# The Role of GABA Co-release from Dopamine Neurons in Ethanol Consumption

> **NIH NIH F31** · STANFORD UNIVERSITY · 2021 · $38,431

## Abstract

PROJECT SUMMARY
Alcohol use disorder is a serious public health concern, yet its cause remains elusive; we still do not fully
understand the neurophysiological mechanisms that drive EtOH consumption. All addictive drugs activate
dopamine (DA) neurons, and this was assumed to only cause a synaptic increase of the neurotransmitter
DA. However, recent evidence suggests that DA neurons also release the inhibitory neurotransmitter
GABA, which equips DA neurons with another level of control over the striatum. Using transgenic mice,
viral manipulations, and EtOH drinking behavior, the experiments proposed here will provide a
mechanistic account of the role of GABA co-release from DA neurons in EtOH consumption. The results
will also provide another level of mechanism – using two-photon imaging, optogenetics, and
electrophysiology, the post-synaptic consequences of DA and GABA co-release on dendritic excitability
will be defined. The mechanistic insight gained from these studies could inform novel treatment strategies
for alcohol use disorder.

## Key facts

- **NIH application ID:** 10116964
- **Project number:** 5F31AA027432-03
- **Recipient organization:** STANFORD UNIVERSITY
- **Principal Investigator:** Konstantin Kaganovsky
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $38,431
- **Award type:** 5
- **Project period:** 2019-03-01 → 2022-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10116964

## Citation

> US National Institutes of Health, RePORTER application 10116964, The Role of GABA Co-release from Dopamine Neurons in Ethanol Consumption (5F31AA027432-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10116964. Licensed CC0.

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