Effects of halothane on excitatory neurotransmission to medullary expiratory neurons in a decerebrate dog model.
Effects of halothane on excitatory neurotransmission to medullary expiratory neurons in a decerebrate dog model.
复制标题
氟烷对去大脑狗模型中髓质呼气神经元兴奋性神经传递的影响。
DOI：
10.1097/00000542-200012000-00020
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发表时间：
2000
期刊：
影响因子：
8.8
通讯作者：
Zuperku,EJ
中科院分区：
文献类型：
--
作者：
Stuth,EA;Krolo,M;Stucke,AG;Tonkovic-Capin,M;Tonkovic-Capin,V;Hopp,FA;Kampine,JP;Zuperku,EJ
研究背景犬尾侧腹侧呼吸组呼气（E）神经元的活动主要依赖于N-甲基-D-天冬氨酸（NMDA）受体介导的兴奋性化学驱动输入，并受γ-氨基丁酸A（GABA（A））受体介导的抑制机制的调节。在一个完整的犬准备，氟烷抑制这些神经元的活动，主要是通过减少整体amatergic兴奋。一个新的decerebrate制备允许比较氟烷对这些突触机制与麻醉剂的基线states.MethodsTwo独立的研究进行decerebrate，迷走神经切断，瘫痪，机械通气的狗在hypercapnic hyperoxia。在研究1中，研究了在通过局部压力喷射荷包牡丹碱完全阻断GABA（A）受体之前和期间，1最小肺泡浓度（MAC）氟烷对细胞外记录的E神经元活动的影响。抑制机制的完全阻断使得氟烷对GABA（A）介导的总体抑制和对NMDA受体介导的总体兴奋的作用之间存在差异。在研究2中，1 MAC氟烷对神经元对谷氨酸激动剂NMDA的局部皮可喷射的剂量反应的影响被用来估计氟烷对突触后谷氨酸能兴奋性神经transmission.ResultsIn研究1，自发活动的14个E神经元被1 MAC氟烷抑制38.6+/-20.6%（平均值+/-SD）。总体兴奋降低31.5+/-15.5%。氟烷给药期间，GABA能抑制增强11.7+/-18.3%。在研究2中，1 MAC氟烷再次显著抑制13个E神经元的自发活动（27.9 ± 10.6%），但氟烷对神经元对外源性NMDA的突触后反应无明显抑制作用（3.3+/-38.4%）。结论这些结果共同表明，在我们的E神经元范例中，氟烷的抑制作用主要是通过减少多巴胺能突触前机制发挥的。
BackgroundThe activity of canine expiratory (E) neurons in the caudal ventral respiratory group is primarily dependent on N-methyl-D-aspartic acid (NMDA) receptor-mediated excitatory chemodrive inputs and modulated by an inhibitory mechanism mediated via gamma-aminobutyric acidA (GABA (A)) receptors. In an intact canine preparation, halothane depressed the activity of these neurons mainly by reduction in overall glutamatergic excitation. A new decerebrate preparation allows comparison of the effects of halothane on these synaptic mechanisms with an anesthetic-free baseline state.MethodsTwo separate studies were performed in decerebrate, vagotomized, paralyzed, mechanically ventilated dogs during hypercapnic hyperoxia. In study 1, the effect of 1 minimum alveolar concentration (MAC) halothane on extracellularly recorded E neuronal activity was studied before and during complete GABA (A) receptor blockade by localized pressure ejection of bicuculline. Complete blockade of the inhibitory mechanism allowed differentiation between the effects of halothane on overall GABA (A)-mediated inhibition and on overall NMDA receptor-mediated excitation. In study 2, the effect of 1 MAC halothane on the dose response of neurons to localized picoejection of the glutamate agonist NMDA was used to estimate halothane effect on postsynaptic glutamatergic excitatory neurotransmission.ResultsIn study 1, the spontaneous activity of 14 E neurons was depressed 38.6+/-20.6%(mean+/-SD) by 1 MAC halothane. Overall excitation was depressed 31.5+/-15.5%. The GABAergic inhibition showed a 11.7+/-18.3% enhancement during halothane. In study 2, the spontaneous activity of 13 E neurons was again significantly depressed by 1 MAC halothane (27.9+/-10.6%), but the postsynaptic response of the neurons to exogenous NMDA was not significantly depressed by halothane (3.3+/-38.4%).ConclusionsTogether these results suggest that in our E neuron paradigm, halothane exerted its depressive effect mainly via reduction of glutamatergic presynaptic mechanisms.