TY - JOUR
T1 - Endocannabinoids at the synapse and beyond
T2 - implications for neuropsychiatric disease pathophysiology and treatment
AU - Scheyer, Andrew
AU - Yasmin, Farhana
AU - Naskar, Saptarnab
AU - Patel, Sachin
N1 - Publisher Copyright:
© 2022, The Author(s), under exclusive licence to American College of Neuropsychopharmacology.
PY - 2023/1
Y1 - 2023/1
N2 - Endocannabinoids (eCBs) are lipid neuromodulators that suppress neurotransmitter release, reduce postsynaptic excitability, activate astrocyte signaling, and control cellular respiration. Here, we describe canonical and emerging eCB signaling modes and aim to link adaptations in these signaling systems to pathological states. Adaptations in eCB signaling systems have been identified in a variety of biobehavioral and physiological process relevant to neuropsychiatric disease states including stress-related disorders, epilepsy, developmental disorders, obesity, and substance use disorders. These insights have enhanced our understanding of the pathophysiology of neurological and psychiatric disorders and are contributing to the ongoing development of eCB-targeting therapeutics. We suggest future studies aimed at illuminating how adaptations in canonical as well as emerging cellular and synaptic modes of eCB signaling contribute to disease pathophysiology or resilience could further advance these novel treatment approaches.
AB - Endocannabinoids (eCBs) are lipid neuromodulators that suppress neurotransmitter release, reduce postsynaptic excitability, activate astrocyte signaling, and control cellular respiration. Here, we describe canonical and emerging eCB signaling modes and aim to link adaptations in these signaling systems to pathological states. Adaptations in eCB signaling systems have been identified in a variety of biobehavioral and physiological process relevant to neuropsychiatric disease states including stress-related disorders, epilepsy, developmental disorders, obesity, and substance use disorders. These insights have enhanced our understanding of the pathophysiology of neurological and psychiatric disorders and are contributing to the ongoing development of eCB-targeting therapeutics. We suggest future studies aimed at illuminating how adaptations in canonical as well as emerging cellular and synaptic modes of eCB signaling contribute to disease pathophysiology or resilience could further advance these novel treatment approaches.
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U2 - 10.1038/s41386-022-01438-7
DO - 10.1038/s41386-022-01438-7
M3 - Review article
C2 - 36100658
AN - SCOPUS:85138184906
SN - 0893-133X
VL - 48
SP - 37
EP - 53
JO - Neuropsychopharmacology
JF - Neuropsychopharmacology
IS - 1
ER -