AI Article Synopsis
- Synaptic inhibition is essential for normal brain function, primarily controlled by the neurotransmitters glycine and GABA.
- These neurotransmitters can be released separately or together and activate their corresponding receptors on the postsynaptic neuron.
- The protein gephyrin plays a key role in the accumulation of these receptors at synapses, with differences observed in receptor localization between lower and higher brain regions, influencing the effectiveness of synaptic inhibition.
Article Abstract
The control of synaptic inhibition is crucial for normal brain function. More than 20 years ago, glycine and gamma-aminobutyric acid (GABA) were shown to be the two major inhibitory neurotransmitters. They can be released independently from different terminals or co-released from the same terminal to activate postsynaptic glycine and GABA(A) receptors. The anchoring protein gephyrin is involved in the postsynaptic accumulation of both glycine and GABA(A) receptors. In lower brain regions, both receptors can be concentrated in synapses, whereas in higher brain regions, glycine receptors are mostly excluded from postsynaptic sites. The activation of glycine and/or GABA(A) receptors determines the strength and precise timing of inhibition. Therefore, tight regulation of postsynaptic glycine versus GABA(A) receptor localization is crucial for optimizing synaptic inhibition in neurons. This review focuses on recent findings and discusses questions concerning the specificity of postsynaptic inhibitory neurotransmitter receptor accumulation during inhibitory synapse formation and development.
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| http://dx.doi.org/10.1007/s00441-002-0694-9 | DOI Listing |
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