Abstract
We investigated the alterations of hippocampal and reticulo-thalamic (RT) GABAergic parvalbumin (PV) interneurons and their synaptic re-organizations underlying the prodromal local sleep disorders in the distinct rat models of Parkinson’s disease (PD). We demonstrated for the first time that REM sleep is a predisposing state for the high-voltage sleep spindles (HVS) induction in all experimental models of PD, particularly during hippocampal REM sleep in the hemiparkinsonian models. There were the opposite underlying alterations of the hippocampal and RT GABAergic PV+ interneurons along with the distinct MAP2 and PSD-95 expressions. Whereas the PD cholinopathy enhanced the number of PV+ interneurons and suppressed the MAP2/PSD-95 expression, the hemiparkinsonism with PD cholinopathy reduced the number of PV+ interneurons and enhanced the MAP2/PSD-95 expression in the hippocampus. Whereas the PD cholinopathy did not alter PV+ interneurons but partially enhanced MAP2 and suppressed PSD-95 expression remotely in the RT, the hemiparkinsonism with PD cholinopathy reduced the PV+ interneurons, enhanced MAP2, and did not change PSD-95 expression remotely in the RT. Our study demonstrates for the first time an important regulatory role of the hippocampal and RT GABAergic PV+ interneurons and the synaptic protein dynamic alterations in the distinct rat models of PD neuropathology.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disease that predominantly affects the motor system as a result of dopaminergic (DA) neuronal loss within the substantia nigra pars compacta (SNpc) [1]
In order to investigate the cellular substrate of the local prodromal sleep disorders in the distinct rat models of PD neuropathology, we quantified the PV+ interneurons of dentate gyrus (DG) by using the hippocampal sections from our previous study, where we have already verified and quantified the lesions: the bilateral PPT
Whereas the PD cholinopathy enhanced, the hemiparkinsonism with PD cholinopathy reduced the number of hippocampal PV+ interneurons in DG (Figures 1 and 2)
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disease that predominantly affects the motor system as a result of dopaminergic (DA) neuronal loss within the substantia nigra pars compacta (SNpc) [1]. The clinical diagnosis of PD is dominantly based on identification of motor impairments such as bradykinesia, rigidity, resting tremor, and posture and gait problems [2]. These motor symptoms appear rather late, following a substantial nigrostriatal dopaminergic neurodegeneration. Over the past few years, the concept of PD pathology has been changed: instead of being regarded as a motor disease induced by the selective loss of DA neurons within the SNpc, PD is being recognized as a severe multisystem neurodegenerative disorder [4]. Gastrointestinal abnormalities, sleep disturbances, visual alterations, and cognitive and mood disorders have been recognized as the non-motor manifestations that precede and accompany the classical motor impairments in PD [4,6]
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