NDLI: beta -Amyloid peptide blocks the response of alpha 7-containing nicotinic receptors on hippocampal neurons.

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beta -Amyloid peptide blocks the response of alpha 7-containing nicotinic receptors on hippocampal neurons.

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beta -Amyloid peptide blocks the response of alpha 7-containing nicotinic receptors on hippocampal neurons.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kawai, H. Liu, Q. Berg, D. K.
Description	Author Affiliation: Liu Q ( Neurobiology Section, Division of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.);
Abstract	Alzheimer's disease produces a devastating decline in mental function, with profound effects on learning and memory. Early consequences of the disease include the specific loss of cholinergic neurons in brain, diminished cholinergic signaling, and the accumulation of beta-amyloid peptide in neuritic plaques. Of the nicotinic acetylcholine receptors at risk, the most critical may be those containing the alpha7 gene product (alpha7-nAChRs), because they are widespread, have a high relative permeability to calcium, and regulate numerous cellular events in the nervous system. With the use of whole-cell patch-clamp recording we show here that nanomolar concentrations of beta-amyloid peptides specifically and reversibly block alpha7-nAChRs on rat hippocampal neurons in culture. The block is noncompetitive, voltage-independent, and use-independent and is mediated through the N-terminal extracellular domain of the receptor. It does not appear to require either calcium influx or G protein activation. beta-Amyloid blockade is likely to be a common feature of alpha7-nAChRs because it applies to the receptors at both somato-dendritic and presynaptic locations on rat hippocampal neurons and extends to homologous receptors on chick ciliary ganglion neurons as well. Because alpha7-nAChRs in the central nervous system are thought to have numerous functions and recently have been implicated in learning and memory, impaired receptor function in this case may contribute to cognitive deficits associated with Alzheimer's disease.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	8
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amyloid Beta-Peptides Pharmacology Hippocampus Drug Effects Neurons Peptide Fragments Receptors, Nicotinic Animals Cells, Cultured Cytology Metabolism Rats, Sprague-Dawley Receptors, Serotonin Receptors, Serotonin, 5-HT3 Recombinant Fusion Proteins Antagonists & Inhibitors Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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