Item Details

abstract

The development of alcohol use disorder is heavily influenced by the age at which an individual begins drinking. Specifically, the younger a person starts drinking alcohol, the more likely they are to develop an alcohol use disorder. Individuals with alcohol use disorder report severe withdrawal-induced anxiety that drives relapse and perpetuates the cycle of a substance use disorder. At the hub of the underlying neural circuitry driving withdrawal-induced anxiety is the basolateral amygdala (BLA). The BLA is susceptible to neural plasticity following chronic ethanol exposure that drives the output of glutamatergic principal cells, which promotes fear and anxiety-related behaviors. The output from principal cells is tightly regulated by a group of inhibitory interneurons, the lateral paracapsular cells (LPCs), that uniquely develop diminished GABA release probability following bouts of chronic ethanol exposure. The purpose of these experiments was to determine (1) if adults were vulnerable to the effects of chronic ethanol exposure on LPCs, (2) if females were susceptible to this development, & (3) to examine the underlying mechanism driving decreases in LPC GABA release. These experiments find that male adolescent rats are uniquely vulnerable to developing decreases in presynaptic GABA release that may be dependent on dopamine D1 receptor signaling.

subject

adolescence

alcohol

development

dopamine

paracapsular

withdrawal

contributor

Koucheki, Ashkon (author)

McCool, Brian (committee chair)

Martin, Thomas J. (committee member)

Chen, Rong (committee member)

date

2022-01-15T09:35:30Z (accessioned)

2022-07-14T08:30:12Z (available)

2022 (issued)

degree

Neuroscience (discipline)

embargo

2022-07-14 (terms)

identifier

http://hdl.handle.net/10339/99387 (uri)

language

en (iso)

publisher

Wake Forest University

title

ISLANDS OF DEVELOPMENTAL VULNERABILITY: EXAMINING THE EFFECT OF CHRONIC ETHANOL EXPOSURE ON LATERAL PARACAPSULAR CELLS

type

Thesis