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γ-氨基丁酸对脑电刺激诱发的防御反应的调节作用

GABA modulation of the defense reaction induced by brain electrical stimulation.

作者信息

Schenberg L C, De Aguiar J C, Graeff F G

出版信息

Physiol Behav. 1983 Oct;31(4):429-37. doi: 10.1016/0031-9384(83)90062-8.

DOI:10.1016/0031-9384(83)90062-8
PMID:6318241
Abstract

Earlier behavioral results led to the suggestion that GABA exerts a tonic inhibitory influence in the dorsal periaqueductal gray (DPAG) matter of the rat integrating defensive behavior. In the present experiments, the role of GABAergic mechanisms in the modulation of the autonomic component of the defense reaction was studied. Thus, the effects of intravenous (IV) injections of chlordiazepoxide as well as of intracerebral (IC) injections of midazolam in the dorsal midbrain, on the blood pressure (BP), heart rate (HR) and respiratory increases induced by electrical stimulation of the DPAG were measured in rats anesthetized with urethane. Chlordiazepoxide (10 mg/kg, IV) as well as midazolam (40 and 160 nmol, IC) attenuated the centrally-induced hypertension, without affecting basal BP. The tachycardia induced by aversive brain stimulation was similarly decreased by the benzodiazepines. In addition, the HR baseline was significantly raised by chlordiazepoxide and by the highest dose of midazolam. The tachypnea induced by brain electrical stimulation was also reduced by both benzodiazepines. Basal respiratory rate was slightly, but significantly decreased by chlordiazepoxide as well as by the two doses of midazolam used and to a lesser extent by the vehicle alone. Chlordiazepoxide attenuated the increase in respiratory depth caused by brain stimulation, while basal respiratory amplitude was not affected. The effects of midazolam on this parameter were unclear. Microinjection of bicuculline (5 and 10 nmol) or picrotoxin (0.3 and 1 nmol) into the DPAG increased the BP, HR and respiration, like the electrical stimulation. The latency and duration of bucuculline effects were shorter than those of picrotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

早期的行为学研究结果表明,γ-氨基丁酸(GABA)对整合防御行为的大鼠中脑导水管周围灰质背侧(DPAG)发挥着紧张性抑制作用。在本实验中,研究了GABA能机制在防御反应自主成分调节中的作用。因此,在以乌拉坦麻醉的大鼠中,测量了静脉注射氯氮卓以及向中脑背侧脑室内注射咪达唑仑对电刺激DPAG所诱导的血压(BP)、心率(HR)和呼吸增加的影响。氯氮卓(10mg/kg,静脉注射)以及咪达唑仑(40和160nmol,脑室内注射)可减轻中枢诱导的高血压,而不影响基础血压。苯二氮卓类药物同样可降低厌恶脑刺激所诱导的心动过速。此外,氯氮卓和最高剂量的咪达唑仑可显著提高心率基线。两种苯二氮卓类药物均可降低脑电刺激所诱导的呼吸急促。氯氮卓以及所使用的两种剂量的咪达唑仑可使基础呼吸频率轻微但显著降低,单独使用溶剂时降低程度较小。氯氮卓可减轻脑刺激引起的呼吸深度增加,而基础呼吸幅度不受影响。咪达唑仑对该参数的影响尚不清楚。向DPAG微量注射荷包牡丹碱(5和10nmol)或苦味毒(0.3和1nmol)可像电刺激一样增加血压、心率和呼吸。荷包牡丹碱作用的潜伏期和持续时间比苦味毒短。(摘要截短至250字)

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