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Elucidating the Role of Cortical Astrocytes in Heroin Seeking

Award Number: F31DA064399
ORGANIZATION: NATIONAL INSTITUTE ON DRUG ABUSE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/01/2026
PERIOD OF PERFORMANCE END DATE: 07/31/2028

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Elucidating the Role of Cortical Astrocytes in Heroin Seeking - PROJECT SUMMARY / ABSTRACT Opioid use disorder (OUD) is devastating public health crisis characterized by vulnerability to drug seeking and relapse when exposed to drug-related cues. Chronic opioid use causes maladaptive excitatory neuronal activity in the prelimbic cortex (PrL), enabling drug-paired cues to trigger drug seeking despite negative consequences. Emerging data from our own labs demonstrate that key subsets of neurons (ensembles) in the PrL form during heroin self-administration (SA), encode drug seeking behavior, and that driving activity in these ensembles promotes reward-motivated behavior. We hypothesize that astroglia, critical mediators of heroin- linked synaptic plasticity, are required to shape excitatory neuronal activity dynamics during seeking. Therefore, investigating how these neuronal ensembles are formed and maintained would provide insight into adaptations caused by heroin use and identify therapeutic targets to prevent relapse. Throughout this F31, I will broaden my technical training to identify how astrocytic activity influences and regulates the ensembles that direct heroin seeking. Very little is known about how astrocytic activity patterns adapt across drug-reward learning or how the formation of astrocytic ensembles coincides with and directs neuronal ensemble formation. Astrocytes respond to altered patterns of synaptic activity by engaging mobilization of internal calcium (Ca2+) stores to drive Ca2+- mediated astrocytic cellular processes that coordinate and integrate action potential firing within neuronal networks. Accordingly, astrocytes serve as an excellent candidate for a regulatory force required to shape drug reward-learning neuronal ensemble formation. Our overarching hypothesis is that dmPFC astrocyte activity is required to shape the neuronal ensemble dynamics that direct heroin-seeking behavior. Throughout the proposal, I will hone my skills in intersectional viral vector strategies and novel head-fixed reward self-administration. In Aim 1 we will utilize viral astrocyte specific Ca2+ pump (CalEx) to analyze the effect of astrocytic inhibition on heroin- and sucrose-seeking behavior. In Aim 2, I will be trained in two-photon microscopy and will employ the astrocyte-specific inhibition virus with a neuron-specific genetically encoded Ca2+ indicator (GECI) to measure PrL neuronal activity in animals engaged in heroin or sucrose SA, extinction, and seeking in the presence or absence of astroglial activity. Collectively, I will gain unparalleled training in advanced neuroscience approaches to establish how astroglial inhibition, via depletion of internal Ca2+, impacts neuronal ensemble encoding and coordination of naturalistic- and drug-motivated behaviors.


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: 2026 ( Subtotal = $50,114 )
2026	2026	THE MEDICAL UNIVERSITY OF SOUTH CAROLINA	179 ASHLEY AVE	CHARLESTON	SC	29425	CHARLESTON	USA	Drug Use and Addiction Research Programs	001	1	7/17/2026	NEW	$0
2026	2026	THE MEDICAL UNIVERSITY OF SOUTH CAROLINA	179 ASHLEY AVE	CHARLESTON	SC	29425	CHARLESTON	USA	Drug Use and Addiction Research Programs	000	1	7/17/2026	NEW	$50,114
														Subtotal = $50,114

Grand Total All Awards = $50,114

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Elucidating the Role of Cortical Astrocytes in Heroin Seeking

Award Number: F31DA064399

ORGANIZATION: NATIONAL INSTITUTE ON DRUG ABUSE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/01/2026

PERIOD OF PERFORMANCE END DATE: 07/31/2028

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