Source:http://linkedlifedata.com/resource/pubmed/id/19103648
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2009-4-1
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pubmed:abstractText |
Plasma membrane chloride (Cl(-)) pathways play an important role in neuronal physiology. Here, we investigated the role of NKCC1 cotransporters (a secondary active Cl(-) uptake mechanism) in Cl(-) handling in cultured rat dorsal root ganglion neurons (DRGNs) and motor neurons (MNs) derived from fetal stage embryonic day 14. Gramicidin-perforated patch-clamp recordings revealed that DRGNs accumulate intracellular Cl(-) through a bumetanide- and Na(+)-sensitive mechanism, indicative of the functional expression of NKCC1. Western blotting confirmed the expression of NKCC1 in both DRGNs and MNs, but immunocytochemistry experiments showed a restricted expression in dendrites of MNs, which contrasts with a homogeneous expression in DRGNs. Both MNs and DRGNs could be readily loaded with or depleted of Cl(-) during GABA(A) receptor activation at depolarizing or hyperpolarizing membrane potentials. After loading, the rate of recovery to the resting Cl(-) concentration (i.e., [Cl(-)](i) decrease) was similar in both cell types and was unaffected by lowering the extracellular Na(+) concentration. In contrast, the recovery on depletion (i.e., [Cl(-)](i) increase) was significantly faster in DRGNs in control conditions but not in low extracellular Na(+). The experimental observations could be reproduced by a mathematical model for intracellular Cl(-) kinetics, in which DRGNs show higher NKCC1 activity and smaller Cl(-)-handling volume than MNs. On the basis of these results, we conclude that embryonic DRGNs show a higher somatic functional expression of NKCC1 than embryonic MNs. The high NKCC1 activity in DRGNs is important for maintaining high [Cl(-)](i), whereas lower NKCC1 activity in MNs allows large [Cl(-)](i) variations during neuronal activity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Bumetanide,
http://linkedlifedata.com/resource/pubmed/chemical/Chlorides,
http://linkedlifedata.com/resource/pubmed/chemical/Gramicidin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, GABA,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, GABA-A,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Chloride Symporters,
http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1530-6860
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1168-76
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pubmed:meshHeading |
pubmed-meshheading:19103648-Animals,
pubmed-meshheading:19103648-Anti-Bacterial Agents,
pubmed-meshheading:19103648-Bumetanide,
pubmed-meshheading:19103648-Cells, Cultured,
pubmed-meshheading:19103648-Chlorides,
pubmed-meshheading:19103648-Electrophysiology,
pubmed-meshheading:19103648-Embryo, Mammalian,
pubmed-meshheading:19103648-Ganglia, Spinal,
pubmed-meshheading:19103648-Gramicidin,
pubmed-meshheading:19103648-Immunohistochemistry,
pubmed-meshheading:19103648-Kinetics,
pubmed-meshheading:19103648-Models, Statistical,
pubmed-meshheading:19103648-Motor Neurons,
pubmed-meshheading:19103648-Patch-Clamp Techniques,
pubmed-meshheading:19103648-Rats,
pubmed-meshheading:19103648-Rats, Inbred Strains,
pubmed-meshheading:19103648-Receptors, GABA,
pubmed-meshheading:19103648-Receptors, GABA-A,
pubmed-meshheading:19103648-Sodium-Potassium-Chloride Symporters,
pubmed-meshheading:19103648-gamma-Aminobutyric Acid
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pubmed:year |
2009
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pubmed:articleTitle |
Differential contribution of the Na(+)-K(+)-2Cl(-) cotransporter NKCC1 to chloride handling in rat embryonic dorsal root ganglion neurons and motor neurons.
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pubmed:affiliation |
Department of Molecular and Cell Biology, Katholieke Universiteit Leuven, Leuven, Belgium. jo.nsimy@gmail.com
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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