Effect of Carbon Monoxide-Induced Hypoxia on Synaptosomal Uptake and Release of Dopamine in Rat Striatum.
10.3349/ymj.1988.29.2.129
- Author:
Kyoung Ja CHAI
1
;
Soo Kyung BAE
Author Information
1. Department of Biochemistry, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article ; In Vitro
- Keywords:
Carbon monoxide-induced hypoxia;
dopamine;
uptake;
release;
striatum;
synaptosomes
- MeSH:
Animal;
Carbon Monoxide Poisoning/*complications;
Corpus Striatum/*ultrastructure;
Culture Media;
Dopamine/*metabolism;
Female;
Hypoxia, Brain/chemically induced/*pathology;
In Vitro;
Male;
Rats;
Synaptosomes/*metabolism
- From:Yonsei Medical Journal
1988;29(2):129-138
- CountryRepublic of Korea
- Language:English
-
Abstract:
We studied the effect of carbon monoxide (CO)-induced hypoxia on synaptosomal uptake and release of dopamine (DA) in rat striatum. When the rats were intoxicated at a blood level of carboxyhemoglobin (HbCO), 60-70% for 3-4hrs, [3H] DA uptake was inhibited as much as 80% of control activity. This suppressed activity remained as long as 12 hrs after termination of the intoxication. After a week recovery period, the suppressed uptake activity was restored completely. When the rats were intoxicated maintaining a blood level of HbCO at 30-40% for 6-7hrs, the uptake was inhibited to 57% of the control actvity and this suppressed activity was restored within 12hrs. For the rats maintaining a blood level of HbCO at 15-25% for 6-7hrs, uptake inhibition was not shown. Acute CO intoxication(at 60-70% of HbCO for 3-4 hrs) caused an increase in K+-stimulated DA release to 147% of the control value. In conclusion, the diminished uptake and increased release of striatal DA in a CO intoxicated brain would cause an extraneuronal accumulation of DA with depletion of intraneuronal DA level, which may play a role in CO-induced hypoxic cell damage.
