Metabotropic Glutamate Receptors at the Aged Mossy Fiber – CA3 Synapse of the Hippocampus

•Metabotropic glutamate receptors modulate both excitability and synaptic transmission of hippocampal CA3 neurons.•Group I mGluRs couple to Gq proteins, have a preferential postsynaptic expression and increase excitability.•Groups II and III mGluRs couple to Gi/o proteins, has a presynaptic expressi...

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Veröffentlicht in:Neuroscience 2021-02, Vol.456, p.95-105
Hauptverfasser: Griego, Ernesto, Galván, Emilio J.
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Sprache:eng
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Zusammenfassung:•Metabotropic glutamate receptors modulate both excitability and synaptic transmission of hippocampal CA3 neurons.•Group I mGluRs couple to Gq proteins, have a preferential postsynaptic expression and increase excitability.•Groups II and III mGluRs couple to Gi/o proteins, has a presynaptic expression and reduces glutamate release.•Aging alters the expression of mGluRs and modifies the modulation exerted by mGluRs on the CA3 network. Metabotropic glutamate receptors (mGluRs) are a group of G-protein-coupled receptors that exert a broad array of modulatory actions at excitatory synapses of the central nervous system. In the hippocampus, the selective activation of the different mGluRs modulates the intrinsic excitability, the strength of synaptic transmission, and induces multiple forms of long-term plasticity. Despite the relevance of mGluRs in the normal function of the hippocampus, we know very little about the changes that mGluRs functionality undergoes during the non-pathological aging. Here, we review data concerning the physiological actions of mGluRs, with particular emphasis on hippocampal area CA3. Later, we examine changes in the expression and functionality of mGluRs during the aging process. We complement this review with original data showing an array of electrophysiological modifications observed in the synaptic transmission and intrinsic excitability of aged CA3 pyramidal cells in response to the pharmacological stimulation of the different mGluRs.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2019.12.016