High-voltage-activated calcium current in developing neurons is insensitive to nifedipine

Philip E. Hockberger*, Sang Chae Nam

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


We have analyzed the effect of nifedipine on the macroscopic high-threshold, voltage-activated (HVA) calcium current in four cell types: postnatal rat Purkinje and dorsal root ganglion (DRG) neurons, embryonic chick DRG neurons, and adult cat ventricular myocytes. As is consistent with previous reports, nifedipine reduced HVA current in myocytes in a voltage-sensitive manner. Analysis of nifedipine actions on neurons, however, was compromised by slow inactivation of the current at holding potentials between -80mV and -40 mV. The slow inactivation was voltage-dependent, irreversible after 5 min, and contributed to "rundown" of the current. At -40 mV, slow inactivation displayed two time constants: 12±8 s and 7±4 min. When slow inactivation was taken into account, we found no evidence for a nifedipine-sensitive component of the HVA current in these neurons. Consistent with previous studies, DRG neurons were reduced irreversibly by ω-conotoxin, whereas cardiac and Purkinje cells were unaffected. Our biophysical and pharmacological results are consistent with two types of neuronal HVA currents (N type and P type) in developing neurons that are distinct from cardiac HVA currents (L type).

Original languageEnglish (US)
Pages (from-to)402-411
Number of pages10
JournalPflügers Archiv European Journal of Physiology
Issue number5
StatePublished - Mar 1994


  • Cardiac myocyte
  • DRG neuron
  • Patch clamp
  • Purkinje neuron
  • Slow inactivation

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)


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