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首页> 外文期刊>The European Journal of Neuroscience >Activation and desensitization of neuronal nicotinic receptors modulate glutamatergic transmission on neonatal rat hypoglossal motoneurons.
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Activation and desensitization of neuronal nicotinic receptors modulate glutamatergic transmission on neonatal rat hypoglossal motoneurons.

机译：神经元烟碱样受体的激活和脱敏调节新生大鼠舌下运动神经元的谷氨酸能传递。

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摘要

In the neonate the muscles of the tongue, which are exclusively innervated by the XII cranial nerves originating from the brainstem nucleus hypoglossus, must contract rhythmically in coincidence with breathing, suckling and swallowing. These motor commands are generated by hypoglossal motoneurons excited by glutamatergic inputs. Because in forebrain areas the efficiency of glutamatergic transmission is modulated by neuronal nicotinic receptors (nAChRs), the role and identity of nAChRs within the nucleus hypoglossus of the neonatal rat were explored using an in vitro brainstem slice preparation. This area expressed immunoreactivity for alpha4, alpha7 and beta2 nAChR subunits. Whole-cell patch-clamp recording from hypoglossal motoneurons showed lack of spontaneous cholinergic events mediated by nAChRs even in the presence of a cholinesterase inhibitor. However, pharmacological antagonism of alpha7- or beta2-containing receptors depressed glutamatergic currents arising either spontaneously or by electrical stimulation of the reticular formation. Hypoglossal motoneurons expressed functional nAChRs with characteristics of alpha4beta2 and alpha7 receptor subunits. Such receptors underwent fast desensitization (time constant of 200 ms) with full recovery within 1 min. Low (0.5 microm) concentration of nicotine first facilitated glutamatergic transmission on motoneurons and later depressed it through receptor desensitization. When 0.1 microm nicotine was used, only depression of synaptic transmission occurred, in keeping with the suggestion that nAChRs can be desensitized without prior activation. These results highlight the role of tonic nAChR activity in shaping excitatory inputs to hypoglossal motoneurons, and suggest that nAChR desensitization by ambient nicotine could contribute to disorders of tongue muscle movements.
机译：在新生儿中，舌头的肌肉必须完全由呼吸干，吮吸和吞咽的节律性收缩，而舌头的肌肉仅由源自脑干核下垂的XII颅神经支配。这些运动命令是由谷氨酸能输入激发的舌下运动神经元产生的。因为在前脑区域，神经元烟碱样受体（nAChRs）调节了谷氨酸能传递的效率，因此使用体外脑干切片制剂探索了新生大鼠核下丘脑内nAChRs的作用和特性。该区域表达了对α4，α7和β2nAChR亚基的免疫反应性。来自舌下运动神经元的全细胞膜片钳记录表明，即使存在胆碱酯酶抑制剂，也缺乏由nAChR介导的自发胆碱能事件。然而，含α7或β2的受体的药理拮抗作用抑制了自发或通过电刺激网状结构形成的谷氨酸能电流。舌下运动神经元表达功能性nAChRs，具有alpha4beta2和alpha7受体亚基的特征。此类受体经历了快速脱敏（时间常数为200 ms），并在1分钟内完全恢复。低浓度（0.5微米）的尼古丁首先促进了运动神经元上的谷氨酸能传播，随后通过受体脱敏作用抑制了它的传播。当使用0.1微米的尼古丁时，仅发生突触传递降低，这与nAChRs无需先激活即可脱敏的建议保持一致。这些结果突显了补剂nAChR活性在塑造向舌下运动神经元的兴奋性输入中的作用，并表明环境烟碱引起的nAChR脱敏可能导致舌肌运动异常。

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