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ABSTRACT: Rationale
Methamphetamine (MA) addiction is a major public health issue in the USA, with a poorly understood genetic component. We previously identified heterogeneous nuclear ribonucleoprotein H1 (Hnrnph1; H1) as a quantitative trait gene underlying sensitivity to MA-induced behavioral sensitivity. Mice heterozygous for a frameshift deletion in the first coding exon of H1 (H1+/-) showed reduced MA phenotypes including oral self-administration, locomotor activity, dopamine release, and dose-dependent differences in MA conditioned place preference. However, the effects of H1+/- on innate and MA-modulated reward sensitivity are not known.Objectives
We examined innate reward sensitivity and facilitation by MA in H1+/- mice via intracranial self-
SUBMITTER: Borrelli KN
PROVIDER: S-EPMC8715365 | biostudies-literature | 2021 Jul
REPOSITORIES: biostudies-literature