Sleep deprivation-induced pre- and postsynaptic modulation of orexin neurons

Briggs, Chantalle; Bowes, Sherri C.; Semba, Kazue; Hirasawa, Michiru

doi:10.1016/j.neuropharm.2018.12.025

Cited by 16 publications

(7 citation statements)

References 48 publications

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“…Key parameters on the relationship of SD and orexinergic system seems to be the type and duration of SD. Previous studies utilized various durations of either total SD, REMSD or sleep fragmentation to understand the role of orexinergic system (Deadwyler et al 2007 ; Arthaud et al 2015 ; Matsuki et al 2015 ; Mehta et al 2015 ; Ran et al 2015 ; Toossi et al 2016 ; Briggs et al 2018 , 2019 ). Plasma OXA level was shown to decrease in rats following 24 h REMSD (Ran et al 2015 ) and to increase in insomnia patients (Tang et al 2017 ).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies suggest that the diverse findings from different sleep disturbance cases might be due to the modulation of orexinergic activity at the synapses, rather than the regulation on gene expression or other intracellular events. In the case of 6 h total SD, the activity of D-type orexin neurons and the presynaptic inhibition of sparse excitatory inputs in both D-type and H-type orexin neurons increased (Briggs et al 2019 ), while it also reduced the astrocytic modulation of glutamatergic synapses around orexinergic neurons via reduced glutamate uptake (Brigss et al 2018 ). SD and orexinergic system activity is closely related with the GABAergic activity on orexinergic neurons and also with the innervation of GABAergic neurons by orexinergic neurons.…”

Section: Discussionmentioning

confidence: 99%

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Baseline prepulse inhibition dependency of orexin A and REM sleep deprivation

Öz,

Kamalı,

Saka

et al. 2024

Psychopharmacology

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Rationale Prepulse inhibition (PPI) impairment reflects sensorimotor gating problems, i.e. in schizophrenia. This study aims to enlighten the role of orexinergic regulation on PPI in a psychosis-like model. Objectives In order to understand the impact of orexinergic innervation on PPI and how it is modulated by age and baseline PPI (bPPI), chronic orexin A (OXA) injections was carried on non-sleep-deprived and sleep-deprived rats that are grouped by their bPPI. Methods bPPI measurements were carried on male Wistar rats on P45 or P90 followed by grouping into low-PPI and high-PPI rats. The rats were injected with OXA twice per day for four consecutive days starting on P49 or P94, while the control groups received saline injections. 72 h REMSD was carried on via modified multiple platform technique on P94 and either OXA or saline was injected during REMSD. PPI tests were carried out 30 min. after the last injection. Results Our previous study with acute OXA injection after REMSD without bPPI grouping revealed that low OXA doses might improve REMSD-induced PPI impairment. Our current results present three important conclusions: (1) The effect of OXA on PPI is bPPI-dependent and age-dependent. (2) The effect of REMSD is bPPI-dependent. (3) The effect of OXA on PPI after REMSD also depends on bPPI. Conclusion Orexinergic regulation of PPI response with and without REMSD can be predicted by bPPI levels. Our findings provide potential insights into the regulation of sensorimotor gating by sleep/wakefulness systems and present potential therapeutic targets for the disorders, where PPI is disturbed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Baseline prepulse inhibition dependency of orexin A and REM sleep deprivation

Öz,

Kamalı,

Saka

et al. 2024

Psychopharmacology

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“…The treatment of rats with 1 and 10 nmol·L −1 orexin-A impaired spatial memory [ 174 ]. The expression of OX1R and OX2R in the brain tissue of SD rats exposed to SD for 9 days increased after 6 h of SD [ 175 ]. The expression significantly increased in the hypothalamus [ 54 , 165 ].…”

Section: Potentially Relevant Mechanismsmentioning

confidence: 99%

The Devastating Effects of Sleep Deprivation on Memory: Lessons from Rodent Models

et al. 2023

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In this narrative review article, we discuss the role of sleep deprivation (SD) in memory processing in rodent models. Numerous studies have examined the effects of SD on memory, with the majority showing that sleep disorders negatively affect memory. Currently, a consensus has not been established on which damage mechanism is the most appropriate. This critical issue in the neuroscience of sleep remains largely unknown. This review article aims to elucidate the mechanisms that underlie the damaging effects of SD on memory. It also proposes a scientific solution that might explain some findings. We have chosen to summarize literature that is both representative and comprehensive, as well as innovative in its approach. We examined the effects of SD on memory, including synaptic plasticity, neuritis, oxidative stress, and neurotransmitters. Results provide valuable insights into the mechanisms by which SD impairs memory function.

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“…Orexins suppress REM sleep and enhance wakefulness in periods of starvation . Sleep deprivation in rats showed an increased firing and a deceased adaptation of spike frequency in response to excitatory drive in the orexin neurons . Activation of OX 2 R will promote wakefulness and suppress NREM sleep …”

Section: Neurotransmitters and Receptors On Sleep–wake Cycle In Ad Pa...mentioning

confidence: 99%

“…144 Sleep deprivation in rats showed an increased firing and a deceased adaptation of spike frequency in response to excitatory drive in the orexin neurons. 145 Activation of OX 2 R will promote wakefulness and suppress NREM sleep. 146 A higher level of orexins usually contributes to deterioration in AD, and orexins can regulate the oscillation circadian of the oscillator in the hippocampus.…”

Section: Neurotransmitters and Receptors On Sleep−wake Cycle In Ad Pa...mentioning

confidence: 99%

Sleep–Wake Disorders in Alzheimer’s Disease: A Review

Sun

Wang

Zhou

et al. 2022

ACS Chem. Neurosci.

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Alzheimer’s disease (AD) is a multifactorial disease, and it has become a serious health problem in the world. Senile plaques (SPs) and neurofibrillary tangles (NFTs) are two main pathological characters of AD. SP mainly consists of aggregated β-amyloid (Aβ), and NFT is formed by hyperphosphorylated tau protein. Sleep–wake disorders are prevalent in AD patients; however, the links and mechanisms of sleep–wake disorders on the AD pathogenesis remain to be investigated. Here, we referred to the sleep–wake disorders and reviewed some evidence to demonstrate the relationship between sleep–wake disorders and the pathogenesis of AD. On one hand, the sleep–wake disorders may lead to the increase of Aβ production and the decrease of Aβ clearance, the spreading of tau pathology, as well as oxidative stress and inflammation. On the other hand, the ApoE4 allele, a risk gene for AD, was reported to participate in sleep–wake disorders. Furthermore, some neurotransmitters, such as acetylcholine, glutamate, serotonin, melatonin, and orexins, and their receptors were suggested to be involved in AD development and sleep–wake disorders. We discussed and suggested some possible therapeutic strategies for AD treatment based on the view of sleep regulation. In general, this review explored different views to find novel targets of diagnosis and therapy for AD.

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Sleep deprivation-induced pre- and postsynaptic modulation of orexin neurons

Cited by 16 publications

References 48 publications

Baseline prepulse inhibition dependency of orexin A and REM sleep deprivation

Baseline prepulse inhibition dependency of orexin A and REM sleep deprivation

The Devastating Effects of Sleep Deprivation on Memory: Lessons from Rodent Models

Sleep–Wake Disorders in Alzheimer’s Disease: A Review

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