Ischemia-induced Changes of Biogenic Amines in Rat Brain and the Effect of Nimodipine of Them.
- Author:
Yong Ki PARK
1
;
Jeong Taeg SEO
;
Hye Ryun BAHNG
;
Kyung Hwan KIM
Author Information
1. Department of Neurology, College of Medicine, Hallym University.
- Publication Type:Original Article
- MeSH:
Animals;
Biogenic Amines*;
Brain Ischemia;
Brain*;
Calcium;
Calcium Channels;
Carotid Artery, Common;
Cerebellum;
Cerebral Cortex;
Corpus Striatum;
Cromakalim;
Decapitation;
Hippocampus;
Hypothalamus;
Ischemia;
Ligation;
Neurotransmitter Agents;
Nimodipine*;
Potassium Channels;
Rats*;
Substantia Nigra;
Thalamus
- From:Journal of the Korean Neurological Association
1992;10(4):515-530
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It has been reported that ischernia causes changes in the concentration and tumover of monoamine neurotransmitters in brain. For the mechanism of cellular death in brain ischernia it is suggested that accumulation of intracellular calcium during ischemia is one of the main causes. Present study was undertaken to investigate the influence of ischemia on the contents and tumover of the biogenic anines in rat brain and further to investigate the effects of nimodipine, a calcium channel blocker, and cromakalim, a potassium channel opener, on them. Brain ischemia was induced by partial ligation of bilateral common carotid artery. Nimodipine (36 ,ug/kg, I.p.) or cromakalim (0.5mg/kg, I.p.) was administered 20 minutes before ligation. Nimodipine was administered every 4 hours in 24-hour ischemic group. Rats were sacrificed by decapitation 3 or 24 hours after induction of ischemia and whole brains were excised. The brain was divided into follow ing regions; cerebral cortex, corpus striatum, hippocampus, thalamus, hypothalamus, substantia nigra and cerebellum. The concentrations of biogenic amines and their metabolites were measured by high performance liquid chromatography-electrochemical detector (HPLC-ECD).
