Nimodipine prevents early loss of hippocampal CA1 parvalbumin immunoreactivity after focal cerebral ischemia in the rat

Brain Res Bull. 1995;36(6):569-72. doi: 10.1016/0361-9230(94)00246-w.

Abstract

The effect of focal cerebral ischemia induced by middle cerebral artery occlusion on hippocampal interneurons containing the calcium-binding protein parvalbumin (PV) was studied in rats. Four hours after the onset of ischemia, a reduced number of PV-immunoreactive (-ir) neurons was observed in the lateral part of the CA1 region, while PV-ir was not altered in the CA2 and CA3 areas. Pretreatment with the L-type Ca2+ channel blocker nimodipine prevented the ischemia-induced loss of PV-ir in the CA1, suggesting a role for L-type voltage sensitive calcium channels in the mechanism of early neuronal alterations in the hippocampus CA1 region after focal cerebral ischemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterial Occlusive Diseases / complications*
  • Hippocampus / cytology
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Immunohistochemistry
  • Interneurons / drug effects*
  • Interneurons / metabolism
  • Ischemic Attack, Transient / drug therapy*
  • Ischemic Attack, Transient / etiology
  • Male
  • Nimodipine / pharmacology*
  • Parvalbumins / analysis*
  • Rats
  • Rats, Wistar
  • Time Factors

Substances

  • Parvalbumins
  • Nimodipine