Research On Altered Features In The Electrocorticogram And Local Field Potential Of The Globus Pallidus Of 6-OHDA-lesioned Rat Models Stimulating Parkinson Disease During Rapid Eye Movement Sleep

Parkinson's disease (PD) is a disease caused by the degeneration of substantia nigra and nigrostriatal pathway and usually occurrs in middle-aged people. Dopamine (DA) insufficiency of corpus striatum is the main pathological changes, which is caused by decreased DA biosynthesis in the surviving neurons and degeneration of dopaminergic neurons. The clinical symptoms of PD include motor symptoms and non-motor symptoms. While the motor symptoms is characterized by bradykinesia, resting tremor, rigidity and postural instability, the non-motor symptoms typical clinical symptoms are also common and can significantly debilitate patients'activities as well as the quality of life, which includes sleep, sensory, psychiatric and cognitive disorders. The incidence of Parkinson's disease is rising in the world in recent years, and the numbers of PD patients are increasing with the aging of population in our country as well. However, the pathogenesis of PD is unclear. At present, the research focuses on the occurrence of motor symptoms, but there is little reasearch on the mechanisms of sleep disorders. And there is still no ideal treatment for the sleep disorders of PD at home and abroad, which is becoming a focus for neural disciplines gradually. Through multi-point simultaneous recordings of electrocorticogram (ECoG) and local field potential of globus pallidus of rats during rapid eye movement sleep (REM) in the experiment, we tried to explore the altered features of motor cortex and Globus Pallidus in PD rats during rapid eye movement (REM) sleep, to further undertand the electrical physiology characteristic of REM sleep and PD.Objective To investigate altered features of the electrocorticogram (ECoG) and local field potential of the globus pallidus of Parkinson disease (PD) rat models during rapid eye movement sleep.Methods Sprague-Dawley rats with unilateral 6-hydroxydopamine (6-OHDA) lesions were used as the model of PD. Apomorphine induced contralateral rotations in PD rat models were examined to assure proper lesioning. Continuous video, Electromyography(EMG), local field potential(LFP) of the globus pallidus(GP), and Electrocorticogram(ECoG) of primary motor cortex (M1) and the secondary motor cortex (M2) were detected simultaneously for 24 hours or more. Power spectral densities (PSD) were computed to decompose distinct frequency components of signals recording at each electrode positions. Coherence analysis was used to assess the coupling or synchronization of brain activity between distributed neuronal populations at each electrode position.Results Compared with the saline-treated rats, 6-OHDA-lesioned rats showed some differences during rapid eye movement sleep:θrhythm in the ECoGs of primary motor cortex (M1) disappeared;θrhythm in the ECoGs of the secondary motor cortex (M2) andθrhythm in LFP of GP on the injected side increased;γrhythm in the ECoGs of primary motor cortex (M 1) increased;γrhythm in the LFP of GP did not change.Conclusion 6-OHDA lesions of midbrain dopaminergic neurons of rat can induce the disappearance ofθrhythm and enhancedγrhythm in the ECoGs of M1 and increase contralateralγrhythm synchronization between the ECoGs of M1 and M2. These abnormal rhythms may be induced by the damage of ventra tegmental area (VTA) and have relationships with rapid eye movement sleep behavior disorder of PD. Whether these abnormal rhythms activities are related to rapid eye movement sleep behavior disorder of PD or not needs further experiments to study.