Linked Life Data

11050128

Source:http://linkedlifedata.com/resource/pubmed/id/11050128

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2000-11-1
pubmed:abstractText
Chloride (Cl(-)) homeostasis is critical for many cell functions including cell signaling and volume regulation. The action of GABA at GABA(A) receptors is primarily determined by the concentration of intracellular Cl(-). Developmental regulation of intracellular Cl(-) results in a depolarizing response to GABA in immature neocortical neurons and a hyperpolarizing or shunting response in mature neocortical neurons. One protein that participates in Cl(-) homeostasis is the neuron-specific K(+)-Cl(-) cotransporter (KCC2). Thermodynamic considerations predict that in the physiological ranges of intracellular Cl(-) and extracellular K(+) concentrations, KCC2 can act to either extrude or accumulate Cl(-). To test this hypothesis, we examined KCC2 function in pyramidal cells from rat neocortical slices in mature (18-28 d postnatal) and immature (3-6 d postnatal) rats. Intracellular Cl(-) concentration was estimated from the reversal potential of whole-cell currents evoked by local application of exogenous GABA. Both increasing and decreasing the extracellular K(+) concentration resulted in a concomitant change in intracellular Cl(-) concentration in neurons from mature rats. KCC2 inhibition by furosemide caused a change in the intracellular Cl(-) concentration that depended on the concentration of pipette Cl(-); in recordings with low pipette Cl(-), furosemide lowered intracellular Cl(-), whereas in recordings with elevated pipette Cl(-), furosemide raised intracellular Cl(-). In neurons from neonatal rats, manipulation of extracellular K(+) had no effect on intracellular Cl(-) concentration, consistent with the minimal KCC2 mRNA levels observed in neocortical neurons from immature animals. These data demonstrate a physiologically relevant and developmentally regulated role for KCC2 in Cl(-) homeostasis via both Cl(-) extrusion and accumulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8069-76
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11050128-Aging, pubmed-meshheading:11050128-Animals, pubmed-meshheading:11050128-Carrier Proteins, pubmed-meshheading:11050128-Chlorides, pubmed-meshheading:11050128-Diuretics, pubmed-meshheading:11050128-Dose-Response Relationship, Drug, pubmed-meshheading:11050128-Evoked Potentials, pubmed-meshheading:11050128-Furosemide, pubmed-meshheading:11050128-Gene Expression Regulation, Developmental, pubmed-meshheading:11050128-Intracellular Fluid, pubmed-meshheading:11050128-Ion Transport, pubmed-meshheading:11050128-Neocortex, pubmed-meshheading:11050128-Patch-Clamp Techniques, pubmed-meshheading:11050128-Potassium, pubmed-meshheading:11050128-Pyramidal Cells, pubmed-meshheading:11050128-RNA, Messenger, pubmed-meshheading:11050128-Rats, pubmed-meshheading:11050128-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11050128-Symporters, pubmed-meshheading:11050128-Thermodynamics, pubmed-meshheading:11050128-gamma-Aminobutyric Acid
pubmed:year
2000
pubmed:articleTitle
Potassium-coupled chloride cotransport controls intracellular chloride in rat neocortical pyramidal neurons.
pubmed:affiliation
Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't