Morales F R, Engelhardt J K, Soja P J, Pereda A E, Chase M H
J Neurophysiol. 1987 Apr;57(4):1118-29. doi: 10.1152/jn.1987.57.4.1118.
It is well established that cholinergic agonists, when injected into the pontine reticular formation in cats, produce a generalized suppression of motor activity (1, 3, 6, 14, 18, 27, 33, 50). The responsible neuronal mechanisms were explored by measuring ventral root activity, the amplitude of the Ia-monosynaptic reflex, and the basic electrophysiological properties of hindlimb motoneurons before and after carbachol was microinjected into the pontine reticular formation of decerebrate cats. Intrapontine microinjections of carbachol (0.25-1.0 microliter, 16 mg/ml) resulted in the tonic suppression of ventral root activity and a decrease in the amplitude of the Ia-monosynaptic reflex. An analysis of intracellular records from lumbar motoneurons during the suppression of motor activity induced by carbachol revealed a considerable decrease in input resistance and membrane time constant as well as a reduction in motoneuron excitability, as evidenced by a nearly twofold increase in rheobase. Discrete inhibitory postsynaptic potentials were also observed following carbachol administration. The changes in motoneuron properties (rheobase, input resistance, and membrane time constant), as well as the development of discrete inhibitory postsynaptic potentials, indicate that spinal cord motoneurons were postsynaptically inhibited following the pontine administration of carbachol. In addition, the inhibitory processes that arose after carbachol administration in the decerebrate cat were remarkably similar to those that are present during active sleep in the chronic cat. These findings suggest that the microinjection of carbachol into the pontine reticular formation activates the same brain stem-spinal cord system that is responsible for the postsynaptic inhibition of alpha-motoneurons that occurs during active sleep.
胆碱能激动剂注入猫的脑桥网状结构时，会产生全身运动活动抑制，这一点已得到充分证实（1, 3, 6, 14, 18, 27, 33, 50）。通过测量在向去大脑猫的脑桥网状结构微量注射卡巴胆碱前后的腹根活动、Ia单突触反射的幅度以及后肢运动神经元的基本电生理特性，对相关神经元机制进行了探索。向脑桥内微量注射卡巴胆碱（0.25 - 1.0微升，16毫克/毫升）导致腹根活动的持续性抑制以及Ia单突触反射幅度的降低。对卡巴胆碱诱导运动活动抑制期间腰段运动神经元的细胞内记录分析显示，输入电阻和膜时间常数显著降低，运动神经元兴奋性也降低，这表现为基强度几乎增加了两倍。在给予卡巴胆碱后还观察到离散的抑制性突触后电位。运动神经元特性（基强度、输入电阻和膜时间常数）的变化以及离散抑制性突触后电位的出现表明，在脑桥给予卡巴胆碱后脊髓运动神经元受到了突触后抑制。此外，去大脑猫给予卡巴胆碱后出现的抑制过程与慢性猫活跃睡眠期间存在的抑制过程非常相似。这些发现表明，向脑桥网状结构微量注射卡巴胆碱激活了与活跃睡眠期间α运动神经元突触后抑制所负责的相同脑干 - 脊髓系统。
