Lai Y Y, Siegel J M
Veterans Administration Medical Center, Sepulveda, California 91343.
J Neurosci. 1988 Dec;8(12):4790-6. doi: 10.1523/JNEUROSCI.08-12-04790.1988.
Electrical stimulation studies have implicated the medial medulla in the inhibition of muscle tone. In the present report we present evidence for suppression of muscle tone by chemical activation of the medial medulla. We find 2 distinct zones within the classically defined medial medullary inhibitory area. A rostral region corresponding to the nucleus magnocellularis (NMC) is sensitive to glutamate. Atonia produced by activation of this region is mediated by non-NMDA receptors. A caudal region, corresponding to the nucleus paramedianus (NPM) is sensitive to ACh. Atonia produced by activation of this region is mediated by muscarinic receptors. Activation of these regions both in acute decerebrate and intact cats suppresses muscle tone. We find that the cholinoceptive dorsolateral pontine region, previously implicated in atonia control, can be activated by glutamate-sensitive non-NMDA receptors. Microinjection of atropine into the NPM or of glutamylglycine into the NMC blocks atonia elicited by pontine carbachol injection. The medullary regions identified here are hypothesized to mediate the suppression of muscle tone that occurs in rapid eye movement sleep and in cataplexy and may have a role in postural control in waking.
电刺激研究表明延髓中部参与肌张力抑制。在本报告中，我们提供了通过化学激活延髓中部来抑制肌张力的证据。我们在经典定义的延髓内侧抑制区内发现了两个不同的区域。对应于巨细胞网状核（NMC）的头侧区域对谷氨酸敏感。激活该区域产生的弛缓由非NMDA受体介导。对应于旁正中核（NPM）的尾侧区域对乙酰胆碱敏感。激活该区域产生的弛缓由毒蕈碱受体介导。在急性去大脑猫和完整猫中激活这些区域均能抑制肌张力。我们发现，先前认为参与弛缓控制的胆碱能背外侧脑桥区域可被谷氨酸敏感的非NMDA受体激活。向NPM微量注射阿托品或向NMC微量注射谷氨酰甘氨酸可阻断脑桥注射卡巴胆碱引起的弛缓。此处确定的延髓区域被认为介导快速眼动睡眠和猝倒时发生的肌张力抑制，并且可能在清醒时的姿势控制中起作用。
