Modulating role of serotonergic signaling in sleep and memory

Vaseghi, Salar; Arjmandi-Rad, Shirin; Eskandari, Maliheh; Ebrahimnejad, Mahshid; Kholghi, Gita; Zarrindast, Mohammad‐Reza

doi:10.1007/s43440-021-00339-8

Cited by 19 publications

(10 citation statements)

References 300 publications

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“…The sleep duration and sleep quality were significantly reduced in flies with the knocked-out gene of 5-HT 1A receptor . It has been reported that serotonin, as a strong inhibitory neurotransmitter in the body, could also improve sleep and anxiety, which may play a role in the coupling of downstream GABAergic pathways . 5-HT 1A R was significantly upregulated at the protein level after YPVEPF treatment (Figure F), which was in accordance with the variation tendency in 5-HT levels.…”

Section: Resultssupporting

confidence: 79%

“…45 It has been reported that serotonin, as a strong inhibitory neurotransmitter in the body, could also improve sleep and anxiety, which may play a role in the coupling of downstream GABAergic pathways. 39 5-HT 1A R was significantly upregulated at the protein level after YPVEPF treatment (Figure 4F), which was in accordance with the variation tendency in 5-HT levels. A preliminary deduction was presented that the strong sleepenhancing and anxiolytic effects of YPVEPF were the result of multitarget coupling by acting on the GABA/Glu-5-HT systems.…”

Section: Effects Of Ypvepf On Related Neurotransmitter Receptors In S...supporting

confidence: 80%

“…To summarize, it revealed that the GABA/Glu ratio might be one powerful indicator for reflecting the hexapeptide YPVEPF to play roles. A series of investigations have revealed the bidirectional communication between anxiety and sleep regulation via the GABAergic or serotoninergic system, and the presynaptic GABA uptake has a great influence on the inhibitory cotransmission from midbrain DA neurons. , Recently, limited studies about the mechanisms of sleep-enhancing peptides have been done, which were focused on simple GABA or 5-HT receptor actions or regulating circadian rhythms. , Hence, we presumed that YPVEPF could have an influence on the GABA-Glu metabolic pathway and serotoninergic system to cause sleep-enhancing and anxiolytic effects.…”

Section: Resultsmentioning

confidence: 99%

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Potential Mechanisms of Casein Hexapeptide YPVEPF on Stress-Induced Anxiety and Insomnia Mice and Its Molecular Effects and Key Active Structure

Qian,

Zheng,

Huang

et al. 2024

J. Agric. Food Chem.

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The hexapeptide YPVEPF with strong sleep-enhancing effects could be detected in rat brain after a single oral administration as we previously proved. In this study, the mechanism and molecular effects of YPVEPF in the targeted stress-induced anxiety mice were first investigated, and its key active structure was further explored. The results showed that YPVEPF could significantly prolong sleep duration and improve the anxiety indexes, including prolonging the time spent in the open arms and in the center. Meanwhile, YPVEPF showed strong sleep-enhancing effects by significantly increasing the level of the GABA/Glu ratio, 5-HT, and dopamine in brain and serum and regulating the anabolism of multiple targets, but the effects could be blocked by bicuculline and WAY100135. Moreover, the molecular simulation results showed that YPVEPF could stably bind to the vital GABAA and 5-HT1A receptors due to the vital structure of Tyr-Pro-Xaa-Xaa-Pro-, and the electrostatic and van der Waals energy played dominant roles in stabilizing the conformation. Therefore, YPVEPF displayed sleep-enhancing and anxiolytic effects by regulating the GABA-Glu metabolic pathway and serotoninergic system depending on distinctive self-folding structures with Tyr and two Pro repeats.

