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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
Published on: January 22, 2016
Does elevated peripheral benzodiazepine receptor gene expression relate to cognitive deficits in methamphetamine
Siriluk Veerasakul1,2, Samur Thanoi1,2, Paritat Watiktinkorn3
1Department of Anatomy, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.
Chronic methamphetamine (METH) abuse increases peripheral benzodiazepine receptor (PBR) gene expression, indicating systemic inflammation. This elevation persists over a year post-abstinence and correlates with cognitive deficits in METH-dependent individuals.
Area of Science:
- Neuroscience
- Psychiatry
- Toxicology
Background:
- Methamphetamine (METH) is a neurotoxin and psychostimulant.
- Chronic METH use induces neurotoxicity and a glial inflammatory response.
- Peripheral benzodiazepine receptor (PBR) is a marker of inflammation.
Purpose of the Study:
- To investigate changes in PBR expression in METH dependence.
- To determine if altered PBR expression correlates with cognitive deficits.
Main Methods:
- PBR gene expression analyzed using reverse transcriptase-polymerase chain reaction.
- Blood samples from 14 METH-dependent males and 14 controls.
Main Results:
- Significantly elevated PBR gene expression observed in METH dependence, suggesting systemic inflammation.
- Elevated PBR levels persisted for over a year after METH abstinence.
- Subjects with high PBR showed deficits in Wisconsin Card Sorting Test.
Conclusions:
- Systemic inflammation is associated with chronic METH abuse.
- Elevated PBR may contribute to cognitive deficits in METH dependence.
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