HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 570/3/553    most recent jphysiol.2005.093781v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McDermott, C. M. Articles by Magee, J. C. Search for Related Content PubMed PubMed Citation Articles by McDermott, C. M. Articles by Magee, J. C. Related Collections Neuroscience

¹ Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA

Although the function of sleep remains elusive, there is compelling evidence to suggest that sleep plays an important role in learning and memory. A number of studies have now shown that sleep deprivation (SD) results in significant impairment of long-term potentiation (LTP) in the hippocampus. In this study, we have attempted to determine the mechanisms responsible for this impairment. After 72 h SD using the multiple-platform technique, we observed a reduction in the whole-cell recorded NMDA/AMPA ratio of CA1 pyramidal cells in response to Schaffer collateral stimulation. This impairment was specific to sleep deprivation as rats placed over a single large platform, which allowed sleep, had a normal NMDA/AMPA ratio. mEPSCs evoked by local application of a high osmolarity solution revealed no differences in the AMPA receptor function. NMDA currents recorded from outside-out patches excised from the distal dendrites of CA1 cells displayed a reduction in amplitude after SD. While there were no alterations in the glutamate sensitivity, channel open probability or the single channel conductance of the receptor, a crosslinking assay demonstrated that the NR1 and NR2A subunits of NMDA receptors were preferentially retained in the cytoplasm after SD, indicating that SD alters NMDAR surface expression. In summary, we have identified a potential mechanism underlying SD-induced LTP impairment. This synaptic alteration may underlie the cognitive deficits seen following sleep deprivation and could represent a target for future intervention studies.

(Received 5 July 2005; accepted after revision 29 November 2005; first published online 1 December 2005)
Corresponding author C. M. McDermott: Neuroscience Center, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, LA 70115, USA. Email: cmcder{at}lsuhsc.edu

This article has been cited by other articles:

				H. Murck, A. Steiger, R. M. Frieboes, and I. A. Antonijevic Pituitary adenylate cyclase-activating peptide affects homeostatic sleep regulation in healthy young men Am J Physiol Endocrinol Metab, March 1, 2007; 292(3): E853 - E857. [Abstract] [Full Text] [PDF]

				C. Kopp, F. Longordo, J. R. Nicholson, and A. Luthi Insufficient Sleep Reversibly Alters Bidirectional Synaptic Plasticity and NMDA Receptor Function J. Neurosci., November 29, 2006; 26(48): 12456 - 12465. [Abstract] [Full Text] [PDF]

				M. L. Furey and W. C. Drevets Antidepressant efficacy of the antimuscarinic drug scopolamine: a randomized, placebo-controlled clinical trial. Arch Gen Psychiatry, October 1, 2006; 63(10): 1121 - 1129. [Abstract] [Full Text] [PDF]