO (n=5), intra-VTA baclofen/muscimol+ i.p. vehicle (n=8). For bilateral VTA gabazine, animals also underwent 2–3 reinstatement tests, after vehicle and 10 μM (n=7 rats), and 100 μM (n=4) gabazine (high dose testing was discontinued due to intense nonspecific locomotor activation). Vehicle/CNO injection order was counterbalanced in all cases.
Mahler S.V., Vazey E.M., Beckley J.T., Keistler C.R., McGlinchey E.M., Kaufling J., Wilson S.P., Deisseroth K., Woodward J.J, & Aston-Jones G. (2014). Designer Receptors Show Role for Ventral Pallidum Input to Ventral Tegmental Area in Cocaine Seeking. Nature neuroscience, 17(4), 577-585.
Publication 2014
5
Patch-Clamp Recordings of Neuronal Electrophysiology
Cited 11 times
Whole cell patch clamp recordings were made using Axopatch 200B or Multiclamp 700B amplifier, a Digidata 1440 digitizer, and a PC running pClamp (Molecular Devices). For in vitro current-clamp recordings, neurons were patched 14–18 DIV (10–14 days post-transfection) to allow for sodium channel maturation. Neurons were bathed in room temperature Tyrode containing 125 mM NaCl, 2 mM KCl, 3 mM CaCl2, 1 mM MgCl2, 10 mM HEPES, 30 mM glucose, 0.01 mM NBQX and 0.01 mM GABAzine. The Tyrode pH was adjusted to 7.3 with NaOH and the osmolarity was adjusted to 300 mOsm with sucrose. For in vitro voltage-clamp recordings, neurons were patched 11–14 DIV (7–10 days post-transfection) and were done under similar conditions as current-clamp recordings, except tyrode also contains 1 μM of tetrodotoxin (TTX, Tocris Bioscience). No retinal was supplemented for any cultured neuron recordings.
For slice recordings, room temperature artificial cerebrospinal fluid (ACSF) was continuously perfused over slices and no blockers were used. ACSF contained: 127 mM NaCl, 2.5 mM KCl, 25 mM NaHCO3, 1.25 mM NaH2PO4, 12 mM D-glucose, 0.4 mM sodium ascorbate, 2 mM CaCl2, 1 mM MgCl2, and was bubbled continuously with carbogen.
For both in vitro and slice recordings, borosilicate glass pipettes (Warner Instruments) with an outer diameter of 1.2 mm and a wall thickness of 0.255 mm were pulled to a resistance of 3–7 MΩ with a P-97 Flaming/Brown micropipette puller (Sutter Instruments) and filled with a solution containing 125 mM K-gluconate, 8 mM NaCl, 0.1 mM CaCl2, 0.6 mM MgCl2, 1 mM EGTA, 10 mM HEPES, 4 mM Mg-ATP, and 0.4 mM Na-GTP. The pipette solution pH was adjusted to 7.3 with KOH and the osmolarity was adjusted to 298 mOsm with sucrose. For voltage clamp experiments, cells were clamped at −65 mV for in vitro (HEK293, cultured neuron) recordings and between −65 to −80 mV for slice recordings. For current clamp experiments, <50 pA constant current injection was used for in vitro recordings and no current injection was used for slice recordings. To ensure accurate measurements, cells with access resistance between 5–35 MΩ, holding current less than ± 100 pA (at −65 mV, in voltage clamp) were used. Access resistance was monitored throughout recording. Data was analyzed using Clampfit (Molecular Devices) and custom MATLAB scripts (Mathworks, Inc.)
Klapoetke N.C., Murata Y., Kim S.S., Pulver S.R., Birdsey-Benson A., Cho Y.K., Morimoto T.K., Chuong A.S., Carpenter E.J., Tian Z., Wang J., Xie Y., Yan Z., Zhang Y., Chow B.Y., Surek B., Melkonian M., Jayaraman V., Constantine-Paton M., Wong G.K, & Boyden E.S. (2014). Independent Optical Excitation of Distinct Neural Populations. Nature methods, 11(3), 338-346.
Publication 2014
2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline Bicarbonate, Sodium carbogen Cells Cerebrospinal Fluid Egtazic Acid gabazine gluconate Glucose HEPES Magnesium Chloride Medical Devices Neurons Osmolarity Retina Sodium Ascorbate Sodium Channel Sodium Chloride Sucrose Transfection

Most recents protocols related to «Gabazine»

