Post-ischemic administration of bifemelane hydrochloride prohibits ischemia-induced depletion of the muscarinic M1-receptor and its mRNA in the gerbil hippocampus

Brain Res. 1992 Sep 18;591(1):171-5. doi: 10.1016/0006-8993(92)90993-j.

Abstract

Parallel determinations of muscarinic cholinergic M1 receptor (M1-R) binding and of M1-R mRNA levels were carried out in the gerbil hippocampus 14 days after 5 min of transient ischemia. Both were reduced in the ischemic tissue to about 50% of the levels found in sham-operated controls, indicating that the late loss of M1-R is probably dependent on decreased synthesis. Three administrations of bifemelane hydrochloride (15 mg/kg, i.p., just after ischemia and 6 and 12 h later) completely prevented neuronal death in the hippocampus and ischemia-induced losses of hippocampal M1-R and its mRNA. Since vascular dementia may depend upon the ischemia-induced losses in cholinergic communication in the hippocampus, these findings suggest that it may be possible to prevent its occurrence by post-ischemic treatment with bifemelane hydrochloride.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzhydryl Compounds / administration & dosage*
  • Blotting, Northern
  • Gerbillinae
  • Hippocampus / blood supply*
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Immunoblotting
  • Ischemic Attack, Transient / drug therapy*
  • Ischemic Attack, Transient / metabolism
  • Ischemic Attack, Transient / pathology
  • RNA, Messenger / drug effects*
  • Receptors, Muscarinic / drug effects*
  • Receptors, Muscarinic / genetics
  • Receptors, Muscarinic / metabolism
  • Time Factors

Substances

  • Benzhydryl Compounds
  • RNA, Messenger
  • Receptors, Muscarinic
  • bifemelane