Techniques have been developed to maintain neural cultures and conduct experiments for many months59 . Here, cells from embryonic day 18 Wistar rat cortices were dissociated in 2 ml of trypsin with 0.25% EDTA (Invitrogen) with trituration, and 10,000–40,000 cells were seeded over an area of ~12 mm2 on top of the CMOS chip. A thin layer of poly(ethyleneimine) (Sigma), 0.05% by weight in borate buffer (Chemie Brunschwig) at 8.5 pH, followed by a 10-μl drop of 0.02 mg ml−1 laminin (Sigma) in Neurobasal (Invitrogen) were used for cell adhesion. After 24 h, the plating media was changed to growth media. Plating media consisted of 850 μl of Neurobasal supplemented with 10% horse serum (HyClone), 0.5 mM GlutaMAX (Invitrogen) and 2% B27 (Invitrogen). Growth media consisted of 850 μl of DMEM (Invitrogen) supplemented with 10% horse serum, 0.5 mM GlutaMAX and 1 mM sodium pyruvate (Invitrogen). Cultures matured for 3–4 weeks before experimentation, and experiments were conducted inside an incubator for a control of environmental conditions (36 °C and 5% CO2). The MEAs were sealed using a Potter ring containing a hydrophobic membrane (fluorinated ethylene–propylene) that is selectively permeable to O2 and CO2, and relatively impermeable to water vapour, bacteria and fungus60 (link); this allows long-term, non-invasive experimentation. To block synaptic activity, antagonists of fast synaptic receptors were used: 50 μM bicuculline methiodide, 100 μM 2-amino-5-phosphonovaleric acid and 10 μM 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX; Sigma), dissolved in growth media. These inhibit GABA-R, NMDA-R and AMPA-R, respectively, and effectively silence network activity. Cultures were allowed to equilibrate for an additional 30 min before experimentation. To visualize whole neurons, cells were sparsely transfected with a human synapsin I promoter driving DsRedExpress from the Callaway lab (Addgene plasmid 22909) using Lipofectamine 2000 (Invitrogen 11668)35 (link). Images were collected at room temperature on a Leica DM6000 FS microscope with a × 10 long working distance objective lens and a Leica DFC 345 FX camera using the Leica Application Suite software. The monochrome camera captured 1600 × 1200 pixel images (0.35 μm per pixel edge) at a 12-bit resolution, which were later pseudo-coloured and inverted.
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Bicuculline methiodide
Bicuculline methiodide
Bicuculline methiodide is a potent and selective GABA(A) receptor antagonist used extensively in neuroscience research.
It blocks the inhibitory effects of GABA, allowing researchers to study the role of GABAergic signaling in various neurological processes.
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It blocks the inhibitory effects of GABA, allowing researchers to study the role of GABAergic signaling in various neurological processes.
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Most cited protocols related to «Bicuculline methiodide»
Action Potentials
Axon
Bicarbonate, Sodium
bicuculline methiodide
Calcium
Cells
Cytoplasmic Granules
Dendritic Cells
Egtazic Acid
GABA-A Receptor
gabazine
Glucose
HEPES
Induced Pluripotent Stem Cells
Kidney Glomerulus
Magnesium Chloride
Neoplasm Metastasis
Pufferfish
Pulses
Sodium Chloride
We used C57BL/6J WT mice aged 3–12 weeks of both sex (experiments shown in Figures 3 , 4 , 5 , 7 , 8 ), as well as 16–28-day-old C57BL/6J/129 hybrid mice, which were either WT, App-KO, Aplp2-KO, or App/Aplp2-dKO (experiments shown in Figures 9 , 11, 12 ). The experimenter was blind to genotype and/or treatment. Coronal brain slices containing the hippocampal formation were prepared as previously described (Talani et al., 2011 (link)). In brief, animals were anesthetized with isoflurane, following the University of California San Diego Institutional Animal Care and Use Committee (IACUC) approved protocol. Brains were rapidly removed from the skull and placed in an ice-cold modified ACSF solution containing (in mM): 215 sucrose, 2.5 KCl, 1.6 NaH2PO4, 4 MgSO4, 1 