Differential effects of acute and repeated electrically and chemically induced seizures on [3H]Nimodipine and [125I]omega-conotoxin GVIA binding in rat brain.

Abstract

[3H]Nimodipine and high-affinity [125I]omega-conotoxin GVIA (CgTX) binding were investigated in membranes from rat cerebral cortex, cerebellum, and hippocampus after electrically and chemically induced seizures. Animals were decapitated 30 min after a single electroconvulsive shock (ECS) or lidocaine-induced seizure and 24 h after the last of 10 once-daily ECS or six once-daily lidocaine-induced seizures. After a single ECS, [3H]nimodipine and [125I]CgTX binding sites decreased in cerebral cortex (by 10% and 17%, respectively). A downregulation of [3H]nimodipine binding sites in hippocampus occurred after single and repeated lidocaine-induced seizures (by 24% and 11%, respectively), whereas [125I]CgTX binding remained unaltered. An earlier report on changes in [3H]nitrendipine binding after chronic ECS in cortex and hippocampus was not confirmed.

• Authors: C H Gleiter, C J Cain, S R Weiss, R M Post, P J Marangos
• Journal: Epilepsia (Epilepsia) 1989 Jul-Aug Vol. 30 Issue 4 Pg. 487-92 ISSN: 0013-9580 [Print] United States
• PMID: 2753000 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Calcium Channel Blockers
• Iodine Radioisotopes
• Mollusk Venoms
• Tritium
• Nimodipine
• omega-Conotoxin GVIA
• Lidocaine

Topics

• Animals
• Binding Sites
• Brain (metabolism)
• Calcium Channel Blockers (metabolism)
• Cerebellum (metabolism)
• Cerebral Cortex (metabolism)
• Electroshock
• Hippocampus (metabolism)
• Iodine Radioisotopes
• Lidocaine
• Male
• Mollusk Venoms (metabolism)
• Nimodipine (metabolism)
• Rats
• Rats, Inbred Strains
• Seizures (chemically induced, etiology, metabolism)
• Tritium
• omega-Conotoxin GVIA