Chloral hydrate anesthesia alters the responsiveness of central serotonergic neurons in the cat.

Chloral hydrate anesthesia alters the responsiveness of central serotonergic neurons in the cat.
复制标题

水合氯醛麻醉改变猫中枢血清素能神经元的反应性。

DOI:
10.1016/0006-8993(84)90651-6
复制
发表时间:
1984
期刊:
影响因子:
2.9
通讯作者:
Jacobs,BL
Jacobs,BL
中科院分区:
医学3区
文献类型:
--
作者:
Heym,J;Steinfels,GF;Jacobs,BL

文献摘要

相似文献

给大鼠腹腔注射水合氯醛(300 mg/kg),观察水合氯醛麻醉对多巴胺能神经元自发活动和反应性的影响。自由活动的猫,中缝背核(DRN)的多巴胺能单位的活动被记录。虽然水合氯醛给药在注射后15分钟内产生了手术麻醉水平,但它仅使DRN神经元的自发活动略有下降(约20%)。与此相反,这些相同的神经元的反应性大大改变水合氯醛管理。通过检查注射水合氯醛前后的同一神经元,发现水合氯醛麻醉完全消除了DRN能神经元对听觉和视觉刺激的兴奋性反应,以及它们对电刺激脑桥网状结构中的神经细胞被盖区(FTG)的兴奋性反应。另一方面,全身给予WB 4101(1.0 mg/kg,i. p.),选择性α 1肾上腺素能受体拮抗剂,水合氯醛麻醉时可明显增强其作用。因此,这些数据表明,水合氯醛麻醉产生了深刻的变化,在中枢多巴胺能神经元的生理和药理学反应,这是不能预测的自发活动单独检查。此外,如前所述,如果不清楚这些混淆影响在多大程度上可能会推广到其他麻醉或固定制剂。因此,除了允许研究神经元活动和行为之间的关系的明显优势之外,在清醒的、自由移动的动物中进行的单个单元研究对于基础生理学和药理学研究也可能具有更大的价值。
The influence of chloral hydrate anesthesia on the spontaneous activity and responsiveness of serotonergic neurons was examined by administering chloral hydrate (300 mg/kg, i.p.) to freely moving cats from which serotonergic unit activity in the dorsal raphe nucleus (DRN) was being recorded. Although chloral hydrate administration produced a surgical level of anesthesia within 15 min following injection, it produced only a small decrease (∼ 20%) in the spontaneous activity of DRN serotonergic neurons. In contrast, the responsiveness of these same neurons was greatly altered by chloral hydrate administration. By examining the same neuron before and after chloral hydrate injection, it was found that chloral hydrate anesthesia completely abolished the excitatory responses of DRN serotonergic neurons to auditory and visual stimuli, as well as their excitatory response to electrical stimulation of the gigantocellular tegmental field (FTG) in the pontine reticular formation. On the other hand, the inhibition of serotonergic neuron firing resulting from systemic administration of WB 4101 (1.0 mg/kg, i.p.), a selective α1adrenergic receptor antagonist, was greatly potentiated by chloral hydrate anesthesia. Therefore, these data indicate that chloral hydrate anesthesia produces profound changes in the physiological and pharmacological responses of central serotonergic neurons which are not predictable by examination of spontaneous activity alone. Furthermore, as discussed, if it not clear to what extent these confounding influences might generalize to other anesthetized or immobilized preparations. Thus, beyond the obvious advantage which allows for the study of relationships between neuronal activity and behavior, single unit studies conducted in awake, freely moving animals also may be of greater value for basic physiological and pharmacological studies.