CaCl2, 4 MgCl2, 20 glucose, 26 NaHCO3 (pH 7.4 equilibrated with 95% O2 and 5% CO2).Coronal brain slices (400 μm thick) were prepared with a Vibratome VT1200S (Leica Microsystems, Germany) and then incubated at room temperature in a physiologic ACSF, containing (in mM): 120 NaCl, 3.3 KCl, 1.2 Na2HPO4, 26 NaHCO3, 1.3 MgSO4, 1.8 CaCl2, 11 Glucose (pH 7.4 equilibrated with 95% O2 and 5% CO2). The hemi-slices were transferred to a recording chamber perfused with ACSF at a flow rate of ~2 ml/min using a peristaltic pump; experiments were performed at 28.0 ± 0.1°C. All recordings were performed using a multiclamp 700B amplifier (Molecular Devices). For extracellular field recordings (fEPSP recordings), a patch-type pipette was fabricated on a micropipette puller (Sutter Instruments, Novato, CA, USA), filled with 1M NaCl, and placed in the middle third of stratum radiatum in area CA1. Field excitatory postsynaptic potentials (fEPSPs) were evoked by activating SCs with a patch-type pipette (monopolar stimulation) filled with ACSF and placed in the middle third of stratum radiatum 150–200 μm away from the recording pipette and at approximately the same slice depth (150–200 μm). Square-wave current pulses (60 μs pulse width) were generated by a stimulus generator (Master 8, AMPI) and delivered through a stimulus isolator (Isoflex, AMPI). I/O function was generated by stimulating in 0.1 mA steps from 0.1 to 1.0/1.2 mA. Paired-pulse ratio (PPR) was measured by delivering two stimuli at 20, 40, 80, 200, 500, and 1000 ms inter-stimulus intervals. Synaptic facilitation was examined by repetitive stimulation (10 stimuli) at 1, 5, 10, and 20 Hz. Depletion of synaptic transmission was elicited by a long train (500 stimuli, 28 Hz) in 5 mM extracellular Ca2+ and in the presence of the NMDA receptor antagonist 2-amino-5-phosphopentanoic acid (DL-AP5) (100 µM). Recovery was assessed with nine stimuli at 2 Hz. Depletion and recovery plots were generated by normalizing responses to the peak amplitude of the fEPSP in the depletion train. The stimulus strength was adjusted so that the basal synaptic amplitude was similar (e.g., 0.5–1.0 mV) across experiments. To monitor miniature excitatory postsynaptic currents (mEPSCs), patch-clamp whole-cell recordings were performed from CA1 pyramidal cells, and we used an infrared differential interference contrast microscope (Nikon eclipse E600FN, Morrel Instrument Company Inc, Melville New York). The cells were voltage-clamped at -65 mV, and the patch pipette (resistance 3–6 MΩ) was filled with an internal solution containing (in mM): 131 CsCl, 8 NaCl, 1 CaCl2, 10 EGTA, 10 Glucose, 10 HEPES (pH = 7.3, 286 mmol/Kg). Series resistance (5 and 15 MΩ) was constantly monitored throughout the experiments by delivering a -5 mV, 80 ms voltage step, and cells with >10% change in series resistance were excluded from analysis. mEPSCs were recorded in the presence of 1 μM TTX and 15 μM 1(S), 9(R)(−)bicuculline methiodide, to block action potentials and GABA-A receptors, respectively. To calculate average mEPSCs recorded from at least three (Figures 4 and 8 ) and five (Figure 12 ) CA1 pyramidal neurons (between ~1000 and 600 events each) were normalized, aligned, and averaged.
Data acquisition and statistical analysis. Output signals were acquired at 5 kHz, filtered at 2.4 kHz, and stored online using pCLAMP 10.3 Electrophysiology Data Acquisition and Analysis Software (Molecular Devices). mEPSCs were analyzed using Mini Analysis software (Synaptosoft). In all cases the experimenter was blind to genotype and/or treatment. Data are presented as means ± SEM. Statistical comparisons of pooled data were performed by unpaired t-test or ANOVA (one- or two-way) using Prism software (GraphPad, San Diego,CA, USA). A p value of <0.05 was considered statistically significant.
Drugs were obtained from Sigma-Aldrich 1(S), 9(R)(−)bicuculline methiodide, Biotium (TTX) and Enzo Life Science (DL-AP5). Stock solutions were prepared in water and dimethyl sulfoxide (DMSO) and added to the ACSF as needed.
