Sedatives and hypnotics

Sobolewski, Kristine

doi:10.1016/bs.seda.2021.09.013

Cited by 3 publications

(1 citation statement)

References 23 publications

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“…While NSAIDs directly inhibit inflammatory mediators, cannabinoids exert broader immunomodulatory effects. ECS modulation may offer a more nuanced and targeted approach to inflammation, potentially mitigating side effects associated with non-specific inhibition of inflammatory pathways [ 171 , 172 , 173 , 174 ].…”

Section: Therapeutic Implications and Future Directionsmentioning

confidence: 99%

Sleep, Glial Function, and the Endocannabinoid System: Implications for Neuroinflammation and Sleep Disorders

Camberos-Barraza,

Camacho-Zamora,

Bátiz-Beltrán

et al. 2024

IJMS

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The relationship between sleep, glial cells, and the endocannabinoid system represents a multifaceted regulatory network with profound implications for neuroinflammation and cognitive function. The molecular underpinnings of sleep modulation by the endocannabinoid system and its influence on glial cell activity are discussed, shedding light on the reciprocal relationships that govern these processes. Emphasis is placed on understanding the role of glial cells in mediating neuroinflammatory responses and their modulation by sleep patterns. Additionally, this review examines how the endocannabinoid system interfaces with glia-immune signaling to regulate inflammatory cascades within the central nervous system. Notably, the cognitive consequences of disrupted sleep, neuroinflammation, and glial dysfunction are addressed, encompassing implications for neurodegenerative disorders, mood disturbances, and cognitive decline. Insights into the bidirectional modulation of cognitive function by the endocannabinoid system in the context of sleep and glial activity are explored, providing a comprehensive perspective on the potential mechanisms underlying cognitive impairments associated with sleep disturbances. Furthermore, this review examines potential therapeutic avenues targeting the endocannabinoid system to mitigate neuroinflammation, restore glial homeostasis, and normalize sleep patterns. The identification of novel therapeutic targets within this intricate regulatory network holds promise for addressing conditions characterized by disrupted sleep, neuroinflammation, and cognitive dysfunction. This work aims to examine the complexities of neural regulation and identify potential avenues for therapeutic intervention.

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