Maloney K J, Mainville L, Jones B E
Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, Montreal, Quebec H3A 2B4, Canada.
J Neurosci. 2000 Jun 15;20(12):4669-79. doi: 10.1523/JNEUROSCI.20-12-04669.2000.
The brainstem contains the neural systems that are necessary for the generation of the state of paradoxical sleep (PS) and accompanying muscle atonia. Important for its initiation are the pontomesencephalic cholinergic neurons that project into the pontomedullary reticular formation and that we have recently shown increase c-Fos expression as a reflection of neural activity in association with PS rebound after deprivation in rats (Maloney et al. , 1999). As a continuation, we examined in the present study c-Fos expression in the pontomedullary reticular and raphe neurons, including importantly GABAergic neurons [immunostained for glutamic acid decarboxylase (GAD)] and serotonergic neurons [immunostained for serotonin (Ser)]. Numbers of single-labeled c-Fos+ neurons were significantly increased with PS rebound only in the pars oralis of the pontine reticular nuclei (PnO), where numbers of GAD+/c-Fos+ neurons were conversely significantly decreased. c-Fos+ neurons were positively correlated with PS, whereas GAD+/c-Fos+ neurons were negatively correlated with PS, suggesting that disinhibition of reticular neurons in the PnO from locally projecting GABAergic neurons may be important in the generation of PS. In contrast, through the caudal pons and medulla, GAD+/c-Fos+ cells were increased with PS rebound, covaried positively with PS and negatively with the electromyogram (EMG). In the raphe pallidus-obscurus, Ser+/c-Fos+ neurons were positively correlated, in a reciprocal manner to GAD+/c-Fos+ cells, with EMG, suggesting that disfacilitation by removal of a serotonergic influence and inhibition by imposition of a GABAergic influence within the lower brainstem and spinal cord may be important in the development of muscle atonia accompanying PS.
脑干包含产生异相睡眠（PS）状态及伴随的肌肉张力缺失所必需的神经系统。对其起始很重要的是脑桥中脑胆碱能神经元，这些神经元投射到脑桥延髓网状结构，并且我们最近发现，在大鼠睡眠剥夺后PS反弹时，这些神经元会增加c-Fos表达，以此反映神经活动（马洛尼等人，1999年）。作为后续研究，我们在本研究中检测了脑桥延髓网状和中缝神经元中的c-Fos表达，其中重要的包括γ-氨基丁酸能神经元[用谷氨酸脱羧酶（GAD）免疫染色]和5-羟色胺能神经元[用5-羟色胺（Ser）免疫染色]。仅在脑桥网状核口部（PnO），单标记c-Fos+神经元的数量随着PS反弹显著增加，而GAD+/c-Fos+神经元的数量则相反显著减少。c-Fos+神经元与PS呈正相关，而GAD+/c-Fos+神经元与PS呈负相关，这表明来自局部投射的γ-氨基丁酸能神经元对PnO网状神经元的去抑制作用可能在PS的产生中起重要作用。相比之下，在脑桥尾端和延髓，GAD+/c-Fos+细胞随着PS反弹而增加，与PS呈正相关，与肌电图（EMG）呈负相关。在中缝苍白核-中缝隐核中，Ser+/c-Fos+神经元与EMG呈正相关，与GAD+/c-Fos+细胞呈相反关系，这表明在脑干下部和脊髓内，去除5-羟色胺能影响导致的去易化作用以及施加γ-氨基丁酸能影响导致的抑制作用，可能在伴随PS的肌肉张力缺失的发展中起重要作用。
