REM sleep deprivation and dopaminergic D2 receptors modulation increase recognition memory in an animal model of Parkinson’s disease

Targa, Adriano; Noseda, Ana Carolina D.; Rodrigues, Laís S.; Aurich, Mariana F.; Lima, Marcelo M.S.

doi:10.1016/j.bbr.2017.11.008

Cited by 15 publications

(13 citation statements)

References 70 publications

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“…Accordingly, our results demonstrated that riluzole did not affected memory processes of control groups and also not rescued the impairment impinged by rotenone, REMSD or their combination. Furthermore, REMSD generated remarkable memory impairment, corroborating with previous reports 49 , 50 . Such result is opposite to other studies that tested riluzole in different chronic and systemic protocols showing levels of improvement of cognitive performance 51 , 52 .…”

Section: Discussionsupporting

confidence: 91%

Absence of a synergic nigral proapoptotic effect triggered by REM sleep deprivation in the rotenone model of Parkinson´s disease

et al. 2019

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Excitotoxicity has been related to play a crucial role in Parkinson's disease (PD) pathogenesis. Pedunculopontine tegmental nucleus (PPT) represents one of the major sources of glutamatergic afferences to nigrostriatal pathway and putative reciprocal connectivity between these structures may exert a potential influence on rapid eye movement (REM) sleep control. Also, PPT could be overactive in PD, it seems that dopaminergic neurons are under abnormally high levels of glutamate and consequently might be more vulnerable to neurodegeneration. We decided to investigate the neuroprotective effect of riluzole administration, a N-methyl-D-aspartate (NMDA) receptor antagonist, in rats submitted simultaneously to nigrostrial rotenone and 24h of REM sleep deprivation (REMSD). Our findings showed that blocking NMDA glutamatergic receptors in the SNpc, after REMSD challenge, protected the dopaminergic neurons from rotenone lesion. Concerning rotenone-induced hypolocomotion, riluzole reversed this impairment in the control groups. Also, REMSD prevented the occurrence of rotenone-induced motor impairment as a result of dopaminergic supersensitivity. In addition, higher Fluoro Jade C (FJC) staining within the SNpc was associated with decreased cognitive performance observed in rotenone groups. Such effect was counteracted by riluzole suggesting the occurrence of an antiapoptotic effect. Moreover, riluzole did not rescue cognitive impairment impinged by rotenone, REMSD or their combination. These data indicated that reductions of excitotoxicity, by riluzole, partially protected dopamine neurons from neuronal death and appeared to be effective in relieve specific rotenone-induce motor disabilities.

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Section: Discussionsupporting

confidence: 91%

Absence of a synergic nigral proapoptotic effect triggered by REM sleep deprivation in the rotenone model of Parkinson´s disease

et al. 2019

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“…In the present study, we did not investigate the effect of rotenone‐induced desynchronisation on the motor activity of the rats. In fact, at the chosen dose and protocol, rotenone does not affect motor function, effectively mimicking an early stage of the disease (Fagotti et al., 2019; Targa et al., 2018). In turn, we observed that the rotenone‐induced desynchronisation was associated with a decrease in SWS and impairment in object recognition memory.…”

Section: Discussionmentioning

confidence: 99%

“…To further investigate these aspects, we used the rotenone animal model of Parkinson’s disease. This model mimics an early stage of the disease with different features such as anxiety (Noseda, Targa, Rodrigues, Aurich, & Lima, 2016), depressive‐like behaviour (Noseda et al., 2014), olfactory dysfunction (Ilkiw et al., 2018; Rodrigues et al., 2014), cognitive impairment (Targa, Noseda, Rodrigues, Aurich, & Lima, 2018), and sleep disturbances (Targa et al., 2016). In addition, we employed a recently developed technique to characterise the fine temporal structure of intermittent phase‐locking in a wide range of oscillatory systems (Ahn, Park, & Rubchinsky, 2011; dos Santos Lima et al., 2019; Park, Worth, & Rubchinsky, 2010).…”

Section: Introductionmentioning

confidence: 99%

Disruption of neocortical synchronisation during slow‐wave sleep in the rotenone model of Parkinson’s disease

Lima

Targa

Cavalcante

et al. 2020

Journal of Sleep Research

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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.

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“…Cognitive deficits in PD patients are diverse with particular impairment in attentional, executive function, episodic learning, memory, and visuospatial domains ( Dubois et al, 2007 ; Aarsland et al, 2011 ). Several mechanisms including spread of α-synuclein Lewy pathology to limbic and neocortical structures ( Braak et al, 2005 ), involvement of basal ganglia and the pedunculopontine nucleus (PPT) ( Targa et al, 2018 ), and hyperphosphorylated tau- as well as amyloid-β deposition ( Hepp et al, 2016 ) seem to contribute to cognitive decline in PD. However, in comparison to Alzheimer’s disease, memory impairment in PD seems to result predominantly from ineffective strategies in encoding and retrieval due to executive dysfunction ( Pillon et al, 1993 ; Bosboom et al, 2004 ; Kalbe et al, 2008 ).…”

Section: Introductionmentioning

confidence: 99%

Sleep Disturbances and Sleep Disordered Breathing Impair Cognitive Performance in Parkinson’s Disease

et al. 2020

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Background Sleep disturbances and impairment of cognitive function are among the most frequent non-motor symptoms in Parkinson’s disease (PD) with negative implications on quality of life of patients and caregivers. Despite the fact that sleep disturbances are a major issue in PD patients, only limited data are available regarding interactions of sleep disturbances and cognitive performance. Objective This post hoc analysis of the RaSPar trial was therefore designed to further elucidate sleep disturbances and their impact on cognition in PD. Methods Twenty-six PD patients with sleep disturbances were evaluated thoroughly including assessments of patients’ subjective and objective sleep quality by interview, questionnaires, and polysomnography (PSG). Cognitive performance was assessed by Parkinson Neuropsychometric Dementia Assessment (PANDA) and Test of Attentional Performance (TAP), and associations of sleep and cognitive function were evaluated. Results We did not detect differences in cognitive performance between patients with and without rapid eye movement (REM) sleep behavior disorder (RBD). Instead, cognitive impairment, particularly affecting cognitive domains attention, executive function/working memory, and semantic memory, was associated with impaired PSG-measured sleep quality (e.g., sleep efficiency) and sleep disordered breathing (SDB) (Apnea-Hypopnea Index > 5/h). Global cognitive performance was decreased in patients with SDB (PANDA score 23.2 ± 3.5 vs. 26.9 ± 2.2, P = 0.020, unpaired two-sided t -test). Conclusion Sleep apnea and other sleep disturbances impair cognitive performance in PD and should be evaluated in routine care, and treatment options such as continuous airway pressure therapy should be considered.

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REM sleep deprivation and dopaminergic D2 receptors modulation increase recognition memory in an animal model of Parkinson’s disease

Cited by 15 publications

References 70 publications

Absence of a synergic nigral proapoptotic effect triggered by REM sleep deprivation in the rotenone model of Parkinson´s disease

Absence of a synergic nigral proapoptotic effect triggered by REM sleep deprivation in the rotenone model of Parkinson´s disease

Disruption of neocortical synchronisation during slow‐wave sleep in the rotenone model of Parkinson’s disease

Sleep Disturbances and Sleep Disordered Breathing Impair Cognitive Performance in Parkinson’s Disease

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