Logo image
Back
Neurotensin in the posterior thalamic paraventricular nucleus: inhibitor of pharmacologically relevant ethanol drinking
Journal article   Open access   Peer reviewed

Neurotensin in the posterior thalamic paraventricular nucleus: inhibitor of pharmacologically relevant ethanol drinking

Surya Pandey, Preeti S Badve, Genevieve R Curtis, Sarah F Leibowitz and Jessica R Barson
Addiction biology, v 24(1), pp 3-16
Jan 2019
DOI: https://doi.org/10.1111/adb.12546
PMID: 28877396
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1111/adb.12546View
Accepted (AM)Open Access (License Unspecified),  Open

Abstract

Alcohol Drinking - genetics Alcohol Drinking - metabolism Animals Behavior, Animal - drug effects Behavior, Animal - physiology Central Nervous System Depressants - administration & dosage Ethanol - administration & dosage Midline Thalamic Nuclei - metabolism Neurotensin - antagonists & inhibitors Neurotensin - genetics Neurotensin - metabolism Neurotensin - pharmacology Rats Rats, Long-Evans RNA, Messenger - metabolism Self Administration
Individuals prone to ethanol overconsumption may have preexisting neurochemical disturbances that contribute to their vulnerability. This study examined the paraventricular nucleus of the thalamus (PVT), a limbic structure recently shown to participate in ethanol intake. To identify individuals prone to ethanol overconsumption, we tested Long-Evans rats in behavioral paradigms and found high levels of vertical time (rearing behavior) in a novel activity chamber to be a consistent predictor of subsequent excessive 20 percent ethanol drinking under the intermittent access model. Examining neurochemicals in the PVT, we found before ethanol exposure that prone rats with high rearing, compared with non-prone rats, had significantly lower levels of neurotensin (NTS) mRNA and peptide in the posterior (pPVT) but not anterior (aPVT) subregion of the PVT. Our additional finding that ethanol intake has no significant impact on either rearing or NTS levels indicates that these measures, which are different in prone rats before ethanol consumption, remain stable after ethanol consumption. The possibility that NTS directly controls ethanol drinking is supported by our finding that NTS administration specifically suppresses ethanol drinking when injected into the pPVT but not aPVT, with this effect occurring exclusively in higher drinkers that presumably have lower endogenous levels of NTS. Further, an NTS antagonist in the pPVT augments intake in lower drinkers with presumably more endogenous NTS, while NTS in the pPVT inhibits novelty-induced rearing that predicts excessive drinking. Together, these results provide strong evidence that low endogenous levels of NTS in the pPVT contribute to an increased propensity toward excessive ethanol drinking.

Metrics

11 Record Views
24 citations in Web of Science
22 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Substance Abuse
Logo image