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Trends Neurosci. 2014 Nov;37(11):663-73. doi: 10.1016/j.tins.2014.07.010. Epub 2014 Aug 24.

Presynaptic long-term depression mediated by Gi/o-coupled receptors.

Author information

1
Section on Synaptic Pharmacology, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, 5625 Fishers Lane, MSC 9411, Bethesda, MD 20852-9411, USA.
2
Department of Pharmacology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA. Electronic address: bmathur@som.umaryland.edu.

Abstract

Long-term depression (LTD) of the efficacy of synaptic transmission is now recognized as an important mechanism for the regulation of information storage and the control of actions, as well as for synapse, neuron, and circuit development. Studies of LTD mechanisms have focused mainly on postsynaptic AMPA-type glutamate receptor trafficking. However, the focus has now expanded to include presynaptically expressed plasticity, the predominant form being initiated by presynaptically expressed Gi/o-coupled metabotropic receptor (Gi/o-GPCR) activation. Several forms of LTD involving activation of different presynaptic Gi/o-GPCRs as a 'common pathway' are described. We review here the literature on presynaptic Gi/o-GPCR-mediated LTD, discuss known mechanisms, gaps in our knowledge, and evaluate whether all Gi/o-GPCRs are capable of inducing presynaptic LTD.

KEYWORDS:

G(i/o)-GPCR; long-term synaptic plasticity; neurotransmitter release; plasticity mechanisms; presynaptic plasticity; synaptic inhibition; vesicle release machinery

PMID:
25160683
PMCID:
PMC4252515
DOI:
10.1016/j.tins.2014.07.010
[Indexed for MEDLINE]
Free PMC Article

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