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Cerebral Cortex Advance Access originally published online on September 29, 2007
Cerebral Cortex 2008 18(6):1326-1334; doi:10.1093/cercor/bhm164
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© 2007 The Authors
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

β-Adrenoreceptors Comprise a Critical Element in Learning-Facilitated Long-Term Plasticity

Anne Kemp1,2 and Denise Manahan-Vaughan1,2

1 Learning and Memory Research, Medical Faculty, Ruhr University Bochum, 44780 Bochum, Germany, 2 International Graduate School for Neuroscience, Ruhr University Bochum, 44780 Bochum, Germany

Address correspondence to Denise Manahan-Vaughan, PhD, Learning and Memory Research, Medical Faculty, Ruhr University Bochum, FNO 1/116, Universitaetsstrasse 150, 44780 Bochum, Germany. Email: dmv-igsn{at}rub.de.

A novel spatial environment consists of several different types of information that may be encoded by cellular information storage mechanisms such as long-term potentiation (LTP) and long-term depression (LTD). Arousal, mediated, for example, by activation of the noradrenergic system, is a critical factor in information acquisition and may enhance the encoding of novel spatial information. Using electrophysiological recordings of hippocampal responses in freely moving rats during spatial learning, we investigated the role of the β-adrenoreceptor in Schaeffer collateral–CA1 synaptic plasticity. We found that novel exploration of spatial context facilitates induction of LTD that is inhibited by intracerebroventricular application of the β-adrenoreceptor antagonist, propranolol. Long-lasting homosynaptic LTD, that was electrically induced by low-frequency stimulation, was unaffected by the antagonist. Although application of a β-adrenoreceptor agonist (isoproterenol) did not affect electrically induced LTD, agonist application facilitated short-term depression (STD) into LTD and mimicked the augmentation, through spatial exploration, of STD into LTD. Exploration of a novel empty environment facilitated LTP that was prevented by application of propranolol. These results suggest that β-adrenoreceptors may facilitate encoding of spatial information through synaptic plasticity in the hippocampus and that noradrenaline is a key factor in effective information acquisition.

Key Words: beta-adrenergic receptor • CA1 • long-term depression • long-term potentiation • noradrenaline • novelty exploration • spatial learning


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