Microdialysis studies of basal levels and stimulus-evoked overflow of dopamine and metabolites in the striatum of young and aged Fischer 344 rats

被引:32
|
作者
Gerhardt, GA
Maloney, RE
机构
[1] Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Neurosci Training Program, Denver, CO 80262 USA
[2] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Neurosci Training Program, Denver, CO 80262 USA
[3] Univ Colorado, Hlth Sci Ctr, Rocky Mt Ctr Sensor Technol, Denver, CO 80262 USA
[4] Louisiana State Univ, Med Ctr, Dept Pharmacol, Shreveport, LA 71130 USA
关键词
dopamine; intracranial microdialysis; Fischer; 344; rat; D-amphetamine; potassium; basal level; aging; striatum;
D O I
10.1016/S0006-8993(98)01095-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The technique of intracranial microdialysis was used to investigate the effects of aging on the striatal dopaminergic system of the anesthetized Fischer 344 rat. Microdialysis probes were implanted into the striatum of young (2-8 months) and aged (24-28 months) urethane anesthetized rats. Striatal dialysate levels were analyzed for dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and serotonin (5-HT) by high performance liquid chromatography with electrochemical detection. As compared to the young animals, basal extracellular levels of DA and DOPAC were significantly decreased in two groups of aged animals. Stimulation with excess potassium added through the microdialysis probe produced a robust overflow of DA in the young and aged rat striatum, but the evoked overflow of DA was not diminished in the aged rat striatum as compared to young animals. In contrast, D-amphetamine-evoked overflow of DA was again robust in young and aged animals, but was greatly decreased in the aged rat striatum as compared to the signals recorded in the young rats. Taken together with previous reports, these data support the hypothesis that a major change in the regulation of DA release that occurs in aging involves changes in the function of the neuronal uptake of DA, which may be a compensatory property of DA neurons in senescence. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:68 / 77
页数:10
相关论文
共 13 条