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Potassium (K + ) channel expression in basal forebrain cholinergic neurons
Author(s) -
Betancourt L.,
Colom L.V.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20000915)61:6<646::aid-jnr8>3.0.co;2-b
Subject(s) - basal forebrain , cholinergic neuron , cholinergic , protein subunit , neuroscience , acetylcholine , microbiology and biotechnology , biology , chemistry , endocrinology , biochemistry , gene
Basal forebrain cholinergic neurons (BFCN) are depleted early in the course of Alzheimer's disease (AD). BFCN voltage‐gated K + channels regulate acetylcholine release and may play a role in BFCN neurodegeneration. Neuronal voltage‐gated K + channels are heterotetrameric assemblies of K v and accessory subunits. Currently, there is no available information about the K v proteins expressed in BFCN. Immunohistochemical techniques were used to investigate the expression of specific K v subunits in rat brain BFCN. Our results showed that BFCN express both K v 3.1 and K v 2.1 subunits. However, the K v 2.1 subunit showed a wider distribution in noncholinergic neurons than the K v 3.1 subunit. K v 3.1 and K v 2.1 immunostaining was noticeable not only in neuronal cell bodies but also in the dendritic ramifications of these neurons. Insofar as the K v 3.1 subunit has been classically associated with “fast‐spiking neurons” and BFCN have low firing rates and long‐duration action potentials, K v 3.1 subunits may have functions other than facilitating high‐frequency firing in BFCN. J. Neurosci. Res. 61:646–651, 2000. © 2000 Wiley‐Liss, Inc.