Data acquisition and statistical analysis. Output signals were acquired at 5 kHz, filtered at 2.4 kHz, and stored online using pCLAMP 10.3 Electrophysiology Data Acquisition and Analysis Software (Molecular Devices). mEPSCs were analyzed using Mini Analysis software (Synaptosoft). In all cases the experimenter was blind to genotype and/or treatment. Data are presented as means ± SEM. Statistical comparisons of pooled data were performed by unpaired t-test or ANOVA (one- or two-way) using Prism software (GraphPad, San Diego,CA, USA). A p value of <0.05 was considered statistically significant.
Drugs were obtained from Sigma-Aldrich 1(S), 9(R)(−)bicuculline methiodide, Biotium (TTX) and Enzo Life Science (DL-AP5). Stock solutions were prepared in water and dimethyl sulfoxide (DMSO) and added to the ACSF as needed.
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One day after HSV injection, the rats were anaesthetized with ketamine/xylazine or pentobarbital, acute brain slices were prepared and whole-cell recordings were performed as previously described12 (link). No viral injection was performed for the analysis of the AMPA/NMDA ratio (Fig. 3b ). Briefly, the brain was quickly perfused with ice-cold dissection buffer (25.0 mM NaHCO3, 1.25 mM NaH2PO4, 2.5 mM KCl, 0.5 mM CaCl2, 7.0 mM MgCl2, 25.0 mM glucose, 110.0 mM choline chloride, 11.6 mM ascorbic acid and 3.1 mM pyruvic acid) and gassed with 5%CO2/95%O2. Coronal brain slices were cut (350 μm, Leica vibratome, VT-1200S) in dissection buffer and transferred into physiological solution (22–25 °C, 118 mM NaCl, 2.5 mM KCl, 26 mM NaHCO3, 1 mM NaH2PO4, 10 mM glucose, 4 mM MgCl2, 4 mM CaCl2, pH 7.4, and gassed with 5%CO2/95%O2). The recording chamber was perfused with physiological solution containing 0.1 mM picrotoxin, 4 μM 2-chloroadenosine at 22–25 °C. For the rectification experiments, we added 0.1 mM D,L-2-amino-5-phosphonopentanoic acid to the perfusate to block NMDA receptors. For the miniature response recordings, we used the physiological solution containing 0.5 μM tetrodotoxin to block Na+ channels.
Patch-recording pipettes (4–7 MΩ) were filled with intracellular solution (115 mM caesium methanesulfonate, 20 mM CsCl, 10 mM HEPES, 2.5 mM MgCl2, 4 mM Na2ATP, 0.4 mM Na3GTP, 10 mM sodium phosphocreatine and 0.6 mM EGTA at pH 7.25)42 (link). For miniature recordings, we used modified intracellular solution to adjust the reversal potential of the γ-aminobutyric acid-A receptor response (127.5 mM caesium methanesulfonate, 7.5 mM CsCl, 10 mM HEPES, 2.5 mM MgCl2, 4 mM Na2ATP, 0.4 mM Na3GTP, 10 mM sodium phosphocreatine, 0.6 mM EGTA, pH 7.25). Whole-cell recordings were obtained from infected or uninfected CA1 pyramidal neurons of rat hippocampus with an Axopatch–700B amplifier (Axon Instruments). There were no significant differences in input or series resistance among groups. Bipolar tungsten stimulating electrodes were placed in CA1 ~200–300 μm lateral from the recorded cells. The stimulus intensity was increased until a synaptic response of amplitude >~10 pA was recorded. When recording simultaneously from two cells, the stimulus intensity was increased until both cells showed a response >~10 pA. Synaptic AMPA receptor-mediated responses at –60 and +40 mV were averaged over 50–100 trials, and their ratio (averaged response at −60 mV/+40 mV) was used as an index of rectification. For paired recordings, infected and nearby uninfected cells (~100 μm) were accessed as whole cells, and the synaptic response to a stimulus was recorded from both cells simultaneously.
