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

Gereau RW, Conn PJ
Neuron. 1994 12 (5): 1121-9

PMID: 8185947 · DOI:10.1016/0896-6273(94)90319-0

Coactivation of metabotropic glutamate receptors (mGluRs) and beta-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 mGluRs and beta-adrenergic receptors induces an acute depression of EPSCs at the Schaffer collateral-CA1 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.

MeSH Terms (23)

Alkaloids Analysis of Variance Animals Cyclic AMP Cyclic AMP-Dependent Protein Kinases Cycloleucine Electric Stimulation Evoked Potentials Hippocampus In Vitro Techniques Isoproterenol Male Models, Neurological Neurons Neurotoxins Protein Kinase C Rats Rats, Sprague-Dawley Receptors, Adrenergic, beta Receptors, Glutamate Staurosporine Synapses Synaptic Transmission

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