Publications by authors named "Sarah E Ewin"

Alcohol use disorder (AUD) and anxiety/stressor disorders frequently co-occur and this dual diagnosis represents a major health and economic problem worldwide. The basolateral amygdala (BLA) is a key brain region that is known to contribute to the aetiology of both disorders. Although many studies have implicated BLA hyperexcitability in the pathogenesis of AUD and comorbid conditions, relatively little is known about the specific efferent projections from this brain region that contribute to these disorders.

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Alcohol use disorder (AUD) differentially impacts men and women and a growing body of evidence points to sex-dependent adaptations in a number of brain regions. In a prior study, we explored the effect of a chronic intermittent ethanol exposure (CIE) model of AUD on neuronal and molecular adaptations in the dorsal and ventral domains of the hippocampus (dHC and vHC, respectively) in male rats. We found the vHC to be particularly sensitive to CIE, showing an increase in neuronal excitability and synaptic proteins associated with augmented excitation.

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The hippocampus, particularly its ventral domain, can promote negative affective states (i.e. stress and anxiety) that play an integral role in the development and persistence of alcohol use disorder (AUD).

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Many studies have implicated hippocampal dysregulation in the pathophysiology of alcohol use disorder (AUD). However, over the past twenty years, a growing body of evidence has revealed distinct functional roles of the dorsal (dHC) and ventral (vHC) hippocampal subregions, with the dHC being primarily involved in spatial learning and memory and the vHC regulating anxiety- and depressive-like behaviors. Notably, to our knowledge, no rodent studies have examined the effects of chronic ethanol exposure on synaptic transmission along the dorsal/ventral axis.

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Adolescent nicotine exposure has been shown to lead to further psychostimulant use in adulthood. Previous preclinical research in rats has shown that environmental enrichment may protect against drug abuse vulnerability. The current study was designed to examine whether environmental enrichment can block the ability of adolescent nicotine exposure to increase d-amphetamine self-administration in adulthood.

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It has long been appreciated that adolescence represents a uniquely vulnerable period when chronic exposure to stressors can precipitate the onset of a broad spectrum of psychiatric disorders and addiction in adulthood. However, the neurobiological substrates and the full repertoire of adaptations within these substrates making adolescence a particularly susceptible developmental stage are not well understood. Prior work has demonstrated that a rodent model of adolescent social isolation (aSI) produces robust and persistent increases in phenotypes relevant to anxiety/stressor disorders and alcohol addiction, including anxiogenesis, deficits in fear extinction, and increased ethanol consumption.

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Environmental enrichment has previously been shown to alter sensitivity to psychostimulants and opiates in various preclinical models. However, little research has been conducted studying the effects of environmental enrichment on the more commonly abused drug, nicotine. The current study raised male rats in either enriched conditions (EC) or isolated conditions (IC) and tested the animals' sensitivity to acquisition, extinction and reinstatement of nicotine conditioned place preference (CPP).

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