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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Halothane prevents MK-801 neurotoxicity in the rat cingulate cortex.
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Halothane prevents MK-801 neurotoxicity in the rat cingulate cortex.

机译：氟烷可防止MK-801对大鼠扣带回皮层的神经毒性。

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摘要

Subcutaneous administration of the N-methyl-D-aspartic acid (NMDA) antagonist, MK-801, to adult rats causes a toxic vacuole reaction in neurons of the posterior cingulate cortex which is readily detected in histological sections 4 h following MK-801 administration. Certain drugs that facilitate neurotransmission at gamma-aminobutyric acidA (GABAA) receptors block this neurotoxic action of MK-801. The anesthetic actions of halothane (fluothane) are thought to be due, at least in part, to an interaction with GABAA receptors. In the present study, we investigated the effect of halothane on MK-801 neurotoxicity. When halothane was administered for either 1 or 2 h, then terminated immediately prior to MK-801 treatment, the vacuole reaction detected 4 h later was almost as severe as in controls not exposed to halothane. Administration of halothane for 1 h after MK-801 injection postponed but did not prevent a relatively full vacuole reaction. However, when rats were kept under halothane anesthesia continuously throughout the 4 h period following MK-801 administration, the vacuole reaction was completely prevented. We postulate that halothane blocks MK-801 neurotoxicity by a facilitative action at GABAA receptors. Because halothane's duration of action is fleeting compared to the very long duration of action of MK-801, the efficacy of halothane in blocking MK-801 neurotoxicity varies in direct proportion to the length of time following MK-801 treatment that the rat brain is exposed to halothane.
机译：对成年大鼠皮下施用N-甲基-D-天冬氨酸（NMDA）拮抗剂MK-801会在扣带后皮层神经元中产生毒性液泡反应，在MK-801施用4小时后的组织学切片中很容易检测到该反应。某些促进在γ-氨基丁酸A（GABAA）受体上神经传递的药物会阻断MK-801的这种神经毒性作用。氟烷（氟烷）的麻醉作用被认为至少部分是由于与GABAA受体的相互作用。在本研究中，我们调查了氟烷对MK-801神经毒性的影响。当给予氟烷1或2小时，然后在MK-801处理之前立即终止时，4小时后检测到的液泡反应几乎与未接触氟烷的对照组一样严重。注射MK-801后，氟烷的给药1小时推迟了，但并没有阻止相对充分的液泡反应。然而，当大鼠在MK-801给药后的4小时内连续处于氟烷麻醉下，则完全避免了液泡反应。我们推测氟烷通过对GABAA受体的促进作用来阻断MK-801神经毒性。由于氟烷的作用持续时间与MK-801的非常长的作用时间相比是短暂的，因此氟烷在阻断MK-801神经毒性方面的功效与MK-801治疗后大鼠大脑暴露的时间长短成正比氟烷。

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