首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Ethanol attenuates sensory stimulus-evoked responses in cerebellar granule cells via activation of GABA_A receptors in vivo in mice
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Ethanol attenuates sensory stimulus-evoked responses in cerebellar granule cells via activation of GABA_A receptors in vivo in mice

机译:乙醇通过激活小鼠体内的GABA_A受体来减弱小脑颗粒细胞中的感觉刺激诱发的反应

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摘要

Acute alcohol intoxication affects cerebellar motor regulation possibly by altering the transfer and integration of external information in cerebellar cortical neurons, resulting in a dysfunction of cerebellar motor regulation or a cerebellar atexia. However, the synaptic mechanisms of ethanol induced impairments of sensory information processing in cerebellar cortical neurons are not fully understand. In the present study, we used electrophysiological and pharmacological methods to study the effects of ethanol on the sensory stimulation-evoked responses in cerebellar granule cells (GCs) in vivo in uret-hane anesthetized mice. Air-puff stimulation of the ipsilateral whisker-pad evoked stimulus-on (P1) and stimulus-off responses (P2) in GCs of cerebellar Crus II. Cerebellar surface perfusion of ethanol did not alter the onset latency of the sensory stimulation-evoked responses, but reversible reduced the amplitude of P1 and P2. The ethanol-induced reduction of the GCs sensory responses was concentration-dependent. In the presence of ethanol, the mean half-width, area under curve, rise Tau and decay Tau of P1 were significantly decreased. Blockade of gamma-aminobutyric acid type A (GABA_A) receptors activity induced an increase in amplitude of P1, and abolished the ethanol induced inhibition of the GCs sensory responses. These results indicate that ethanol inhibits the tactile evoked responses in cerebellar GCs through enhancement of GABAa receptors activity.
机译:急性酒精中毒可能通过改变小脑皮质神经元中外部信息的传递和整合来影响小脑运动调节,导致小脑运动调节功能障碍或小脑性共济失调。然而,乙醇诱导的小脑皮质神经元感觉信息处理受损的突触机制尚不完全清楚。在本研究中,我们使用电生理和药理学方法研究了乙醇对尿道麻醉小鼠体内小脑颗粒细胞(GCs)的感觉刺激诱发反应的影响。气喘刺激同侧晶须垫在小脑Crus II的GC中引起刺激刺激(P1)和刺激刺激响应(P2)。乙醇的小脑表面灌注并没有改变感觉刺激诱发反应的发作潜伏期,但可逆地降低了P1和P2的幅度。乙醇诱导的GCs感觉反应的降低是浓度依赖性的。在乙醇存在下,P1的平均半峰宽,曲线下面积,Tau上升和衰减Tau显着降低。 γ-氨基丁酸A型(GABA_A)受体活性的封锁导致P1振幅的增加,并取消了乙醇诱导的GC感觉反应的抑制。这些结果表明乙醇通过增强GABA a受体活性来抑制小脑GC中的触觉诱发反应。

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