Effects of Clavulanic Acid Treatment on Reinstatement to Methamphetamine, Glial Glutamate Transporters, and mGluR 2/3 Expression in P Rats Exposed to Ethanol.
Alcohol-Induced Disorders
/ drug therapy
Amphetamine-Related Disorders
/ drug therapy
Animals
Clavulanic Acid
/ pharmacology
Drug-Seeking Behavior
Ethanol
/ toxicity
Glutamate Plasma Membrane Transport Proteins
/ genetics
Male
Methamphetamine
/ toxicity
Neuroglia
/ drug effects
Rats
Receptors, Metabotropic Glutamate
/ genetics
Recurrence
Repetition Priming
Clavulanic acid
Conditioned place preference
Glutamatergic transporters
Methamphetamine
mGluR2/3
Journal
Journal of molecular neuroscience : MN
ISSN: 1559-1166
Titre abrégé: J Mol Neurosci
Pays: United States
ID NLM: 9002991
Informations de publication
Date de publication:
Jan 2019
Jan 2019
Historique:
received:
11
05
2018
accepted:
01
10
2018
pubmed:
25
11
2018
medline:
1
2
2019
entrez:
25
11
2018
Statut:
ppublish
Résumé
Evidence demonstrated that the glutamatergic system is implicated in mediating relapse to several drugs of abuse, including methamphetamine (METH). Glutamate homeostasis is maintained by a number of glutamate transporters, such as glutamate transporter type 1 (GLT-1), cystine/glutamate transporter (xCT), and glutamate aspartate transporter (GLAST). In addition, group II metabotropic glutamate receptors (mGluR2/3) were found to be implicated in relapse-seeking behavior. Ample evidence showed that β-lactam antibiotics are effective in upregulating GLT-1 and xCT expression, thus improving glutamate homeostasis and attenuating relapse to drugs of abuse. In this study, we investigated the reinstatement of METH using conditioned place preference (CPP) in male alcohol-preferring (P) rats exposed to home-cage free choice ethanol drinking. Here, we tested the effect of clavulanic acid (CA), a β-lactam, on the reinstatement of METH-seeking and ethanol drinking. In addition, we examined the expression of GLT-1, xCT, and GLAST as well as metabotropic glutamate receptor (mGluR2/3) in the nucleus accumbens (NAc) shell, NAc core, and dorsomedial prefrontal cortex (dmPFC). A priming i.p. injection of METH reinstated preference in METH-paired chamber following extinction. Chronic exposure to ethanol decreased the expression of GLT-1 and xCT in the NAc shell, but not in the NAc core or dmPFC. CA treatment blocked the reinstatement of METH-seeking, decreased ethanol intake, and restored the expression of GLT-1 and xCT in the NAc shell. In addition, the expression of mGluR2/3 was increased by CA treatment in the NAc shell and dmPFC. These findings suggest that these glutamate transporters and mGluR2/3 might be potential therapeutic targets for the attenuation of reinstatement to METH-seeking.
Identifiants
pubmed: 30471010
doi: 10.1007/s12031-018-1194-z
pii: 10.1007/s12031-018-1194-z
pmc: PMC6344243
mid: NIHMS1514310
doi:
Substances chimiques
Glutamate Plasma Membrane Transport Proteins
0
Receptors, Metabotropic Glutamate
0
metabotropic glutamate receptor 2
0
metabotropic glutamate receptor 3
0
Clavulanic Acid
23521W1S24
Ethanol
3K9958V90M
Methamphetamine
44RAL3456C
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-15Subventions
Organisme : NIAAA NIH HHS
ID : R01 AA019458
Pays : United States
Organisme : NIAAA NIH HHS
ID : U24 AA015512
Pays : United States
Organisme : National Institute on Alcohol Abuse and Alcoholism
ID : R01AA019458
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