Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-5-8
pubmed:abstractText
A variety of voltage-gated ion channels are expressed on principal cell dendrites and have been proposed to play a pivotal role in the regulation of dendritic excitability. Previous studies at the light microscopic level demonstrated that the K+ channel subunit Kv2.1 expression was polarized to the cell soma and dendrites of principal neurons throughout 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-containing inhibitory interneurons. At the electron microscopic level Kv2.1 immunoreactivity was primarily observed on the plasma membrane of the somata and proximal dendrites of both principal neurons and inhibitory interneurons; expression was low on smaller dendritic branches, and absent on axons and presynaptic terminals. Kv2.1 subunit expression was highly concentrated on the cell surface membrane immediately facing astrocytic processes. Kv2.1 expression was also concentrated in specific cytoplasmic compartments and on the subsurface cisterns underlying the plasma membrane facing astrocytes. In addition, Kv2.1 subunit immunoreactivity was associated with postsynaptic densities of a fraction of inhibitory symmetric synapses; while expression at asymmetric synapses was rare. These data demonstrate that channels formed by Kv2.1 subunits 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 into the extracellular space. This expression pattern suggests that channels formed by Kv2.1 are poised to provide a role in the regulation of neuronal dendritic excitability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-48
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:9522360-Animals, pubmed-meshheading:9522360-Astrocytes, pubmed-meshheading:9522360-Calcium-Binding Protein, Vitamin D-Dependent, pubmed-meshheading:9522360-Cerebral Cortex, pubmed-meshheading:9522360-Delayed Rectifier Potassium Channels, pubmed-meshheading:9522360-Hippocampus, pubmed-meshheading:9522360-Interneurons, pubmed-meshheading:9522360-Microscopy, Immunoelectron, pubmed-meshheading:9522360-Neural Inhibition, pubmed-meshheading:9522360-Neurons, pubmed-meshheading:9522360-Parvalbumins, pubmed-meshheading:9522360-Potassium Channels, pubmed-meshheading:9522360-Potassium Channels, Voltage-Gated, pubmed-meshheading:9522360-Rats, pubmed-meshheading:9522360-Rats, Sprague-Dawley, pubmed-meshheading:9522360-Shab Potassium Channels, pubmed-meshheading:9522360-Somatostatin, pubmed-meshheading:9522360-Synaptic Membranes, pubmed-meshheading:9522360-Tissue Distribution
pubmed:year
1998
pubmed:articleTitle
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.
pubmed:affiliation
Laboratory of Cellular and Molecular Neurophysiology, NICHD-NIH, USA.
pubmed:publicationType
Journal Article