Adolescent alcohol drinking and GABA signaling

NIH RePORTER · NIH · R01 · $399,791 · view on reporter.nih.gov ↗

Abstract

PROJECT SUMMARY Adolescence marks a period of increased risk taking and exploration. As part of this exploratory behavior, many individuals initiate alcohol use during adolescence, which can lead to increased risk for alcohol use disorders later in life. One major site of adolescent maturation in prefrontal cortex are GABAergic inhibitory neurons, including parvalbumin positive chandelier cells. Chandelier cells synapse directly onto the axon potential initiating sites of neighboring glutamatergic pyramidal cells. They are therefore uniquely poised to regulate pyramidal cell spiking. Here, our goal is to understand how the function of these two inhibitory cell classes are affected by adolescent alcohol consumption, and to determine if manipulations to chloride transporter function alters drinking behavior. We will use a combination of electrophysiology and 2-photon imaging to understand how interneuron function is regulated at the cellular level, and viral manipulation of chloride transporter function paired with behavior to understand how prefrontal inhibitory function regulates drinking. Results of this study will provide insight into how inhibitory circuits contribute to drinking behavior and may elucidate potential therapeutic targets to treat alcohol abuse disorders.

Key facts

NIH application ID
9913434
Project number
5R01AA027023-02
Recipient
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Principal Investigator
Kevin J Bender
Activity code
R01
Funding institute
NIH
Fiscal year
2020
Award amount
$399,791
Award type
5
Project period
2019-04-12 → 2024-03-31