Heavy ethanol consumption during adolescence has been linked to neuroimmune response dysregulation and cognitive deficits in the developing adolescent brain. During adolescence, the brain is particularly susceptible to the pharmacological effects of ethanol that are induced by acute and chronic bouts of exposure. Numerous preclinical rodent model studies have used different ethanol administration techniques, such as intragastric gavage, self-administration, vapor, intraperitoneal, and free access, and while most models indicated proinflammatory neuroimmune responses in the adolescent brain, there are various factors that appear to influence this observation.
View Article and Find Full Text PDFEthanol acts directly on the α7 Nicotinic acetylcholine receptor (α7). Adolescent-binge alcohol exposure (ABAE) produces deleterious consequences during adulthood, and data indicate that the α7 receptor regulates these damaging events. Administration of an α7 Negative Allosteric Modulator (NAM) or the cholinesterase inhibitor galantamine can prophylactically prevent adult consequences of ABAE.
View Article and Find Full Text PDFAlcohol consumption in adolescence causes multiple acute negative changes in neural and behavioral function that persist well into adulthood and possibly throughout life. The medial prefrontal cortex (mPFC) and dorsal hippocampus are critical for executive function and memory and are especially vulnerable to adolescent ethanol exposure. We have reported that astrocytes, particularly in the mPFC, change both in morphology and synaptic proximity during adolescence.
View Article and Find Full Text PDFPharmacol Biochem Behav
February 2023
Binge patterns of alcohol use, prevalent among adolescents, are associated with a higher probability of developing alcohol use disorders (AUD) and other psychiatric disorders, like anxiety and depression. Additionally, adverse life events strongly predict AUD and other psychiatric disorders. As such, the combined fields of stress and AUD have been well established, and animal models indicate that both binge-like alcohol exposure and stress exposure elevate anxiety-like behaviors.
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