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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex.
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Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex.

机译：C57BL / 6J小鼠脑桥网状结构中的卡巴胆碱降低前额叶皮层中乙酰胆碱的释放。

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The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (P<0.01) decrease (-28%) in ACh release in the frontal association cortex, a significant (P<0.01) decrease (-23%) in respiratory rate, and a significant (P<0.01) increase (223%) in time to righting after anesthesia. Additional in vitro studies used the [(35)S]guanylyl-5'-O-(gamma-thio)-triphosphate ([(35)S]GTPgammaS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain. In vitro treatment with carbachol (1 mM) caused a significant (P<0.01) increase in [(35)S]GTPgammaS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration-dependent and blocked by atropine, indicating that the carbachol-stimulated [(35)S]GTPgammaS binding was mediated by muscarinic cholinergic receptors. Together, the in vitro and in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.
机译：前额叶皮层和脑干调节自主和唤醒状态的控制，但前额叶皮层和脑干之间的通信的神经递质机制仍然知之甚少。这项研究检查了假说，将卡巴胆碱微透析递送至麻醉的C57BL / 6J（B6）小鼠的脑桥网状结构（PRF）会调节额叶联想皮层中的乙酰胆碱（ACh）释放。向PRF的卡巴胆碱微透析（8.8 mM）导致额叶缔合皮层ACh释放显着（P <0.01）降低（-28％），呼吸频率显着（P <0.01）降低（-23％） ，并且在麻醉后恢复时间显着（P <0.01）增加（223％）。额外的体外研究使用了[（35）S]鸟苷基5'-O-（γ-硫代）-三磷酸（[（（35）S] GTPgammaS）试验来测试有关毒蕈碱胆碱能受体激活鸟嘌呤核苷酸结合蛋白（ G蛋白）在额叶皮质和基底前脑中。用卡巴胆碱（1 mM）进行的体外处理导致额叶缔合皮层（62％）和基底前脑核（包括中隔）（227％），垂直（前额）的[（35）S] GTPgammaS结合显着（P <0.01）增加Broca对角带的水平肢体为210％）和水平肢体（165％），以及无感染性实体（127％）。卡巴胆碱的G蛋白激活是浓度依赖性的，并被阿托品所阻断，表明卡巴胆碱刺激的[（35）S] GTPgammaS结合是由毒蕈碱胆碱能受体介导的。总之，体外和体内数据首次在B6小鼠中表明PRF中的胆碱能神经传递可以显着改变额叶缔合皮层中的ACh释放，麻醉引起的觉醒和呼吸频率。

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