Stielper ZF(1)(2), Fucich EA(1)(2)(3), Middleton JW(2)(4), Hillard CJ(5), Edwards S(1)(2), Molina PE(1)(2), Gilpin NW(1)(2)(6). Author information:
(1)Department of Physiology, Louisiana State University Health Sciences Center,
New Orleans, Louisiana, USA.
(2)Alcohol and Drug Abuse Center of Excellence, Louisiana State University
Health Sciences Center, New Orleans, Louisiana, USA.
(3)Neuroscience Program, Tulane University, New Orleans, Louisiana, USA.
(4)Department of Cell Biology and Anatomy, Louisiana State University Health
Sciences Center, New Orleans, Louisiana, USA.
(5)Department of Pharmacology and Toxicology, Medical College of Wisconsin,
Milwaukee, Wisconsin, USA.
(6)Southeast Louisiana VA Healthcare System, New Orleans, Louisiana, USA.
Traumatic brain injury (TBI) affects approximately 3 million Americans yearly and increases vulnerability to developing psychiatric comorbidities. Alcohol use disorder (AUD) is the most prevalent psychiatric diagnosis preceding injury and TBI may increase subsequent alcohol use. The basolateral amygdala (BLA) is a limbic structure commonly affected by TBI that is implicated in anxiety and AUD. Endocannabinoids (eCBs) regulate synaptic activity in the BLA, and BLA eCB modulation alters anxiety-like behavior and stress reactivity. Previous work from our laboratories showed that systemic eCB degradation inhibition ameliorates TBI-induced increases in anxiety-like behavior and motivation to respond for alcohol in male rats. Here, we used a lateral fluid percussion model to test moderate TBI effects on anxiety-like behavior, alcohol drinking, and eCB levels and cell signaling in BLA, as well as the effect of alcohol drinking on anxiety-like behavior and the BLA eCB system, in female rats. Our results show that TBI does not promote escalation of operant alcohol self-administration or increase anxiety-like behavior in female rats. In the BLA, TBI and alcohol drinking alter tissue amounts of 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine (anandamide; AEA) 1 h post-injury, and 2-AG levels remain low 11 days post-injury. Eleven days after injury, BLA pyramidal neurons were hyperexcitable, but measures of synaptic transmission and eCB signaling were unchanged. These data show that TBI impacts BLA 2-AG tissue levels, that this effect is modified by alcohol drinking, and also that TBI increases BLA cell excitability.
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