Potentiation of cAMP responses by metabotropic glutamate receptors depresses excitatory synaptic transmission by a kinase-independent mechanism

Robert W. Gereau IV, P. Jeffrey Conn

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

Coactivation of metabotropic glutamate receptors (mGluRs) and β-adrenergic receptors causes a synergistic increase in cAMP formation in the rat hippocampus. Increases in CAMP are known to have many actions in the hippocampus via activation of CAMP-dependent protein kinase. We now report that coactivation of mGIuRs and β-adrenergic receptors induces an acute depression of EPSCs at the Schaffer collateral-CAl synapse. Interestingly, this depression of EPSCs is dependent upon increases in CAMP levels but independent of protein kinase activity. A series of studies suggests that CAMP-mediated depression of EPSCs is dependent on metabolism of cAMP and release of adenosine or 5′-AMP into the extracellular space with resultant activation of presynaptic adenosine receptors. These studies suggest that cAMP can have local hormone-like effects in the hippocampal formation which are independent of cAMP-dependent protein kinase.

Original languageEnglish
Pages (from-to)1121-1129
Number of pages9
JournalNeuron
Volume12
Issue number5
DOIs
StatePublished - May 1994

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