Alterations of Sleep and Sleep Oscillations in the Hemiparkinsonian Rat

Ciric, Jelena; Kapor, Slobodan; Perović, Milka; Saponjic, Jasna

doi:10.3389/fnins.2019.00148

Cited by 13 publications

(51 citation statements)

References 71 publications

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“…In the substantia nigra, but not in the VTA, this intervention led to increased wakefulness and reduced amounts of NREM and REM sleep during light-on and light-off periods. These results are indicative of insomnia and are in part consistent with findings in rats with a selective dopamine lesion of SNc (see Sleep Disturbances in the 6-Hydroxydopamine Model of Parkinson’s Disease and Sleep Disturbances in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Model of Parkinson’s Disease ) (Lima et al, 2007; Ciric et al, 2019).…”

Section: Introductionsupporting

confidence: 84%

“…When compared to naïve animals, these animals also show increased muscle activity during REM sleep, which is indicative of RBD-like abnormalities (Vo et al, 2014). Sleep analysis has recently been performed in rats injected unilaterally with 6-OHDA in the SNc, which results in a substantial loss of dopamine neurons (Ciric et al, 2019). This intervention leads to increased number and mean duration of wake episodes assessed by cortical and hippocampal EEG during 6 h within the inactive, light-on period (Ciric et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Sleep analysis has recently been performed in rats injected unilaterally with 6-OHDA in the SNc, which results in a substantial loss of dopamine neurons (Ciric et al, 2019). This intervention leads to increased number and mean duration of wake episodes assessed by cortical and hippocampal EEG during 6 h within the inactive, light-on period (Ciric et al, 2019). Increased wake time, particularly evident during the 12-h dark period, has also been observed in rats with a selective 6-OHDA lesion of the SNc (Qiu et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

“…This difference is likely explained by the more generalized effect on multiple components of the catecholamine system exerted by intracerebroventricular (i.c.v.) administration of 6-OHDA, in comparison to selective stereotactic injections in MFB or SNc (Vo et al, 2014; Ciric et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Sleep Disorders in Rodent Models of Parkinson’s Disease

et al. 2019

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Sleep disorders are frequently diagnosed in Parkinson’s disease and manifested in the prodromal and advanced stages of the disease. These conditions, which in some cases affect more than 50% of Parkinson’s disease (PD) patients, include hypersomnia, often manifested as excessive daytime sleepiness, insomnia, characterized by delayed initiation and fragmentation of sleep at night, and disruption of rapid eye movement (REM) sleep, resulting in loss of atonia and dream enactment. Standard dopamine replacement therapies for the treatment of motor symptoms are generally inadequate to combat sleep abnormalities, which seriously affect the quality of life of PD patients. Rodent models still represent a major tool for the study of many aspects of PD. They have been primarily designed to eliminate midbrain dopamine neurons and elicit motor impairment, which are the traditional pathological features of PD. However, rodent models are increasingly employed to investigate non-motor symptoms, which are often caused by degenerative processes affecting multiple monoaminergic and peptidergic structures. This review describes how neurotoxic and genetic manipulations of rats and mice have been utilized to reproduce some of the major sleep disturbances associated with PD and to what extent these abnormalities can be linked to nondopaminergic dysfunction, affecting for instance noradrenaline, serotonin, and orexin transmission. Strengths and limitations are discussed, as well as the consistency of results obtained so far, and the need for models that better reproduce the multisystemic neurodegenerative nature of PD, thereby allowing to replicate the complex etiology of sleep-related disorders.

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Section: Introductionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sleep Disorders in Rodent Models of Parkinson’s Disease

et al. 2019

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“…Thus, we can speculate that this change in the pattern of rest/activity seen in response to 6-OHDA may be similar to the insomnia at night or the hypersomnia during the daytime experimented by PD patients ( De Castro Medeiros et al, 2019 ). Behavioral changes related to circadian cycles were already described in the 6-OHDA model, such as alterations on circadian locomotor rhythm parameters ( Ben and Bruguerolle, 2000 ; Gravotta et al, 2011 ; Masini et al, 2017 ; De Lazzari et al, 2018 ; Souza et al, 2018 ; Ciric et al, 2019 ; De Castro Medeiros et al, 2019 ). In fact, some of these studies associated the circadian disruption with the loss of dopaminergic neurons indicating that dopamine may act as a modulator of the circadian system ( Isobe and Nishino, 2001 ; Gravotta et al, 2011 ; De Lazzari et al, 2018 ; Souza et al, 2018 ; Ciric et al, 2019 ; De Castro Medeiros et al, 2019 ).…”

Section: Discussionmentioning

confidence: 93%

Changes in Day/Night Activity in the 6-OHDA-Induced Experimental Model of Parkinson’s Disease: Exploring Prodromal Biomarkers

et al. 2020

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The search for experimental models mimicking an early stage of Parkinson’s disease (PD) before motor manifestations is fundamental in order to explore early signs and get a better prognosis. Interestingly, our previous studies have indicated that 6-hydroxydopamine (6-OHDA) is a suitable model to induce an early degeneration of the nigrostriatal system without any gross motor impairment. Considering our previous findings, we aim to implement a novel system to monitor rats after intrastriatal injection of 6-OHDA to detect and analyze physiological changes underlying prodromal PD. Twenty male Sprague-Dawley rats were unilaterally injected with 6-OHDA ( n = 10) or saline solution ( n = 10) into the right striatum and placed in enriched environment cages where the activity was monitored. After 2 weeks, the amphetamine test was performed before the sacrifice. Immunohistochemistry was developed for the morphological evaluation and western blot analysis to assess molecular changes. Home-cage monitoring revealed behavioral changes in response to 6-OHDA administration including significant hyperactivity and hypoactivity during the light and dark phase, respectively, turning out in a change of the circadian timing. A preclinical stage of PD was functionally confirmed with the amphetamine test. Moreover, the loss of tyrosine hydroxylase expression was significantly correlated with the motor results, and 6-OHDA induced early proapoptotic events. Our findings provide evidence for a novel prodromal 6-OHDA model following a customized monitoring system that could give insights to detect non-motor deficits and molecular targets to test neuroprotective/neurorestorative agents.

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