1
Targeted Neuromodulation of Vocal Circuitry
Solutions within fabricated glass micropipettes (~20 µm diameter) were pressure-ejected using a picospritzer (Biomedical Engineering; ~25 nl/ pulse, repeated at ~2 Hz, at 25–30 PSI)15 (link),23 (link),45 (link). Fictive calls were monitored continuously before, during and after each injection. Injections of gabazine (Tocris Biosciences; 50-150 nl total volume, ~25 nl/pulse, 1 mM in 0.1 M PB) within forebrain vocal regions induced persistent fictive calling. To block such calling, we pressure injected either muscimol (Sigma-Aldrich, 10 mM in 0.1 M PB; n = 2) or a NBQX (Sigma-Aldrich, 2.5 mM in 0.1 M PB) and APV (Sigma-Aldrich, 2.5 mM in 0.1 M PB) cocktail (n = 2; ~250 nl) into the PAG during extended periods of fictive calling. Bilateral injections were performed sequentially with one micropipette. Either 5% Fluoroscein or 5% Alexa-Fluor 568 (Invitrogen-Fisher Scientific) was included in the pipette solutions to facilitate locating injection sites. For pharmacological mapping of midbrain or hindbrain vocal sites, micropipettes were filled with either 0.5M L-glutamate (GLU, Sigma-Aldrich) in 0.1 M PB (pH8), or 1 mM gabazine (Tocris Bioscience) in 0.1 M PB. To localise the injection sites, 5% neurobiotin was included in the pipette solutions. After baseline recordings searching for vocal sites that were identified using electrical stimulation (see45 (link)), a glass micropipette was guided to possible vocal sites using surface landmarks, effective depths for electrical stimulation, and previous mapping studies15 (link),23 (link),45 (link),69 (link). The pipette solution was pressure-ejected using the picospritzer (total volume, 25–100 nl of GLU or 100–300 nl of gabazine).
Each fish was injected unilaterally with either GLU or gabazine. For each site injected with GLU, injections were repeated at least three times, with at least 5 min between each injection if no calling was evoked, and at least 5 min after the cessation of calling if calling was evoked. Response to at least one injection of GLU was considered a ‘positive’ site. Typically, two specific sites were tested for GLU response in each animal, one on each side of the brain, with more than a 20 min interval between injections in distinct sites that allowed for complete recovery from any effect of the first injection. Midbrain vocal responses following gabazine injection occurred at longer latencies but persisted for longer durations. Because of this, longer periods between injection sites were used (at least 30 min without calling before a new site would be tried), and if the first site produced calling, only one site would be tested in that fish. For both drugs, sites that did not respond were only classified as non-vocal if the fish maintained fictive vocal responses to electrical stimulation throughout the experiment, and later histological examination showed that tracer dye had in fact been released into the brain.
The locations of midbrain injection sites were confirmed in 52 cases for GLU, and 18 cases for gabazine. 26 GLU and 9 gabazine cases were located within the designated boundaries of PAGcs and PAGcd (Fig. S8d, e), and thus considered hits; fictive vocal data from sites outside these regions occurred rarely, and only ever at long latencies. The locations of hindbrain injection sites in the vocal prepacemaker nucleus (VPP) were confirmed in 3 cases for GLU. Following transcardial perfusion with a cold teleost Ringer rinse, brains were removed, post-fixed for 24 h in 4% paraformaldehyde in 0.1 M PB, and then sectioned as described earlier. Where neurobiotin was used as a marker, it was processed for visualisation using either diamionobenzidine (DAB) or Strepavidin-AF596. Injection sites were checked using light or fluorescence microscopy (Nikon Eclipse E800), and the centre of the injection site was taken to be the point of densest stain, or at the end of a visible pipette track in the tissue. These points were registered to a common reference brain based on distance from local anatomical landmarks within the midbrain and hindbrain.
Schuppe E.R., Ballagh I., Akbari N., Fang W., Perelmuter J.T., Radtke C.H., Marchaterre M.A, & Bass A.H. (2024). Midbrain node for context-specific vocalisation in fish. Nature Communications, 15, 189.
Publication 2024
2
Modulation of Neuronal Activity
Adenosine (10–100 µM), 8-Cyclopentyltheophylline (CPT, 1 μM), CGS21680 (30 nM), tetrodotoxin (TTX, 0.5 μM), and gabazine (10 μM) were all bath applied via the perfusion system for 3–7 min; drugs were purchased either from Sigma-Aldrich or Tocris.
Ding C., Yang D, & Feldmeyer D. (2024). Adenosinergic Modulation of Layer 6 Microcircuitry in the Medial Prefrontal Cortex Is Specific to Presynaptic Cell Type. The Journal of Neuroscience, 44(15), e1606232023.
Publication 2024
3
Gabazine-Induced Neural Activity Changes
Based on several in-vivo studies, we used a 10 µM gabazine (GBZ) concentration since this concentration does not trigger any epileptiform neuronal activity (Darbin et al. 2006; Gaucher et al. 2013; Wang et al. 2009). A small quantity of the drug (0.1 ml) was delicately applied in the immediate vicinity of the electrode using a syringe. The drug was allowed to diffuse along the electrode shaft for about 4 min. Then, the cortical surface overlying the electrode (primary visual cortex) was rinsed with saline solution to remove any remaining residue of the drug. The visual inspection of neural activity did not show any epileptic activity in the IC after GBZ application. Moreover, we could observe that neural responses started to change 6 to 8 min after GBZ application. The effect of gabazine in both groups was studied at three different time points after the drug application (15 min, 45 min, and 90 min). The stability of neural activity before GBZ application was assessed (supplementary Fig. 1).
Parameshwarappa V., Siponen M.I., Watabe I., Karkaba A., Galazyuk A, & Noreña A.J. (2024). Noise-induced hearing loss alters potassium-chloride cotransporter KCC2 and GABA inhibition in the auditory centers. Scientific Reports, 14, 10689.
Publication 2024
4
Measuring Fictive Vocalizations in Pharmacology
Latencies and durations of pharmacologically induced calling were measured using Clampfit 9 (Axon Instruments). Latency was measured from the mechanical artifact in the recorded trace created by the first injection pulse to the first spike in a fictive vocalisation. Duration was measured from the first spike in a fictive vocalisation to the last spike of the last fictive vocalisation. In some cases, gabazine injection initiated persistent calling, sometimes lasting up to ~1.5 h; calling was considered terminated when the experiment ended, and the recording ceased. Physiology data (axon binary files) were imported using a preexisting MathWorks script. For analysis of call rate (calls per min) data were then processed using Matlab (Mathworks) with custom written scripts (I.H.B.). For analysis of spontaneous and forebrain-gabazine induced calling rates (and their silencing by midbrain injections), we calculated the number of fictive calls per min for each min of the experiment, before, during and after attempted midbrain silencing.
Schuppe E.R., Ballagh I., Akbari N., Fang W., Perelmuter J.T., Radtke C.H., Marchaterre M.A, & Bass A.H. (2024). Midbrain node for context-specific vocalisation in fish. Nature Communications, 15, 189.
Publication 2024
5
Pharmacological Reagents for Neuroscience
Most drugs were dissolved in water to make stock solutions (typically at 10,000× concentration) that were frozen as aliquots and used as needed during experiments. ACh (Fisher Scientific) was bath-applied with physostigmine hemisulfate (eserine; Tocris Bioscience), a blocker of acetylcholinesterase (AChE). Atropine and pirenzepine dihydrochloride were purchased from Sigma-Aldrich. TTX citrate and CGP 52432 were purchased from HelloBio, Inc. CNO dihydrochloride, DNQX, and D-AP5 were purchased from Tocris Bioscience. SR-95531 (gabazine) was purchased from MedChemExpress and dissolved in DMSO for stock solutions.
, & Gulledge A.T. (2024). Cholinergic Activation of Corticofugal Circuits in the Adult Mouse Prefrontal Cortex. The Journal of Neuroscience, 44(3), e1388232023.
Publication 2024

