Potassium (K+) channel expression in basal forebrain cholinergic neurons

Abstract

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.