ArticleNeurotoxicity research2018
The Role of HINT1 in Methamphetamine-Induced Conditioned Place Preference.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- The influence of HINT1 protein in nucleus accumbens on aggressive behavior and anxiety-like behavior.Psychopharmacology · 2026Article
- The role of HINT1 in methamphetamine-induced behavioral sensitization.Psychopharmacology · 2020Article
- HINT1 in Neuropsychiatric Diseases: A Potential Neuroplastic Mediator.Neural plasticity · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Drug addiction is a chronically relapsing disorder in humans; yet, the underlying mechanism remained unclear. Recent studies suggested that the histidine triad nucleotide binding protein 1 (HINT1) may play significant roles in diverse neuropsychiatric diseases including drug addiction. In our present study, we used different batches of mice to establish the different stages of methamphetamine (METH)-induced conditioned place preference (CPP) to explore the dynamic changes throughout the process of addiction in different brain regions, including prefrontal cortex (PFC), nucleus accumbens (NAc), corpus striatum (CPu), and hippocampus (Hip). We found that in NAc of the METH group mice, the HINT1 expression level initially increased after acquisition phases, and then dropped to the normal level after extinction phase, and again increased after reinstatement phase. However, there was no statistical difference in the HINT1 expression level in other three encephalic regions (PFC, CPu, and Hip). Therefore, the HINT1 protein, particularly in the NAc, plays a vital role in the METH-induced CPP. However, the precise mechanisms will require further investigation.
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