BETA-ADRENERGIC RECEPTOR ACTIVATION INDUCES LONG-LASTING POTENTIATION IN BURST-SPIKING BUT NOT REGULAR-SPIKING CELLS AT CA1-subiculum SYNAPSES

The hippocampus plays a central role in memory formation in the mammalian brain The subiculum is the principal target of CA1 pyramidel cells and thus serves as the major relay station for the outgoing hippocampal information Pyramidal cells in the subiculum have been classified as burst spiking (BS) and regular spiking (RS) cells In this study we demonstrate that application of the beta adrenergic agonist isoproterenol (2 mu M) induces a chemical form of long term potentiation (LTP) of responses to alvear stimulation in (BS) but not in (RS) cells This effect is prevented by the beta-adrenergic receptor antagonist propranolol (2 mu M) The isoproterenol induced LTP in (BS) cells does not depend on postsynaptic Ca2+ signaling, as 1,2 bis(2 aminophenoxy)ethane N,N,N,N tetraacetic acid (BAPTA) does not prevent its induction Furthermore, paired pulse facilitation (PPF) and coefficient of variation (CV) analysis indicate the site of the LTP expression to be presynaptic Our findings show that activation of beta adrenergic receptors (beta ARs) at CA1 subiculum synapses induces a cell type specific form of chemical LTP in subicular (BS) cells that may allow a target specific trafficking of hippocampal output (C) 2010 IBRO Published by Elsevier Ltd All rights reserved