Abstract
Activation of metabotropic glutamate receptors (mGluRs) can potentiate the cAMP response elicited by activation of beta-adrenergic receptors (beta ARs) in the hippocampus. We have shown that co-activation of mGluRs and beta ARs induces both an acute depression of excitatory synaptic transmission and a long-lasting excitation of CA1 pyramidal cells. However, these studies were performed using a non-selective mGluR agonist. We have now used subtype selective mGluR agonists, and report that while the acute depression of transmission exhibits a pharmacology consistent with mediation by this mGluR subtype, the lasting excitation of CA1 pyramidal cells may be mediated by an interaction between beta ARs and mGluRs that are coupled to phosphoinositide hydrolysis.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adrenergic beta-Agonists / pharmacology*
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Animals
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Cyclopropanes / pharmacology
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Evoked Potentials / drug effects
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Glycine / analogs & derivatives
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Glycine / pharmacology
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Hippocampus / cytology
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Hippocampus / drug effects*
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In Vitro Techniques
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Isoproterenol / pharmacology
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Male
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Pyramidal Cells / drug effects
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Rats
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Rats, Sprague-Dawley
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Receptors, Adrenergic, beta / drug effects*
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Receptors, Metabotropic Glutamate / agonists*
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Receptors, Metabotropic Glutamate / antagonists & inhibitors
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Resorcinols / pharmacology
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Synapses / drug effects
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Synaptic Transmission / drug effects
Substances
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Adrenergic beta-Agonists
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Cyclopropanes
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Receptors, Adrenergic, beta
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Receptors, Metabotropic Glutamate
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Resorcinols
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2-(2,3-dicarboxycyclopropyl)glycine
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3,5-dihydroxyphenylglycine
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Isoproterenol
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Glycine