The AMPA/NMDA ratio was calculated as the ratio of the peak current at −60 mV to the current at +40 mV 150 ms after stimulus onset (40–60 traces averaged for each holding potential). For the miniature recordings, the mEPSC (−60 mV holding potential) and mIPSC (0 mV holding potential) were recorded for 5 min in the same CA1 neuron. Bath application of an AMPA receptor blocker (CNQX, 10 μM) or γ-aminobutyric acid-A receptor blocker (bicuculline methiodide, 10 μM) completely blocked the mEPSC (at −60 mV) or mIPSC (at 0 mV) events, respectively. To evaluate the paired-pulse ratio from the EPSC or IPSC average, 30–60 sweeps were recorded with paired stimuli at 100-ms intervals. The EPSC or IPSC amplitudes were measured from the peak of the post-synaptic current to the basal current level immediately before the electrical stimulation.
Patch-recording pipettes (4–7 MΩ) were filled with intracellular solution (115 mM caesium methanesulfonate, 20 mM CsCl, 10 mM HEPES, 2.5 mM MgCl2, 4 mM Na2ATP, 0.4 mM Na3GTP, 10 mM sodium phosphocreatine and 0.6 mM EGTA at pH 7.25)42 (link). For miniature recordings, we used modified intracellular solution to adjust the reversal potential of the γ-aminobutyric acid-A receptor response (127.5 mM caesium methanesulfonate, 7.5 mM CsCl, 10 mM HEPES, 2.5 mM MgCl2, 4 mM Na2ATP, 0.4 mM Na3GTP, 10 mM sodium phosphocreatine, 0.6 mM EGTA, pH 7.25). Whole-cell recordings were obtained from infected or uninfected CA1 pyramidal neurons of rat hippocampus with an Axopatch–700B amplifier (Axon Instruments). There were no significant differences in input or series resistance among groups. Bipolar tungsten stimulating electrodes were placed in CA1 ~200–300 μm lateral from the recorded cells. The stimulus intensity was increased until a synaptic response of amplitude >~10 pA was recorded. When recording simultaneously from two cells, the stimulus intensity was increased until both cells showed a response >~10 pA. Synaptic AMPA receptor-mediated responses at –60 and +40 mV were averaged over 50–100 trials, and their ratio (averaged response at −60 mV/+40 mV) was used as an index of rectification. For paired recordings, infected and nearby uninfected cells (~100 μm) were accessed as whole cells, and the synaptic response to a stimulus was recorded from both cells simultaneously.
The AMPA/NMDA ratio was calculated as the ratio of the peak current at −60 mV to the current at +40 mV 150 ms after stimulus onset (40–60 traces averaged for each holding potential). For the miniature recordings, the mEPSC (−60 mV holding potential) and mIPSC (0 mV holding potential) were recorded for 5 min in the same CA1 neuron. Bath application of an AMPA receptor blocker (CNQX, 10 μM) or γ-aminobutyric acid-A receptor blocker (bicuculline methiodide, 10 μM) completely blocked the mEPSC (at −60 mV) or mIPSC (at 0 mV) events, respectively. To evaluate the paired-pulse ratio from the EPSC or IPSC average, 30–60 sweeps were recorded with paired stimuli at 100-ms intervals. The EPSC or IPSC amplitudes were measured from the peak of the post-synaptic current to the basal current level immediately before the electrical stimulation.
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bicuculline methiodide
Cannula
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
Fentanyl Citrate
Kainic Acid
Microinjections
Neurons
Pharmaceutical Preparations
Sulfate, Morphine
Most recents protocols related to «Bicuculline methiodide»
Acute slices were prepared as described previously (8 (link), 58 (link)). After recovery, the slice was transferred to the recording chamber and superfused with ACSF containing 2.5 mM CaCl2 and 20 µM bicuculline methiodide (Tocris, Bristol, UK) at a rate of 3 to 4 mL/min at RT (22.0 to 24.0 °C). For a detailed description, see SI Appendix .
Allopregnanolone (C21H34O2, 3α-hydroxy-5α-pregnan-20-one, Sigma Chemical Co., St. Louis, MO, USA, CAS Number 516-54-1), Ketamine HCl (Ketonal 50 mg/ml, Richmond Laboratories, Veterinary Division, Buenos Aires, Argentina) and Xylazine (Sedomin 100 mg/ml, König Laboratories, Buenos Aires, Argentina) were used for experimental and surgical procedures.
