Channelpedia

PubMed 9070739


Referenced in: none

Automatically associated channels: Kv1.4 , Kv3.1 , Kv4.2



Title: Clustering of KV4.2 potassium channels in postsynaptic membrane of rat supraoptic neurons: an ultrastructural study.

Authors: G Alonso, H Widmer

Journal, date & volume: Neuroscience, 1997 Apr , 77, 617-21

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/9070739


Abstract
Ion channels play a key role in determining both neuronal membrane excitability and specificity. Neuronal specificity is achieved by several mechanisms, including the properties of the afferent network neurons are involved in, and the expression of specific sets of ion channels at the cellular level. In addition, subcellular distribution of channels might contribute to neuronal specificity, as suggested by the growing number of recent studies. Among ion channels, potassium (K+) channels have been shown to play an essential contribution in repolarization and interspike duration. Recently, K+ channel subtypes examined by light microscopy were reported to display a differential subcellular distribution in central neurons. But the precise localization of the channels on pre- or post-synaptic membrane was only assessed in a few brain areas. Here we used confocal and immunoelectron microscopic approaches to determine the hypothalamic localization of Kv4.2 K+ channels, which encode an A-type current. We found that intense immunostaining was localized to the supraoptic nucleus where it frequently formed rings outlining the somata of magnocellular neurons. Electron microscopy further revealed that this immunostaining was essentially associated with the plasma membrane limitating the somata or the dendrites of these neurons, and that it was particularly concentrated at the site of synaptic contacts. This is the first report showing clusters of voltage-gated channels on postsynaptic membranes in central mammalian neurons. The specific localization of the Kv4.2 channel indicates that this channel may play a role in signal integration at the synapse.