Possible modulatory role of voltage-activated Ca2+ currents determining the membrane properties of isolated pyramidal neurones of the rat dorsal cochlear nucleus

Csaba Harasztosi, Ian D. Forsythe, Géza Szûcs, Peter R. Stanfield, Zoltán Rusznák

Research output: Article

14 Citations (Scopus)


Voltage-activated Ca2+ currents have been studied in pyramidal cells isolated enzymatically from the dorsal cochlear nuclei of 6-11-day-old Wistar rats, using whole-cell voltage-clamp. From hyperpolarized membrane potentials, the neurones exhibited a T-type Ca2+ current on depolarizations positive to -90 mV (the maximum occurred at about -40 mV). The magnitude of the T-current varied considerably from cell to cell (-56 to -852 pA) while its steady-state inactivation was consistent (E50 = -88.2 ± 1.7 mV, s = - 6.0 ± 0.4 mV). The maximum of high-voltage activated (HVA) Ca2+ currents was observed at about -15 mV. At a membrane potential of -10 mV the L-type Ca2+ channel blocker nifedipine (10 μM) inhibited approximately 60% of the HVA current, the N-type channel inhibitor ω-Conotoxin GVIA (2 μM) reduced the current by 25% while the P/Q-type channel blocker ω-Agatoxin IVA (200 nM) blocked a further 10%. The presence of the N- and P/Q-type Ca2+ channels was confirmed by immunochemical methods. The metabotropic glutamate receptor agonist (±)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (200 μM) depressed the HVA current in every cell studied (a block of approximately 7% on an average). The GABA(B) receptor agonist baclofen (100 μM) reversibly inhibited 25% of the HVA current. Simultaneous application of ω-Conotoxin GVIA and baclofen suggested that this inhibition could be attributed to the nearly complete blockade of the N-type channels. Possible physiological functions of the voltage-activated Ca2+ currents reported in this work are discussed.

Original languageEnglish
Pages (from-to)109-119
Number of pages11
JournalBrain research
Issue number1
Publication statusPublished - aug. 21 1999

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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