# Accumbal integration of brain wide glutamatergic inputs and their dysregulation by cocaine self-administration

> **NIH NIH F30** · VANDERBILT UNIVERSITY · 2022 · $32,007

## Abstract

Project Summary/Abstract
 Cocaine use disorder (CUD) has no FDA approved therapies putting stimulant use disorders at a unique
treatment disadvantage, necessitating further research on stimulant use neural dysregulation for novel
interventions. The nucleus accumbens (NAc) is at the core of valence-based stimulus processing and associative
learning, and its dysregulation by cocaine is a primary component underlying the development of CUD in human
and animal models. The NAc is not only an incredibly plastic area but receives numerous glutamatergic inputs
from across the brain that integrate complex information in order to drive the activity of the NAc. Long-term
cocaine exposure leads to plasticity in synaptic strength of glutamatergic inputs into the NAc and this plasticity
has been directly linked to maladaptive behaviors associated with cocaine exposure. While a large body of work
has highlighted the synapse-specific mechanisms that occur following cocaine exposure, this has been largely
done in ex-vivo preparations and on individual inputs into the NAc; however, information encoding within these
projection populations is a dynamic process that occurs on a fast timescale and understanding how their
relationship encodes complex information requires their simultaneous recording in awake and behaving animals.
I will be using a range of calcium imaging and viral-mediated expression approaches to 1. identify the
glutamatergic inputs that modulate and drive neural activity within the NAc and 2. understand how these signals
facilitate the encoding of stimuli to drive behavior at baseline and following cocaine use. First, using multisite
fiber photometry in glutamatergic projections from the basolateral amygdala (BLA-NAc), Hippocampus (vHPC-
NAc) and medial prefrontal cortex (mPFC-NAc) into the NAc, I will define how these circuits are simultaneously
activated by unconditioned and conditioned stimuli to drive behavior (Aim 1). Next, using cocaine self-
administration, I will define how these circuits are altered by repeated drug exposure, leading to neural and
behavioral impairments in learning for non-drug stimuli (Aim 2). As a future physician-scientist, understanding
the complex factors that contribute to addiction, especially as they relate to learning from drug and non-drug
stimuli, are a critical component of effective CUD treatment and intervention. This proposal with provide the
technical training needed to answer such questions in the laboratory, while also providing the theoretical training
to provide optimal care for patients in my clinical practice.

## Key facts

- **NIH application ID:** 10464292
- **Project number:** 1F30DA054764-01A1
- **Recipient organization:** VANDERBILT UNIVERSITY
- **Principal Investigator:** Stephanie Ann Cajigas Gabriel
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $32,007
- **Award type:** 1
- **Project period:** 2022-06-01 → 2026-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10464292

## Citation

> US National Institutes of Health, RePORTER application 10464292, Accumbal integration of brain wide glutamatergic inputs and their dysregulation by cocaine self-administration (1F30DA054764-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10464292. Licensed CC0.

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