J Korean Neurol Assoc.  1992 Dec;10(4):515-530.

Ischemia-induced Changes of Biogenic Amines in Rat Brain and the Effect of Nimodipine of Them

• Park YK
• Seo JT
• Bahng HR
• Kim KH

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).

MeSH Terms

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
Biogenic Amines
Calcium
Calcium Channels
Cromakalim
Neurotransmitter Agents
Nimodipine
Potassium Channels