Potassium ion recycling pathway via gap junction systems in the mammalian cochlea and its interruption in hereditary nonsyndromic deafness

Medical Electron Microscopy

Volumn 33, Issue 2, 2000, Pages 51-56

  Kikuchi, T ^a   Adams, J C ^b   Miyabe, Y ^a   So, E ^a   Kobayashi, T ^a  

^a NAGASAKI UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b MASSACHUSETTS EYE AND EAR INFIRMARY   (United States)

Author keywords

Connexin 26; K+ ion; Na, K ATPase; Na K Cl cotransporter; Nonsyndromic deafness

Indexed keywords

GAP 26 PROTEIN; GAP 30 PROTEIN; GAP 31 PROTEIN; GAP JUNCTION PROTEIN; NEUROMODULIN; POTASSIUM ION; UNCLASSIFIED DRUG;

ANIMAL TISSUE; AUDITORY STIMULATION; COCHLEA; CONNECTIVE TISSUE CELL; CORTI ORGAN; ENDOLYMPH; EPITHELIUM CELL; FIBROBLAST; GAP JUNCTION; GENE EXPRESSION; GENE MUTATION; HAIR CELL; HEARING IMPAIRMENT; ION CURRENT; MOUSE; NONHUMAN; PERCEPTION DEAFNESS; POTASSIUM CONDUCTANCE; POTASSIUM TRANSPORT; PRIORITY JOURNAL; REVIEW; SENSORY NERVE CELL; STRIA VASCULARIS;

ANIMALS; COCHLEA; DEAFNESS; GAP JUNCTIONS; HUMANS; POTASSIUM;

EID: 0034469456     PISSN: 09184287     EISSN: None     Source Type: Journal    
DOI: 10.1007/s007950070001     Document Type: Review

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