Disruption of KCC2 reveals an essential role of K-Cl cotransport already in early synaptic inhibition

Neuron

Volumn 30, Issue 2, 2001, Pages 515-524

  Hübner, Christian A ^a   Stein, Valentin ^a   Hermans Borgmeyer, Irm ^a   Meyer, Torsten ^b   Ballanyi, Klaus ^b   Jentsch, Thomas J ^a  

^a UNIVERSITY MEDICAL CENTER HAMBURG EPPENDORF   (Germany)

^b UNIVERSITY OF GÖTTINGEN   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

4 AMINOBUTYRIC ACID; CALCIUM ION; GLYCINE; ISOPROTEIN; KCC2 PROTEIN; POTASSIUM ION; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ATELECTASIS; CHLORIDE TRANSPORT; CONTROLLED STUDY; ELECTRIC ACTIVITY; ELECTROSTIMULATION; GENE DISRUPTION; HYPOXIA; KNOCKOUT MOUSE; MOTOR DYSFUNCTION; MOUSE; NERVE CONDUCTION; NERVE POTENTIAL; NERVE STIMULATION; NEUROTRANSMISSION; NEWBORN; NONHUMAN; PATCH CLAMP; POTASSIUM TRANSPORT; PRIORITY JOURNAL; RESPIRATORY FAILURE; SCIATIC NERVE; SPINAL CORD; SPINAL CORD MOTONEURON; SYNAPSE; SYNAPTIC INHIBITION;

EID: 0034990498     PISSN: 08966273     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0896-6273(01)00297-5     Document Type: Article

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