Mechanisms of beta-adrenergic facilitation of LTP in rat visual cortex

Mechanisms by which the beta-adrenergic agonist isoproterenol facilitates induction of long-term potentiation (LTP) were studied in visual cortex slices of adult rats. The amplitude of postsynaptic potentials elicited by white matter stimulation was not potentiated by tetanization in normal medium, but was in isoproterenol-containing medium, albeit modestly. This LTP induction was prevented by co-application of either an N-methyl-D-aspartate (NMDA) receptor antagonist, D-(-)-2-amino-5-phosphono-pentanoate, or an L-type Ca2+ channel antagonist, nifedipine. In medium containing the L-type Ca2+ channel agonist BAY K8644, but not isoproterenol, tetanization resulted in LTP. These results suggest that, in visual cortex slices from adult rats, LTP induced under isoproterenol perfusion depends on both NMDA receptors and voltage-sensitive Ca2+ channels.