Unraveling a new circuitry for sleep regulation in Parkinson's disease

Targa, Adriano; Rodrigues, Laís S.; Noseda, Ana Carolina D.; Aurich, Mariana F.; Andersen, Mônica Levy; Tufik, Sérgio; Cunha, Cláudio Da; Lima, Marcelo M.S.

doi:10.1016/j.neuropharm.2016.04.018

Cited by 21 publications

(22 citation statements)

References 49 publications

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“…In the ROT-treated compared to the SHAM animals a selective reduction in the percentage of TH-ir neurons within the SNpc, which is related to several NMS that are landmarks of early-phase features of PD, was observed 9,32,33,37 . Dopamine depletion within the SNpc leads to an increase in striatal D2 receptors, increasing activity of the nigrostriatal indirect-pathway resulting in movement impairment 47 .…”

Section: Discussionmentioning

confidence: 89%

“…The ROT-PD has established itself more and more as a prototypical model to study sleep aspects related to the SNpc dopaminergic lesion. Previous studies have shown that both chronic systemic administration and stereotaxic injection of ROT were associated with sleep alterations, as long-term and progressive deterioration of spontaneous sleep 35 and decrease of the time in NREM sleep 33 .…”

Section: Discussionmentioning

confidence: 99%

“…For ROT (3 groups, 24 animals per group, total number of 72 animals) or vehicle (dimethylsulfoxide - SHAM) (3 groups, 24 animals per group, total number of 72 animals) infusion within the SNpc, the following coordinates was used, bregma as a reference: (AP) −5.0 mm, (ML) ± 2.1 mm and (DV) −8.0 mm 36 . Rotenone (12 µg/µl; Sigma-Aldrich®, St. Louis, MO, United States) or DMSO (Sigma-Aldrich®, St. Louis, MO, United States) infusions of 1 µL into each hemisphere were made at a rate of 0.33 µL/min for 3 min 32,33,37 . These infusions were made using an electronic infusion pump (Insight Instruments, Ribeirão Preto, SP, Brazil).…”

Section: Methodsmentioning

confidence: 99%

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Chronic sleep restriction in the rotenone Parkinson’s disease model in rats reveals peripheral early-phase biomarkers

Fagotti

Targa

Rodrigues

et al. 2019

Sci Rep

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Parkinson’s disease (PD) is a chronic disorder that presents a range of premotor signs, such as sleep disturbances and cognitive decline, which are key non-motor features of the disease. Increasing evidence of a possible association between sleep disruption and the neurodegenerative process suggests that sleep impairment could produce a detectable metabolic signature on the disease. In order to integrate neurocognitive and metabolic parameters, we performed untargeted and targeted metabolic profiling of the rotenone PD model in a chronic sleep restriction (SR) (6 h/day for 21 days) condition. We found that SR combined with PD altered several behavioural (reversal of locomotor activity impairment; cognitive impairment; delay of rest-activity rhythm) and metabolic parameters (branched-chain amino acids, tryptophan pathway, phenylalanine, and lipoproteins, pointing to mitochondrial impairment). If combined, our results bring a plethora of parameters that represents reliable early-phase PD biomarkers which can easily be measured and could be translated to human studies.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Chronic sleep restriction in the rotenone Parkinson’s disease model in rats reveals peripheral early-phase biomarkers

Fagotti

Targa

Rodrigues

et al. 2019

Sci Rep

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“…and striatum [45]. Also, on the base of recent evidence for the functional connectivity of the PPT and deep cerebellar nuclei [46], it was suggested that the PPT, beside its important role in the cortico-basal ganglia circuit, may act as an interface device between the basal ganglia and cerebellum, thereby influencing motor control and cognitive functions [41].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Sleep disorder and altered locomotor activity as biomarkers of the Parkinson’s disease cholinopathy in rat

Ciric

Lazic

Kapor

et al. 2018

Behavioural Brain Research

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In order to find out the possible earliest biomarkers of Parkinson's disease (PD) cholinopathy, we followed the impact of bilateral pedunculopontine tegmental nucleus (PPT) lesion in rat on: the cortical and hippocampal sleep/wake states architectures, all sleep states related EEG microstructures, sleep spindles, the basal and stimulated locomotor activity. Sleep and basal locomotor activity in adult Wistar rats were followed during their inactive circadian phase, and throughout the same aging period. The bilateral PPT lesions were done by 0.1M ibotenic acid (IBO) during the surgical procedure for implantation of the electroencephalographic (EEG) and electromyographic (EMG) electrodes for chronic sleep recording. The cholinergic neuronal loss was identified by NADPH - diaphorase histochemistry. After all sleep and behavioral recording sessions, the locomotor activity was stimulated by d-amphetamine (d-AMPH) and the neuronal activity of striatum was followed by c-Fos immunolabeling. Impaired cholinergic innervation from the PPT was expressed earlier as sleep disorder then as movement disorder, and it was the earliest and long-lasting at hippocampal and thalamo-cortical level, and followed by a delayed "hypokinesia". This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH. In order how they occurred, the hippocampal non rapid eye movement (NREM) sleep disorder, altered high voltage sleep spindle (HVS) dynamics during rapid eye movement (REM) sleep in the hippocampus and motor cortex, and "hypokinesia" may serve as the biomarkers of PD cholinopathy onset and progression.

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“…Accordingly, our recent study published in Neuropharmacology proposed a physiological association between PPT and SNpc that was tested by a protocol of neurotoxic lesions and pharmacological modulation of striatal D2 receptors in Wistar rats [8]. These results showed that D2 striatal receptors have a relevant influence in non-REM sleep regulation because raclopride (a selective antagonist) administration increased the percentage of time spent in non-REM sleep compared to piribedil (a selective agonist).…”

mentioning

confidence: 99%