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: 568/3/881    most recent jphysiol.2005.096081v1 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 Klein, R. C Articles by Yakel, J. L Search for Related Content PubMed PubMed Citation Articles by Klein, R. C Articles by Yakel, J. L

¹ Laboratory of Neurobiology, National Institute of Environmental Health Sciences, NIH, DHHS, PO Box 12233, Research Triangle Park, NC 27709, USA

Diverse subtypes of nicotinic acetylcholine receptors (nAChRs), including fast-desensitizing 7-containing receptors, are expressed in the CNS. While nAChRs appear to regulate cognitive processing and synaptic plasticity, little is known to date about how this regulation occurs, particularly in brain regions known to be important for cognition. By combining patch-clamp electrophysiology with local photolysis of caged carbachol to rapidly activate the 7-containing nAChRs in rat hippocampal CA1 stratum radiatum interneurones in slices, we describe a novel transient up-regulation of channel function. The nAChRs were activated using a paired-pulse uncaging protocol, where the duration of the UV laser pulses (5–25 ms) and the interval between pulses (200 ms to 30 s) were varied. At relatively long interpulse intervals, we observed a strong (> 75%) decrease in the amplitude of the second response due to desensitization. However, when two pulses were applied at a 200 ms interval, a > 3-fold increase in the amplitude of the second response was observed, a phenomenon referred to here as paired-pulse potentiation. Interestingly, this potentiation appeared to be regulated by [Ca²⁺]_i, and/or Ca²⁺-dependent processes, as it was significantly enhanced by dialysing cells with either the Ca²⁺ chelator BAPTA, or with peptide inhibitors of either calcineurin or PKC, and was attenuated by dialysing cells with the CaMKII inhibitor KN-93. No potentiation was observed using caged GABA or glutamate, indicating some specificity for nAChRs. Thus, rat hippocampal 7-containing nAChRs possess a newly described phenomenon of paired-pulse potentiation that may be involved in regulating synaptic plasticity in the hippocampus.

(Received 5 August 2005; accepted after revision 30 August 2005; first published online 1 September 2005)
Corresponding author J. L. Yakel: NIEHS, F2-08, PO Box 12233, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA. Email: yakel{at}niehs.nih.gov

This article has been cited by other articles:

				C. C. Fernandes, A. Pinto-Duarte, J. A. Ribeiro, and A. M. Sebastiao Postsynaptic Action of Brain-Derived Neurotrophic Factor Attenuates {alpha}7 Nicotinic Acetylcholine Receptor-Mediated Responses in Hippocampal Interneurons J. Neurosci., May 21, 2008; 28(21): 5611 - 5618. [Abstract] [Full Text] [PDF]

				D. Fayuk and J. L. Yakel Dendritic Ca2+ signalling due to activation of {alpha}7-containing nicotinic acetylcholine receptors in rat hippocampal neurons J. Physiol., July 15, 2007; 582(2): 597 - 611. [Abstract] [Full Text] [PDF]