Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for their...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
Activation and Inactivation of G Proteins01:22

Activation and Inactivation of G Proteins

Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high affinity and are together...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cardiac MRI for clinical dilated cardiomyopathy: Improved diagnostic power via combined T1, T2, and ECV.

Radiography (London, England : 1995)·2024
Same author

Irisin alleviates renal injury caused by sepsis via the NF-κB signaling pathway.

European review for medical and pharmacological sciences·2020
Same author

Effect of dexmedetomidine on kidney injury in sepsis rats through TLR4/MyD88/NF-κB/iNOS signaling pathway.

European review for medical and pharmacological sciences·2019
Same author

Model research on repairing meniscus injury in rabbits using bone marrow mesenchymal stem cells and silk fibroin meniscus porous scaffold.

European review for medical and pharmacological sciences·2018
Same author

Translational neurocardiology: preclinical models and cardioneural integrative aspects.

The Journal of physiology·2016
Same author

Different impact of two mutations of a novel compound heterozygous protein C deficiency with late onset thrombosis.

Genetics and molecular research : GMR·2014

Related Experiment Video

Updated: May 30, 2026

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
07:51

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Published on: November 14, 2014

GABA(B) restrains release from singly-evoked GABA terminals.

Y-H Jin1, M C Andresen

  • 1Department of Physiology, School of Medicine, Kyung Hee University, Seoul, 130-701, Korea.

Neuroscience
|August 9, 2011
PubMed
Summary

Single neuron boutons in the brain control neurotransmitter release. Researchers studied GABA release from single boutons, finding GABA(B) receptors provide strong negative feedback, regulating release probability.

More Related Videos

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission
07:16

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
09:59

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices

Published on: July 17, 2011

Related Experiment Videos

Last Updated: May 30, 2026

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors
07:51

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Published on: November 14, 2014

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission
07:16

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
09:59

GABA-activated Single-channel and Tonic Currents in Rat Brain Slices

Published on: July 17, 2011

Area of Science:

  • Neuroscience
  • Cell Biology
  • Synaptic Transmission

Background:

  • Neurotransmitter release is complex and varies across the brain.
  • Individual synaptic boutons, the fundamental units of release, are poorly understood.
  • Directly studying single boutons is challenging but crucial for understanding neural communication.

Purpose of the Study:

  • To directly investigate neurotransmitter release from single synaptic boutons.
  • To characterize the mechanisms regulating GABA release from nucleus tractus solitarius (NTS) neurons.
  • To explore the role of GABA receptors in modulating release probability at the single-bouton level.

Main Methods:

  • Mechanically isolated NTS neurons were used to access single boutons.
  • Single boutons were directly activated using focal stimulation under voltage clamp.
  • Evoked postsynaptic currents (ePSCs) were recorded to measure neurotransmitter release.
  • Pharmacological agents (gabazine, TTX, CGP 52432) were used to probe receptor function.

Main Results:

  • Focal stimulation of single boutons evoked either excitatory (eEPSCs) or inhibitory (eIPSCs) postsynaptic currents in an all-or-none manner.
  • GABA release (eIPSCs) was infrequent and subject to use-dependent depression.
  • GABA(A) receptor blockade (gabazine) and TTX abolished eIPSCs.
  • GABA(B) receptor antagonism (CGP 52432) increased initial release rate, slowed depression, and blocked inhibition of spontaneous IPSCs.

Conclusions:

  • Single synaptic boutons exhibit distinct release properties.
  • GABA(B) receptors exert strong, long-lasting negative feedback on GABA release from individual terminals.
  • This feedback mechanism significantly influences release probability, even in isolated boutons.