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Advances in biochemical psychopharmacology最新文献

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Studies on the mechanism of interaction of anesthetics with GABA-A receptors. 麻醉药与GABA-A受体相互作用机制的研究。
B Longoni, R W Olsen
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引用次数: 0
Investigations on the "set-point" theory of benzodiazepine receptor function. 苯二氮卓类受体功能“设定点”理论的研究。
D J Nutt, C F Smith, R Bennett, H C Jackson
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引用次数: 0
Modulation of GABAA receptor subunit mRNAs: assessment by northern hybridization and PCR. GABAA受体亚基mrna的调节:北方杂交和PCR评估。
L G Miller, I Kang
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引用次数: 0
Functional modulation of cloned GABAA receptors expressed in Xenopus oocytes. 克隆GABAA受体在爪蟾卵母细胞中表达的功能调控。
K A Wafford, P Whiting, J A Kemp
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引用次数: 0
Treatment of panic disorder. 治疗恐慌症。
G B Cassano, C Toni, L Musetti
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引用次数: 0
Physiological role of GABAb receptors in the mammalian neostriatum. GABAb受体在哺乳动物新纹状体中的生理作用。
P Calabresi, N B Mercuri, A Stefani, G Bernardi
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引用次数: 0
Decrease in GABAA receptor function induced by pentylenetetrazol kindling in the rat: role of N-methyl-D-aspartate (NMDA) receptors. 戊四唑点燃诱导大鼠GABAA受体功能下降:n -甲基- d -天冬氨酸(NMDA)受体的作用。
M G Corda, M Orlandi, O Giorgi
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引用次数: 0
Neurosteroids: an overview. 神经类固醇:概述。
E E Baulieu
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引用次数: 0
Different sites of action of neurosteroids and benzodiazepines on natural and recombinant GABAA receptors. 神经甾体和苯二氮卓类药物对天然和重组GABAA受体的不同作用位点。
G Puia, S Vicini, P H Seeburg, E Costa
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引用次数: 0
GABA- and glutamate-gated ion channels as molecular sites of alcohol and anesthetic action. GABA-和谷氨酸-门控离子通道作为酒精和麻醉作用的分子位点。
F F Weight, L G Aguayo, G White, D M Lovinger, R W Peoples

The evidence presented above indicates that GABA- and glutamate-activated ion channels are molecular sites of alcohol and anesthetic action. In view of the important role that these channels play in CNS excitability, it seems likely that the actions of alcohol and anesthetics on these channels contribute significantly to the behavioral effects of these agents. Although the behavioral effects of alcohol and anesthetics may well result from a combination of actions on different ion channels and other molecular sites in the CNS, it is of interest to consider whether the actions of these agents on particular types of ion channels may contribute to particular behavioral effects. In this regard, it should be noted that benzodiazepines potentiate GABAA responses, but do not produce intoxication or general anesthesia in their clinical dose range. Benzodiazepines are widely used clinically, primarily for their anxiolytic actions (26), suggesting that the potentiation of GABAA responses by ethanol and barbiturates may contribute to the anxiolytic effects of these agents. Since kainate and quisqualate channels mediate fast excitatory transmission in the CNS, inhibition of kainate and quisqualate receptor-activated responses would be expected to result in general CNS depression. This suggests that inhibition of kainate and quisqualate receptor-mediated responses may contribute to the general anesthetic effects of ethanol, trichloroethanol and barbiturates. NMDA channels are thought to mediate complex excitatory neural phenomena and cognitive function. In view of this, the observation that ethanol inhibits NMDA receptor-mediated responses over the concentration range that produces intoxication and the correlation between the potency of different alcohols for inhibiting NMDA-activated current and their potency for producing intoxication suggest that ethanol-induced inhibition of NMDA receptor-mediated responses may contribute to the intoxicating effects of ethanol. Although these speculations are no doubt oversimplifications, the recognition that GABA- and glutamate-gated ion channels are molecular sites of alcohol and anesthetic action provides a basis for investigating the molecular mechanisms involved in the action of these agents and the behavioral significance of those actions.

上述证据表明,GABA和谷氨酸激活的离子通道是酒精和麻醉作用的分子位点。鉴于这些通道在中枢神经系统兴奋性中所起的重要作用,酒精和麻醉剂对这些通道的作用似乎可能对这些药物的行为影响起着重要作用。尽管酒精和麻醉剂的行为效应很可能是由作用于中枢神经系统中不同离子通道和其他分子位点的联合作用引起的,但考虑这些药物对特定类型离子通道的作用是否会导致特定的行为效应是很有趣的。在这方面,应该注意的是,苯二氮卓类药物可以增强GABAA反应,但在其临床剂量范围内不会产生中毒或全身麻醉。苯二氮卓类药物在临床上被广泛使用,主要是因为它们的抗焦虑作用(26),这表明乙醇和巴比妥酸盐对GABAA反应的增强可能有助于这些药物的抗焦虑作用。由于kainate和ququate通道介导CNS中的快速兴奋传递,抑制kainate和ququate受体激活的反应可能导致CNS普遍抑制。这表明,抑制海因酸盐和准酸盐受体介导的反应可能有助于乙醇、三氯乙醇和巴比妥类药物的全身麻醉效果。NMDA通道被认为介导复杂的兴奋性神经现象和认知功能。鉴于此,观察到乙醇在产生中毒的浓度范围内抑制NMDA受体介导的反应,以及不同醇抑制NMDA激活电流的效力与其产生中毒的效力之间的相关性表明,乙醇诱导的NMDA受体介导的反应的抑制可能有助于乙醇的中毒作用。尽管这些推测无疑过于简单化,但认识到GABA和谷氨酸门控离子通道是酒精和麻醉作用的分子位点,为研究这些药物作用的分子机制和这些作用的行为意义提供了基础。
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引用次数: 0
期刊
Advances in biochemical psychopharmacology
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