Synaptic Functions of Metabotropic Receptors

Postsynaptically located metabotropic glutamate receptors modulate both transmitter-activated and voltage-gated ion channels and thereby influence the strength of synaptic transmission. Both L-type and N-type Ca2+ channels are inhibited by activation of group I or II mGluR, and L-type channels are additionally inhibited by group III mGluR activation. Inhibition of Ca2+ entry presumably contributes to the observed reduction of Ca2+-dependent K+ currents in many neurons, but in cerebellar granule cells, mGluR activation increases the activity of Ca2+-dependent and inwardly rectifying K+ channels. The net effect on excitability is thus difficult to predict. Many ligand-gated channels are also modulated by mGluRs including AMPA, NMDA, and GABAa receptors. Whether activation of mGluR acts to inhibit or potentiate a receptor is often cell-specific. For example, in hippocampal pyramidal cells, mGluR activation potentiates NMDA receptors (see Fig. 1), but in cerebellar granule cells, mGluR activation inhibits NMDA receptors. In both cases, the effect is reduced by protein kinase C inhibitors.

Some mGluRs are located presynaptically and serve as autoreceptors that limit transmitter release. For example, glutamate-mediated EPSPs are reduced by activation of group II mGluRs at mossy fiber terminals onto CA3 hippocampal pyramidal neurons and by activation of group III mGluRs on Schaffer collateral synapses made onto CA1 pyramidal cells (see Fig. 1). The mechanism may involve reduction of Ca2+ entry into the presynaptic terminal.

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