Ca2+ channel currents in type I carotid body cells of normoxic and chronically hypoxic neonatal rats

C. Peers, E. Carpenter, C. J. Hatton, C. N. Wyatt, D. Bee

Research output: Contribution to journalArticlepeer-review

Abstract

Whole-cell patch-clamp recordings were used to study voltage-gated Ca 2+ channel currents in type I carotid body cells of young rats born and reared in normoxia or in a chronically hypoxic (CH) environment (10% O 2 ). Currents activated at potentials of −40 mV and more positive, and typically peaked at 0 mV in both groups of cells. Steady-state inactivation curves were similar in the two populations. Ca 2+ currents were significantly larger in CH type I cells, but this was accounted for by the increased size of CH cells: current density was similar in both cell types. Nifedipine (5 μM) always partially inhibited currents and Bay K 8644 (2–5 μM) always enhanced currents, indicating the presence of L-type channels. In a small number of cells from each group, the N-type channel blocker ω-conotoxin GVIA caused partial, irreversible inhibition, but in most cells was without discernible effect. These results indicate that type I cells possess L-type Ca 2+ channels, that N-type are expressed in some cells and that non-L, non-N-type channels are also present. Furthermore, chronic hypoxia does not appear to cause specific adaptive changes in the properties of Ca 2+ channels in type I cells.

Original languageEnglish
Pages (from-to)251-257
Number of pages7
JournalBrain Research
Volume739
Issue number1-2
DOIs
StatePublished - Nov 11 1996

ASJC Scopus Subject Areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Keywords

  • ω-conotoxin GVIA
  • Ca channel
  • carotid body
  • chronic hypoxia
  • nifedipine
  • type I cell

Disciplines

  • Medical Cell Biology
  • Medical Neurobiology
  • Medical Physiology
  • Medical Sciences
  • Medicine and Health Sciences
  • Neurosciences
  • Physiological Processes

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