Premium
Disruption of neocortical synchronisation during slow‐wave sleep in the rotenone model of Parkinson’s disease
Author(s) -
Santos Lima Gustavo Zampier,
Targa Adriano D. S.,
Freitas Cavalcante Samantha,
Rodrigues Lais S.,
FonteneleAraújo John,
Torterolo Pablo,
Andersen Monica L.,
Lima Marcelo M. S.
Publication year - 2021
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/jsr.13170
Subject(s) - rotenone , parkinson's disease , neuroscience , pars compacta , substantia nigra , psychology , neocortex , memory consolidation , sleep (system call) , audiology , disease , hippocampus , medicine , chemistry , mitochondrion , computer science , biochemistry , operating system
Parkinson’s disease motor dysfunctions are associated with improperly organised neural oscillatory activity. The presence of such disruption at the early stages of the disease in which altered sleep is one of the main features could be a relevant predictive feature. Based on this, we aimed to investigate the neocortical synchronisation dynamics during slow‐wave sleep (SWS) in the rotenone model of Parkinson’s disease. After rotenone administration within the substantia nigra pars compacta, one group of male Wistar rats underwent sleep–wake recording. Considering the association between SWS oscillatory activity and memory consolidation, another group of rats underwent a memory test. The fine temporal structure of synchronisation dynamics was evaluated by a recently developed technique called first return map. We observed that rotenone administration decreased the time spent in SWS and altered the power spectrum within different frequency bands, whilst it increased the transition rate from a synchronised to desynchronised state. This neurotoxin also increased the probability of longer and decreased the probability of shorter desynchronisation events. At the same time, we observed impairment in object recognition memory. These findings depict an electrophysiological fingerprint represented by a disruption in the typical oscillatory activity within the neocortex at the early stages of Parkinson’s disease, concomitant with a decrease in the time spent in SWS and impairment in recognition memory.