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J Neurophysiol (July 30, 2003). doi:10.1152/jn.00616.2003
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Submitted on June 27, 2003
Accepted on July 25, 2003

{beta}-amyloid peptide activates non-{alpha}7 nicotinic acetylcholine receptors in rat basal forebrain neurons

Wen Fu1 and Jack H. Jhamandas1*

1 Medicine (Neurology) and Centre for Alzheimer and Neurodegenerative Research, University of Alberta, Edmonton, Alberta, Canada

* To whom correspondence should be addressed. E-mail: jack.jhamandas{at}ualberta.ca.

Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by profound deficits in memory and cognitive function. Neuropathological hallmarks of the disease include a loss of basal forebrain cholinergic neurons and the deposition of {beta}-amyloid peptide (A{beta}) in neuritic plaques. At a cellular level, considerable attention has focused on a study of A{beta} interactions with the neuronal nicotinic acetylcholine receptor (nAChR) subtypes. In this study, using cell-attached and outside-out single channel recordings from acutely dissociated rat basal forebrain neurons, we report that A{beta} and nicotine activate nAChRs with two distinct levels of single-channel conductance. Whole-cell recordings from these neurons reveal A{beta} and nicotine, in a concentration-dependant and reversible manner, evoke brisk depolarizing responses and an inward current. The effects of A{beta} on both single channel and whole cell are blocked by the non-competitive nAChR antagonist mecamylamine and competitive nAChR antagonist dihydro-beta-erythroidine, but not the specific {alpha}7-selective nAChR antagonist methyllycaconitine, indicating that A{beta} activated non-{alpha}7 nAChRs on basal forebrain neurons. In addition, the non-{alpha}7 nAChR agonists UB-165, epibatidine, and cytisine but not the selective {alpha}7 agonist AR-R17779 induced similar responses as A{beta} and nicotine. Thus, non-{alpha}7 nAChRs may also represent a novel target in mediating the effects of A{beta} in AD.




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