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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
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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...
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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...
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G-protein Coupled Receptors

G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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Related Experiment Video

Updated: May 13, 2026

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

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Published on: November 14, 2014

GABAB Receptors Regulate Extrasynaptic GABAA Receptors.

William M Connelly1, Sarah J Fyson, Adam C Errington

  • 1Cardiff School of Biosciences, Cardiff University, Cardiff CF10 AX, United Kingdom. connellywm@cardiff.ac.uk

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 1, 2013
PubMed
Summary

Postsynaptic GABA(B) receptor activation enhances tonic GABA(A) currents in rat brain cells. This crosstalk, involving G proteins and protein kinase, impacts neuronal excitability.

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Using an α-Bungarotoxin Binding Site Tag to Study GABA A Receptor Membrane Localization and Trafficking

Published on: March 28, 2014

Area of Science:

  • Neuroscience
  • Cellular Neurophysiology

Background:

  • Tonic inhibitory currents mediated by GABA(A) receptors are crucial in the central nervous system (CNS).
  • These currents are present in various neuronal types, including thalamocortical neurons, dentate gyrus granule cells, and cerebellar granule cells.

Purpose of the Study:

  • To investigate the interaction between postsynaptic GABA(B) receptors and tonic GABA(A) currents.
  • To elucidate the signaling pathway involved in this interaction.

Main Methods:

  • Experiments conducted on rat brain slices.
  • Utilized pharmacology and knockout mouse models.
  • Recorded neuronal currents to assess receptor function.

Main Results:

  • Activation of postsynaptic GABA(B) receptors significantly enhances tonic GABA(A) currents.
  • The enhancement pathway involves G proteins, adenylate cyclase, and cAMP-dependent protein kinase.
  • This modulation is independent of potassium channels and GABA transporters.
  • Increased tonic current alters thalamocortical neuron excitability.

Conclusions:

  • Demonstrates, for the first time, postsynaptic crosstalk between GABA(B) and GABA(A) receptors.
  • Highlights a novel mechanism regulating neuronal excitability through receptor-receptor interactions.