Role Of Endocannabinoids In The Escalation Of Alcohol Use Following Traumatic Brain Injury

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Cellular, Molecular, Physiological, and Behavioral Aspects of Traumatic Brain Injury


Traumatic brain injury (TBI) is a silent epidemic affecting millions of people. TBI can be defined as a primary mechanical insult to the brain followed by a secondary cascade of events including neuroinflammation and neuronal hyperexcitability at the site of injury. Unfortunately, there are few effective therapeutic interventions for treating TBI or preventing the emergence of long-term TBI-associated neurological and psychiatric sequelae. TBI in humans and animal models can lead to cognitive dysfunction, anxiety-like behavior, and increases in alcohol drinking. These long-term functional changes may be related to TBI-induced alterations in neurotransmission and signaling in subcortical brain areas, such as the amygdala. Because the brain endocannabinoid system facilitates synaptic homeostasis and buffers the organism against the effects of trauma, studies have investigated the role of brain endocannabinoids in mediating long-term TBI effects, and those studies have shown that boosting brain endocannabinoid signaling attenuates TBI-induced increases in negative affective behaviors and neuroadaptations in preclinical animal models. Therefore, interventions that increase brain endocannabinoid signaling after TBI may reduce the effects or prevent the emergence of TBI-associated comorbidities, including increases in alcohol drinking that may eventually lead to alcohol use disorder.

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