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Adolescent opioid exposure effects on alcohol-induced hyperalgesia in adult mice

Award Number: F32AA031198
ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 07/30/2024

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Adolescent opioid exposure effects on alcohol-induced hyperalgesia in adult mice - Project Summary Adolescence is a crucial period of brain development with robust hormonal, physiological, behavioral, and neurochemical changes. Long-term use of both alcohol and opioids results in increased pain sensitivity or hyperalgesia. Adolescent opioid use, through prescription and recreational use, is a growing problem in the United States and is known to increase the likelihood of future misuse of substances that include but are not limited to alcohol. That said, very little is known about the neuroplasticity that occurs during adolescent opioid exposure (AOE) and how it may affect alcohol use and alcohol-related outcomes during adulthood – here, we propose a set of experiments that focus on the latter of these two topics by testing AOE effects on alcohol- induced allodynia in adult mice. We will test the prediction that the central nucleus of the amygdala (CeA), a brain region modulated by opioid and alcohol use and important for pain modulation, and more specifically that protein kinase C-δ+ (PKCδ) cells in this brain region, are important in mediating AOE effects on alcohol-induced allodynia later in life. CeA PKCδ cells are hyperexcitable in animals with chronic neuropathic pain, and CeA PKCδ cell function is altered by alcohol and opioids. It is not known how CeA PKCδ cell+ neurons are affected by AOE, what their role is in alcohol-induced allodynia in adults, and what role it might play AOE enhancement of alcohol effects on pain-related outcomes. Our global hypothesis is that early-life exposure to opioids will increase the magnitude of alcohol-induced allodynia in adulthood, and this enhancement will be mediated by CeA PKCδ neurons. To test this, we will expose adolescent male and female wild type and PKCδ:cre mice to chronic oxycodone, then expose them to chronic alcohol during adulthood, with appropriate controls for each condition. We will use circuit-based approaches to inhibit the activity of CeA PKCδ+ cells to investigate the role of these cells in AOE enhancement of alcohol-induced allodynia in adult mice.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = $0 )
2024	2024	LOUISIANA STATE UNIVERSITY HEALTH SCIENCES CENTER NEW ORLEANS	433 BOLIVAR ST RM 619	NEW ORLEANS	LA	70112	ORLEANS	USA	Alcohol Research Programs	000	1	1/30/2024	NEW	$69,500
2024	2024	LOUISIANA STATE UNIVERSITY HEALTH SCIENCES CENTER NEW ORLEANS	433 BOLIVAR ST RM 619	NEW ORLEANS	LA	70112	ORLEANS	USA	Alcohol Research Programs	001	1	5/1/2024	NEW	$4,784
2024	2024	LOUISIANA STATE UNIVERSITY HEALTH SCIENCES CENTER NEW ORLEANS	433 BOLIVAR ST RM 619	NEW ORLEANS	LA	70112	ORLEANS	USA	Alcohol Research Programs	002	1	7/19/2024	NEW	-$74,284
														Subtotal = $0

Grand Total All Awards = $0

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Adolescent opioid exposure effects on alcohol-induced hyperalgesia in adult mice

Award Number: F32AA031198

ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 07/30/2024

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