ArticleProceedings of the National Academy of Sciences of the United States of America2001
GTP-binding protein beta gamma subunits mediate presynaptic calcium current inhibition by GABA(B) receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 83 citations in OpenAlex.
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- Article
- Presynaptic calcium channels: specialized control of synaptic neurotransmitter release.Nature reviews. Neuroscience · 2020Review
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- The expanding roles and mechanisms of G protein-mediated presynaptic inhibition.The Journal of biological chemistry · 2019Review
- Review
- NMDA receptor-dependent presynaptic inhibition at the calyx of Held synapse of rat pups.Open biology · 2017Article
- Roles for Regulator of G Protein Signaling Proteins in Synaptic Signaling and Plasticity.Molecular pharmacology · 2016Review
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
- Strength and precision of neurotransmission at mammalian presynaptic terminals.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2015Review
- Modulation of synaptic depression of the calyx of Held synapse by GABA(B) receptors and spontaneous activity.The Journal of physiology · 2013Article
- GABAB receptor-mediated frequency-dependent and circadian changes in synaptic plasticity modulate retinal input to the suprachiasmatic nucleus.The Journal of physiology · 2013Article
- GPCR mediated regulation of synaptic transmission.Progress in neurobiology · 2012Review
- Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca²+ channel peptides.The Journal of physiology · 2011Article
- Involvement of protein kinase C and protein kinase A in the enhancement of L-type calcium current by GABAB receptor activation in neonatal hippocampus.Neuroscience · 2011Article
- Orchestration of "presto" and "largo" synchrony in up-down activity of cortical networks.Frontiers in neural circuits · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A variety of GTP-binding protein (G protein)-coupled receptors are expressed at the nerve terminals of central synapses and play modulatory roles in transmitter release. At the calyx of Held, a rat auditory brainstem synapse, activation of presynaptic gamma-aminobutyric acid type B receptors (GABA(B) receptors) or metabotropic glutamate receptors inhibits presynaptic P/Q-type Ca(2+) channel currents via activation of G proteins, thereby attenuating transmitter release. To identify the heterotrimeric G protein subunits involved in this presynaptic inhibition, we loaded G protein beta gamma subunits (G beta gamma) directly into the calyceal nerve terminal through whole-cell patch pipettes. G beta gamma slowed the activation of presynaptic Ca(2+) currents (I(pCa)) and attenuated its amplitude in a manner similar to the externally applied baclofen, a GABA(B) receptor agonist. The effects of both G beta gamma and baclofen were relieved after strong depolarization of the nerve terminal. In addition, G beta gamma partially occluded the inhibitory effect of baclofen on I(pCa). In contrast, guanosine 5'-O-(3-thiotriphosphate)-bound G(o)alpha loaded into the calyx had no effect. Immunocytochemical examination revealed that the subtype of G proteins G(o), but not the G(i), subtype, is expressed in the calyceal nerve terminal. These results suggest that presynaptic inhibition mediated by G protein-coupled receptors occurs primarily by means of the direct interaction of G(o) beta gamma subunits with presynaptic Ca(2+) channels.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.