To obtain the stock solution, ALLO was first dissolved in propylene glycol at a concentration of 3.14 mM. Working concentration was obtained after serial dilutions in sterile physiological solution; the resulting propylene glycol concentration was less than 0.2%.
Bicuculline methiodide [1(S),9(R)-(-)-Bicuculline methiodide, Sigma, USA] was used to antagonize GABAARs. A stock solution was prepared in DMSO at an initial concentration of 1 × 10−2 M. Working concentrations were obtained by dilution of the initial one in physiological solution; the resulting DMSO concentration at working solutions was less than 0.2%.
The control group received physiological solution (BRAUN, Buenos Aires, Argentina) with a similar concentration of propylene glycol/DMSO.
Bouin solution (Biopur Diagnostics, Santa Fe, Argentina), hematoxylin, eosin (Merk, Germany) and Canada Balsam Synthetic (Biopack, Buenos Aires, Argentina) were used for histological procedures.
To obtain the stock solution, ALLO was first dissolved in propylene glycol at a concentration of 3.14 mM. Working concentration was obtained after serial dilutions in sterile physiological solution; the resulting propylene glycol concentration was less than 0.2%.
Bicuculline methiodide [1(S),9(R)-(-)-Bicuculline methiodide, Sigma, USA] was used to antagonize GABAARs. A stock solution was prepared in DMSO at an initial concentration of 1 × 10−2 M. Working concentrations were obtained by dilution of the initial one in physiological solution; the resulting DMSO concentration at working solutions was less than 0.2%.
The control group received physiological solution (BRAUN, Buenos Aires, Argentina) with a similar concentration of propylene glycol/DMSO.
Bouin solution (Biopur Diagnostics, Santa Fe, Argentina), hematoxylin, eosin (Merk, Germany) and Canada Balsam Synthetic (Biopack, Buenos Aires, Argentina) were used for histological procedures.
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Action potentials were generated in the presynaptic dGC using 5 ms square current pulses (1 nA). For connectivity analysis, 5 action potentials were induced at 20 Hz (inter-sweep-interval: 10 s; at least 30 repetitions) while recording unitary excitatory postsynaptic currents (uEPSCs) from CA3-PCs. Neurons were considered to be connected if >5% of action potentials evoked time-locked inward uEPSCs [26 (link)]. Recordings were performed in the presence of (-)-bicuculline-methiodide (10 μM, Abcam, Cambridge, UK, #ab120108) to prevent inhibitory synapse recruitment. Moreover, glutamine (200 μM, Gibco, New York, NY, USA, #11539876) was added to the recording medium to avoid synaptic depletion [27 (link)].
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Kynurenic acid (Sigma-Aldrich, Dorset, UK) was directly dissolved in ECS on the day of use. The γ-cyclodextrin (Sigma-Aldrich) was directly dissolved in the intracellular solution. Stock solutions of strychnine hydrochloride (Sigma), TTX, bicuculline methiodide and gabazine hydrobromide (all HelloBio, Bristol, UK), were made in distilled H2O. 5α-pregnane-3α,20α-diol [5α-pregnanediol] (SantaCruz Bio PubChem CID 164,674 (566-58-5), ganaxolone (Bio-Techne Tocris, Oxford, UK), 5α-pregnane,3,20-dione [5α-dihydroprogesterone] (Sigma), SAGE-217 (MedChem Express, Monmouth Junction, NJ, USA), Co2-1970 (synthesised at MDI, Cardiff University), 5α-pregnane-3α-ol-20-one [allopregnanolone] (Tocris), DS2 (Tocris) and picrotoxin (Sigma-Aldrich) stocks were made in DMSO (100%). The maximum final concentration of DMSO in ECS was 0.3%.
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Bicuculline methiodide is a chemical compound used in research laboratories. It functions as a selective antagonist of GABA(A) receptors, which are important for neuronal signaling in the central nervous system.
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Bicuculline methiodide is a chemical compound commonly used as a research tool in neuroscience and pharmacology. It functions as a competitive antagonist of the GABA-A receptor, which is the main inhibitory neurotransmitter receptor in the central nervous system.
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PClamp 10 software is a data acquisition and analysis platform for electrophysiology research. It provides tools for recording, analyzing, and visualizing electrical signals from cells and tissues.
