ACTIVITY OF A9 AND A10 DOPAMINERGIC-NEURONS IN UNRESTRAINED RATS - FURTHER CHARACTERIZATION AND EFFECTS OF APOMORPHINE AND CHOLECYSTOKININ
ACTIVITY OF A9 AND A10 DOPAMINERGIC-NEURONS IN UNRESTRAINED RATS - FURTHER CHARACTERIZATION AND EFFECTS OF APOMORPHINE AND CHOLECYSTOKININ
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DOI：
10.1016/0006-8993(87)90988-7
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发表时间：
1987-03-03
期刊：
影响因子：
2.9
通讯作者：
BUNNEY, BS
中科院分区：
文献类型：
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作者：
FREEMAN, AS;BUNNEY, BS
本实验观察了清醒自由状态下大鼠中脑单个多巴胺能神经元(共77个)的活动。腹侧被盖区(A10)细胞(n=39)的放电频率和放电模式与麻醉和瘫痪大鼠已鉴定的DA神经元相似。在听觉刺激和手动刺激触须的过程中，单位活动被短暂地刺激(更高的放电率和爆发式活动)。在定向反应和嗅觉阶段也发生了类似的变化。记录的A10细胞中有26%似乎是电性偶联的，这与之前在A9神经元中观察到的流行率一致。测定阿朴吗啡和八肽缩胆囊素(CCK-8)对A9和A10 DA细胞活性的影响。阿朴吗啡序贯剂量(5-320微克/公斤，静脉注射)降低每个受试神经元的放电频率(n=19)。这些细胞中有10个被归类为对药物(ED50；20微克/千克)“敏感”，其余细胞则明显“不敏感”(ED50；微克/千克)。在A9和A10中都有可能发现具有这两种敏感性的细胞。硫酸化CCK-8(1-16微克/公斤，静脉注射)兴奋(放电率和爆发率增加)73%的A9神经元被采样，但对A10细胞的放电产生不一致的影响。CCK-8可增加对阿朴吗啡敏感的A9和A10神经元的百分比(82%)。无论CCK-8对单位放电的影响如何，对阿朴吗啡的敏感性都有所增强。因此，正如在麻醉大鼠中发现的那样，CCK-8似乎增强了DA激动剂对DA神经元的抑制作用。
The activity of single dopaminergic (DA) neurons (total n = 77) in the midbrain of awake, unrestrained rats was examined. The firing rates and patterns of ventral tegmental area (A10) cells (n = 39) were similar to those of identified DA neurons in anesthetized and paralyzed rats. Unit activity was briefly stimulated (increased firing rate and burst activity) in response to an auditory stimulus and during manual stimulation of the vibrissae. Similar changes occurred during orienting responses and periods of sniffing. Twenty-six percent of A10 cells recorded appeared to be electrotonically coupled which matched the prevalence previously observed among A9 neurons. The effects on A9 and A10 DA cell activity of apomorphine and the carboxyterminal octapeptide of cholecystokinin (CCK-8) were then determined. Sequential doses of apomorphine (5-320 .mu.g/kg, i.v.) reduced the firing rate of each neuron tested (n = 19). Ten of these cells were classified as ''sensitive'' to the drug (ED50 < 20 .mu.g/kg), while the remainder were considerably ''less sensitive'' (ED50 > .mu.g/kg). Cells of either sensitivity were as likely to be found in A9 as in A10. Sulfated CCK-8 (1-16 .mu.g/kg, i.v.) excited (firing rate and bursting increased) 73% of the A9 neurons sampled but produced inconsistent effects on A10 cell firing. CCK-8 pretreatment increased the percentage of A9 and A10 neurons which were classified as ''sensitive'' to apomorphine (82%). Enhanced sensitivity to apomorphine occurred regardless of effect of CCK-8 on unit firing. Thus, as has been found in anesthetized rats, CCK-8 appeared to enhance the inhibitory effects of a DA agonist on DA neurons.