Roles of the BNST in Response to Acute Drug Withdrawal
2011-08-11
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Roles of the BNST in Response to Acute Drug Withdrawal
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2011-08-11
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•Those experiencing withdrawal from drugs of abuse display symptoms of dysphoria such as anxiety. Anxiety during withdrawal from an acute opiate exposure also causes potentiation of the acoustic startle reflex (“withdrawal-potentiated startle”).1,3,4
•The Gewirtz lab’s research has suggested that anxiety during acute withdrawal from opoids is mediated by levels of dopamine in the brain due to experiments with a general dopamine receptor agonist, apomorphine. Opiates disinhibit dopamenergic neurons in the VTA which project to the BNST and CeA. 2
•Withdrawal is hypothesized to be caused by the drop in dopamine levels in the brain. Apomorphine replaces dopamine at dopamine receptors and prevents withdrawal symptoms as measured by acoustic startle.
•While we know dopamine is important in this phenomena we do not know which brain structures play a role in producing anxiety symptoms during withdrawal.
•Our goal is to discover which brain structures play a role in producing withdrawal-potentiated startle. We will test this by administering apomorphine directly to the BNST, Bed Nucleus of the Stria Terminalis, after subcutaneous injection of morphine with the expectation that, if the BNST is critical for producing withdrawal potentiated startle, then withdrawal potentiated startle will be blocked .
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Additional contributors: Anna Radke; Jonathan Gewirtz (faculty mentor)
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This research was funded by the NIH grants T32-HD007151 and DA018784, the University of Minnesota, and the Undergraduate Research Opportunities Program (UROP).
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Leslie, Jacob. (2011). Roles of the BNST in Response to Acute Drug Withdrawal. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/117658.
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