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Picrotoxin is a chemical compound that acts as a GABA antagonist. It is primarily used in scientific research as a tool to study the function of GABA receptors.
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Dimethyl sulfoxide (dmso) by Merck Group
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

More about "Gabazine"

Gabazine, also known as SR-95531, is a powerful and selective GABA(A) receptor antagonist commonly utilized in neuroscience research.
It plays a crucial role in investigating the function of GABA-mediated inhibition in various neurological processes and disorders.
Gabazine exerts its effects by binding to the GABA(A) receptor, effectively blocking the inhibitory actions of the neurotransmitter GABA and altering neuronal excitability.
This makes it a valuable tool for researchers studying the contribution of GABAergic signaling in areas such as synaptic transmission, neuronal network dynamics, and the pathophysiology of conditions like epilepsy, anxiety, and cognitive dysfunction.
Researchers can employ Gabazine in conjunction with other related compounds, such as Strychnine (a glycine receptor antagonist), the Multiclamp 700B amplifier (a versatile electrophysiology tool), D-AP5 (an NMDA receptor antagonist), and Picrotoxin (another GABA(A) receptor antagonist).
Additionally, the use of DMSO as a solvent can facilitate the administration of Gabazine in experimental settings.
By leveraging the insights gained from the MeSH term description and the Metadescription, researchers can optimize their Gabazine studies with the help of PubCompare.ai.
This platform provides access to the latest protocols from literature, preprints, and patents, enabling researchers to identify the most robust and reliable experimental approaches through intelligent comparisons.
Streamlining the research process with PubCompare.ai's powerful tools can lead to more accurate and reproducible results in the investigation of GABA-mediated neurological processes and disorders.