Traumatic Brain Injury and Alcohol Drinking Alter Basolateral Amygdala Endocannabinoids in Female Rats
Autor: | Elizabeth A Fucich, Scott Edwards, Nicholas W. Gilpin, Patricia E. Molina, Jason W. Middleton, Zachary F. Stielper, Cecilia J. Hillard |
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Rok vydání: | 2021 |
Předmět: |
030506 rehabilitation
medicine.medical_specialty Alcohol Drinking Polyunsaturated Alkamides Traumatic brain injury 2-Arachidonoylglycerol Alcohol Arachidonic Acids Alcohol use disorder Anxiety 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine Brain Injuries Traumatic mental disorders medicine Animals Rats Wistar Basolateral Nuclear Complex business.industry Original Articles Anandamide medicine.disease Endocannabinoid system Rats medicine.anatomical_structure Endocrinology nervous system chemistry Female Neurology (clinical) medicine.symptom 0305 other medical science business 030217 neurology & neurosurgery Endocannabinoids Basolateral amygdala |
Zdroj: | J Neurotrauma |
ISSN: | 1557-9042 0897-7151 |
Popis: | 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. |
Databáze: | OpenAIRE |
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