赛拉嗪诱发大鼠大脑皮质神经元抑制：一项药理学研究。
Xylazine-evoked depression of rat cerebral cortical neurons: a pharmacological study.
作者信息
O'Regan M H
机构信息
Department of Physiology, Medical School, Wayne State University, Detroit 48201.
出版信息
Gen Pharmacol. 1989;20(4):469-74. doi: 10.1016/0306-3623(89)90197-3.
PMID:2568968
Abstract
- Iontophoretic application of the veterinary tranquilizer xylazine suppressed the spontaneous firing of 134/137 neurons tested, an effect not antagonized by adenosine receptor and alpha-adrenergic receptor blocking agents. 2. Depressions in neuronal activity evoked by norepinephrine, gamma-aminobutyric acid or adenosine failed to be potentiated by xylazine. 3. However, the excitatory effects of acetylcholine and glutamate were both inhibited by xylazine. 4. Thus, the depressant effect of locally applied xylazine may involve a decrease in the excitability of the neuronal membrane.
摘要
- 兽用镇静剂赛拉嗪的离子电渗应用抑制了所测试的137个神经元中的134个的自发放电，腺苷受体和α-肾上腺素能受体阻断剂未拮抗该效应。2. 去甲肾上腺素、γ-氨基丁酸或腺苷诱发的神经元活动抑制未被赛拉嗪增强。3. 然而，乙酰胆碱和谷氨酸的兴奋作用均被赛拉嗪抑制。4. 因此，局部应用赛拉嗪的抑制作用可能涉及神经元膜兴奋性的降低。
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