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Bicuculline methiodide (BMI) is a laboratory reagent used in scientific research. It is a GABA-A receptor antagonist, which means it blocks the action of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABA-A receptor. BMI is commonly used in electrophysiology and neurobiological studies to investigate the role of GABA-mediated inhibition in the nervous system.
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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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The BX51WI is an upright microscope designed for upright water immersion imaging. It features a infinity-corrected optical system and a bright LED illumination system. The BX51WI is suitable for a variety of applications requiring high-resolution imaging in an aqueous environment.
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The Multiclamp 700B amplifier is a versatile instrument designed for electrophysiology research. It provides high-quality amplification and signal conditioning for a wide range of intracellular and extracellular recording applications. The Multiclamp 700B offers advanced features and precise control over signal acquisition, enabling researchers to obtain reliable and accurate data from their experiments.
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Bicuculline methiodide is a potent and selective antagonist of GABA-A receptors. It is commonly used in neuroscience research to block inhibitory GABA-A receptor-mediated neurotransmission.
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Strychnine is a chemical compound that can be used as a research tool in laboratory settings. It is a naturally occurring substance found in certain plants. Strychnine has specific chemical and biological properties that may be of interest for certain scientific investigations, though its intended use should be determined by the relevant research protocols and safety guidelines.
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More about "Bicuculline methiodide"
Bicuculline methiodide (BMI) is a powerful and selective GABA(A) receptor antagonist that has been extensively utilized in neuroscience research.
It works by blocking the inhibitory effects of the neurotransmitter GABA, allowing researchers to investigate the role of GABAergic signaling in various neurological processes.
This chemical compound is often used in conjunction with other tools and techniques to study the underlying mechanisms of neural function and behavior.
For example, it may be combined with electrophysiological recording systems like the PClamp 10 software and Multiclamp 700B amplifier to measure the electrical activity of neurons in response to the blockade of GABA receptors.
Bicuculline methiodide is structurally similar to the plant-derived compound picrotoxin, which is another GABA(A) receptor antagonist.
Both of these substances can be used to pharmacologically manipulate GABAergic transmission and explore its impact on neuronal excitability, synaptic plasticity, and other complex brain processes.
In addition to its use in fundamental neuroscience research, BMI may also be employed in the study of neurological disorders characterized by imbalances in inhibitory signaling, such as epilepsy.
By understanding how the disruption of GABA receptor function affects neural network dynamics, researchers can gain insights into the pathophysiology of these conditions and potentially identify new therapeutic targets.
Regardless of the specific application, the availability of PubCompare.ai's AI-driven protocol comparison tool can greatly facilitate the optimization of Bicuculline methiodide-based experiments.
This intuitive platform allows scientists to easily locate and compare research protocols from the literature, preprints, and patents, helping them identify the most effective and efficient methods and products for their investigations.
With this support, researchers can spend more time on generating novel insights and less on navigating the vast array of experimental approaches.
It works by blocking the inhibitory effects of the neurotransmitter GABA, allowing researchers to investigate the role of GABAergic signaling in various neurological processes.
This chemical compound is often used in conjunction with other tools and techniques to study the underlying mechanisms of neural function and behavior.
For example, it may be combined with electrophysiological recording systems like the PClamp 10 software and Multiclamp 700B amplifier to measure the electrical activity of neurons in response to the blockade of GABA receptors.
Bicuculline methiodide is structurally similar to the plant-derived compound picrotoxin, which is another GABA(A) receptor antagonist.
Both of these substances can be used to pharmacologically manipulate GABAergic transmission and explore its impact on neuronal excitability, synaptic plasticity, and other complex brain processes.
In addition to its use in fundamental neuroscience research, BMI may also be employed in the study of neurological disorders characterized by imbalances in inhibitory signaling, such as epilepsy.
By understanding how the disruption of GABA receptor function affects neural network dynamics, researchers can gain insights into the pathophysiology of these conditions and potentially identify new therapeutic targets.
Regardless of the specific application, the availability of PubCompare.ai's AI-driven protocol comparison tool can greatly facilitate the optimization of Bicuculline methiodide-based experiments.
This intuitive platform allows scientists to easily locate and compare research protocols from the literature, preprints, and patents, helping them identify the most effective and efficient methods and products for their investigations.
With this support, researchers can spend more time on generating novel insights and less on navigating the vast array of experimental approaches.