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Review
. 1997 Oct;15(2):193-222.
doi: 10.1007/BF02740634.

Nicotinic acetylcholine receptors in health and disease

J Lindstrom  1
Affiliations
Review

Nicotinic acetylcholine receptors in health and disease

J Lindstrom. Mol Neurobiol. 1997 Oct.

Abstract

Nicotinic acetylcholine receptors (AChRs) are a family of acetylcholine-gated cation channels that form the predominant excitatory neurotransmitter receptors on muscles and nerves in the peripheral nervous system. AChRs are also expressed on neurons in lower amounts throughout the central nervous system. AChRs are even being reported on unexpected cell types such as keratinocytes. Structures of these AChRs are being determined with increasing precision, but functions of some orphan subunits are just beginning to be established. Functional roles for postsynaptic AChRs in muscle are well known, but in neurons the post-, peri-, extra-, and presynaptic roles of AChRs are just being revealed. Pathogenic roles of AChRs are being discovered in many diseases involving mechanisms ranging from mutations, to autoimmune responses, to the unknown; involving cell types ranging from muscles, to neurons, to keratinocytes; and involving signs and symptoms ranging from muscle weakness to epilepsy, to neurodegenerative disease, to psychiatric disease, to nicotine addiction. Awareness of AChR involvement in some of these diseases has provoked new interests in development of therapeutic agonists for specific AChR subtypes and the use of expressed cloned AChR subunits as possible immunotherapeutic agents. Highlights of recent developments in these areas will be briefly reviewed.

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References

    1. Annu Rev Med. 1997;48:341-51 - PubMed
    1. Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2095-7 - PubMed
    1. Mol Pharmacol. 1993 Nov;44(5):1046-50 - PubMed
    1. Biochemistry. 1979 Oct 16;18(21):4465-70 - PubMed
    1. Cell Immunol. 1994 Sep;157(2):353-68 - PubMed

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