Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Neurochem. 2014 Aug;130(3):402-7. doi: 10.1111/jnc.12727. Epub 2014 Apr 19.

Mephedrone alters basal ganglia and limbic neurotensin systems.

Author information

  • 1Department of Pharmacology & Toxicology, College of Pharmacy, University of Utah, Salt Lake City, Utah, USA.

Abstract

Mephedrone (4-methylmethcathinone) is a synthetic cathinone designer drug that alters pre-synaptic dopamine (DA) activity like many psychostimulants. However, little is known about the post-synaptic dopaminergic impacts of mephedrone. The neuropeptide neurotensin (NT) provides inhibitory feedback for basal ganglia and limbic DA pathways, and post-synaptic D1 -like and D2 -like receptor activity affects NT tissue levels. This study evaluated how mephedrone alters basal ganglia and limbic system NT content and the role of NT receptor activation in drug consumption behavior. Four 25 mg/kg injections of mephedrone increased NT content in basal ganglia (striatum, substantia nigra and globus pallidus) and the limbic regions (nucleus accumbens core), while a lower dosage (5 mg/kg/injection) only increased striatal NT content. Mephedrone-induced increases in basal ganglia NT levels were mediated by D1 -like receptors in the striatum and the substantia nigra by both D1 -like and D2 -like receptors in the globus pallidus. Mephedrone increased substance P content, another neuropeptide, in the globus pallidus, but not in the dorsal striatum or substantia nigra. Finally, the NT receptor agonist PD149163 blocked mephedrone self-administration, suggesting reduced NT release, as indicated by increased tissue levels, likely contributing to patterns of mephedrone consumption.

© 2014 International Society for Neurochemistry.

KEYWORDS:

basal Ganglia; dopamine; limbic System; mephedrone; neurotensin; stimulants

PMID:
24678634
[PubMed - indexed for MEDLINE]
PMCID:
PMC4107087
[Available on 2015-08-01]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk