THE K+ CHANNEL, KV2.1, IS APPOSED TO ASTROCYTIC PROCESSES AND IS ASSOCIATED WITH INHIBITORY POSTSYNAPTIC MEMBRANES IN HIPPOCAMPAL AND CORTICAL PRINCIPAL NEURONS AND INHIBITORY INTERNEURONS

A variety of voltage-gated ion channels are expressed on principal cel l dendrites and have been proposed to play a pivotal role in the regul ation of dendritic excitability. Previous studies at the light microsc opic level demonstrated that the K+ channel subunit Kv2.1 expression w as polarized to the cell soma and dendrites of principal neurons throu ghout the central nervous system. Here, using double immunostaining we now show that Kv2.1 protein is similarly expressed in the majority of cortical and hippocampal parvalbumin, calbindin and somatostatin-cont aining inhibitory interneurons. At the electron microscopic level Kv2. 1 immunoreactivity was primarily observed on the plasma membrane of th e somata and proximal dendrites of both principal neurons and inhibito ry interneurons; expression was low on smaller dendritic branches, and absent on axons and presynaptic terminals. Kv2.1 subunit expression w as highly concentrated on the cell surface membrane immediately facing astrocytic processes. Kv2.1 expression was also concentrated in speci fic cytoplasmic compartments and on the subsurface cisterns underlying the plasma membrane facing astrocytes. In addition, Kv2.1 subunit imm unoreactivity was associated with postsynaptic densities of a fraction of inhibitory symmetric synapses; while expression at asymmetric syna pses was rare. These data demonstrate that channels formed by Kv2.1 su bunits are uniquely positioned on the soma and principal dendrites of both pyramidal cells and inhibitory interneurons at sites immediately adjacent to astrocytic processes. This close apposition to astrocytes will ensure a rapid removal and limit the influence of K+ released int o the extracellular space. This expression pattern suggests that chann els formed by Kv2.1 are poised to provide a role in the regulation of neuronal dendritic excitability. (C) 1998 IBRO. Published by Elsevier Science Ltd.