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Journal of Neuroscience, Vol 12, 506-517, Copyright © 1992 by Society for Neuroscience
Long-term increases in excitability in the CA1 region of rat hippocampus induced by beta-adrenergic stimulation: possible mediation by cAMP
TV Dunwiddie, M Taylor, LR Heginbotham and WR Proctor
Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.
The cellular mechanisms underlying beta-adrenergic potentiation in the CA1
region of the rat hippocampus were examined. A 10 min treatment with
isoproterenol (ISO) induced a long-term depolarization of the pyramidal
neurons that persisted for at least 30 min of washout; the ISO-induced
decrease in the calcium-activated potassium conductance
(afterhyperpolarization, or AHP) was similarly prolonged. The long-term
excitability changes induced by ISO did not depend upon the calcium
concentration of the medium and could be elicited in medium containing as
little as 240 microM calcium. The persistent increase in population spike
induced by ISO was mimicked by superfusion with several cAMP analogs and by
forskolin (which directly activates adenylate cyclase), but not by the
inactive dideoxyforskolin. Forskolin and cAMP analogs also induced
decreases in AHPs that could be quite prolonged, but did not depolarize
pyramidal neurons as consistently as did ISO. We hypothesize that
activation of beta-adrenergic receptors in the CA1 region of hippocampus
may induce an alteration of the hippocampal "state" that can persist for as
long as several hours, during which the induction of other forms of
plasticity may be enhanced.
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