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Section: Resultssupporting

confidence: 79%

Section: Effects Of Ypvepf On Related Neurotransmitter Receptors In S...supporting

confidence: 80%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Potential Mechanisms of Casein Hexapeptide YPVEPF on Stress-Induced Anxiety and Insomnia Mice and Its Molecular Effects and Key Active Structure

Qian,

Zheng,

Huang

et al. 2024

J. Agric. Food Chem.

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“…5-hydroxytryptamine (5-HT) is currently acknowledged to act primarily to promote wakefulness and inhibit REM sleep (REMS). 69,70 The relationship between sleep and 5-HT has been verified in both animal and human experiments. During sleep deprivation, the release of 5-HT is even higher than during the preceding waking period, as indicated by the findings in animals.…”

Section: -Hydroxytryp-taminementioning

confidence: 83%

The Underlying Mechanisms of Sleep Deprivation Exacerbating Neuropathic Pain

Zhu¹,

Huang²

2023

NSS

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Pain disrupts sleep, and sleep deprivation or interference can alter pain perception in animals and humans, for example by increasing sensitivity to pain. However, the mechanism by which sleep affects neuropathic pain remains unclear. In this review, we discuss the available evidence from the epidemiologic, clinical, and human, as well as laboratory studies. In previous studies, we have found that sleep deprivation affects various injurious systems, including opioids, dopaminergic, immune, orexins, hypothalamicpituitary-adrenal axis, and adenosine. At the same time, these systems play a crucial role in neuropathic pain regulation. In the complex interactions between these neurobiological systems, there may be potential regulatory pathways through which sleep deprivation amplifies neuropathic pain. Because of the impact sleep problems and neuropathic pain can have on the patients' quality of life, studying the link between sleep and neuropathic pain is important for neuropathic pain prevention and public health.

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“…In addition, unique roles of DR in PD are as follows (Table 2 ): (1) hypo‐connectivity with the left postcentral gyrus is negatively correlated with daytime sleepiness. Modulating role of serotonin in sleep–wake behavior has been widely reported (Monti, 2011 ; Vaseghi et al, 2022 ), thus, impaired connectivity between DR and sensory cortex may be a reason for daytime sleepiness. (2) Hypo‐connectivity with the bilateral ACC/MCC is associated with anxiety.…”

Section: Discussionmentioning

confidence: 99%

Common and unique dysconnectivity profiles of dorsal and median raphe in Parkinson's disease

Wang

Sun

Gao

et al. 2022

Human Brain Mapping

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The serotonergic (5‐HT) system, which undergoes degeneration in Parkinson's disease (PD), is involved in the pathogenesis of motor and nonmotor symptoms. The dorsal raphe (DR) and median raphe (MR) nuclei are the main source of 5‐HT neurons, however, brain connectivity changes in these two nuclei have not been delineated in PD. Here we used resting‐state fMRI (rs‐fMRI) to characterize functional connectivity profiles of DR and MR and further examine the associations between dysconnectivity of raphe nuclei and clinical phenotypes of PD. We found that DR and MR commonly hypo‐connected with the sensorimotor, temporal, and occipital cortex, limbic system, left thalamus, putamen, and cerebellum in PD. DR had unique decreased connectivity with the bilateral prefrontal and cingulate cortices, while MR had lower connectivity with the pons. Moreover, reduced connectivity of DR correlated with depression, drowsiness, and anxiety, whereas dysconnectivity of MR correlated with depression, cognitive deficits, sleep disturbances, and pain. Our findings highlight the complex roles of raphe nuclei in motor and nonmotor symptoms, providing novel insights into the neurophysiological mechanisms underlying pathogenesis of PD.

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Modulating role of serotonergic signaling in sleep and memory

Cited by 19 publications

References 300 publications

Potential Mechanisms of Casein Hexapeptide YPVEPF on Stress-Induced Anxiety and Insomnia Mice and Its Molecular Effects and Key Active Structure

Potential Mechanisms of Casein Hexapeptide YPVEPF on Stress-Induced Anxiety and Insomnia Mice and Its Molecular Effects and Key Active Structure

The Underlying Mechanisms of Sleep Deprivation Exacerbating Neuropathic Pain

Common and unique dysconnectivity profiles of dorsal and median raphe in Parkinson's disease

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