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Cytoskeleton mediates inhibition of the fast Na + current in respiratory brainstem neurons during hypoxia
Author(s) -
Mironov S. L.,
Richter D. W.
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00584.x
Subject(s) - cytoskeleton , depolarization , hypoxia (environmental) , brainstem , cytochalasin b , biophysics , biology , osmotic concentration , microbiology and biotechnology , colchicine , respiratory system , intracellular , chemistry , biochemistry , endocrinology , neuroscience , cell , anatomy , oxygen , genetics , organic chemistry
Whole‐cell Na + currents (I Na ) were recorded in inspiratory neurons in a medullary slice preparation from neonatal mouse that contains the functional respiratory network. Hypoxia and metabolic poisoning with KCN rapidly inhibited I Na by reducing the number of Na + channels available for opening during depolarization. Application of agents specific for G‐proteins, protein kinase C and A, intracellular Ca 2+ and pH did not prevent the hypoxic inhibition of I Na . The effects of hypo‐osmolarity and hypoxia were additive, whereas hyperosmolarity partially prevented a subsequent hypoxic inhibition of I Na . Cytochalasin B and colchicine decreased, and taxol or phalloidin increased I Na and reduced its hypoxic inhibition. We conclude that cytoskeleton rearrangements during hypoxia are responsible for suppression of a fast I Na in brainstem respiratory neurons, which could be mediated by the uncoupling of channel inactivation gates from cytoskeletal elements.