Hypoxic augmentation of fast-inactivating and persistent sodium currents in rat caudal hypothalamic neurons

Eric Horn, Tony G. Waldrop

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Previous work from this laboratory has indicated that TTX-sensitive sodium channels are involved in the hypoxia-induced inward current response of caudal hypothalamic neurons. Since this inward current underlies the depolarization and increased firing frequency observed in these cells during hypoxia, the present study utilized more detailed biophysical methods to specifically determine which sodium currents are responsible for this hypoxic activation. Caudal hypothalamic neurons from ~3-wk-old Sprague-Dawley rats were acutely dissociated and patch-damped in the voltage-clamp mode to obtain recordings from fast-inactivating and persistent (noninactivating) whole cell sodium currents. Using computer-generated activation and inactivation voltage protocols, rapidly inactivating sodium currents were analyzed during normal conditions and during a brief (3-6 min) period of severe hypoxia. In addition, voltage-ramp and extended-voltage-activation protocols were used to analyze persistent sodium currents during normal conditions and during hypoxia. A polarographic oxygen electrode determined that the level of oxygen in this preparation quickly dropped to 10 Torr within 2 min of initiation of hypoxia and stabilized at

Original languageEnglish (US)
Pages (from-to)2572-2581
Number of pages10
JournalJournal of Neurophysiology
Volume84
Issue number5
StatePublished - 2000
Externally publishedYes

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Sodium
Neurons
Oxygen
Cell Hypoxia
Architectural Accessibility
Sodium Channels
Sprague Dawley Rats
Electrodes
Hypoxia

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Hypoxic augmentation of fast-inactivating and persistent sodium currents in rat caudal hypothalamic neurons. / Horn, Eric; Waldrop, Tony G.

In: Journal of Neurophysiology, Vol. 84, No. 5, 2000, p. 2572-2581.

Research output: Contribution to journalArticle

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