Inhibitory effects of Shati/Nat8l overexpression in the medial prefrontal cortex on methamphetamine-induced conditioned place preference in mice.
Acetyltransferases
/ genetics
Animals
Central Nervous System Stimulants
/ pharmacology
Conditioning, Classical
Dopamine
/ metabolism
Gene Knock-In Techniques
Glutamic Acid
/ metabolism
Locomotion
/ drug effects
Male
Methamphetamine
/ pharmacology
Mice
Microdialysis
Nucleus Accumbens
/ metabolism
Prefrontal Cortex
/ metabolism
Receptors, Metabotropic Glutamate
/ metabolism
NAc
Shati/Nat8l
dopamine
drug addiction
glutamate
mPFC
Journal
Addiction biology
ISSN: 1369-1600
Titre abrégé: Addict Biol
Pays: United States
ID NLM: 9604935
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
31
08
2018
revised:
24
02
2019
accepted:
28
02
2019
pubmed:
6
4
2019
medline:
25
6
2021
entrez:
6
4
2019
Statut:
ppublish
Résumé
Shati/Nat8l is a novel N-acetyltransferase identified in the brain of mice treated with methamphetamine (METH). Shati/Nat8l mRNA is expressed in various brain areas, including the prefrontal cortex (PFC), where the expression level is higher than that in other brain regions. Shati/Nat8l overexpression in the nucleus accumbens (NAc) attenuates the pharmacological response to METH via mGluR3. Meanwhile, dopamine (DA) and glutamate dysregulations have been reported in the medial prefrontal cortex (mPFC) and NAc after METH self-administration and during reinstatement. However, the mechanism, the reward system, and function of Shati/Nat8l in the mPFC is unclear. Here, we injected an adeno-associated virus (AAV) vector containing Shati/Nat8l into the mPFC of mice, to overexpress Shati/Nat8l in the mPFC (mPFC-Shati/Nat8l). Interestingly, the METH-induced conditioned place preference (CPP) was attenuated in the mPFC-Shati/Nat8l mice, but locomotor activity was not. Additionally, immunohistochemical results from mice that were injected with AAV-GFP showed fluorescence in the mPFC and other brain regions, mainly the NAc, indicating an mPFC-NAc top-down connection. Finally, in vivo microdialysis experiments revealed that Shati/Nat8l overexpression in the mPFC reduced extracellular DA levels and suppressed the METH-induced DA increase in the NAc. Moreover, decreased extracellular glutamate levels were observed in the NAc. These results indicate that Shati/Nat8l overexpression in the mPFC attenuates METH-induced CPP by decreasing extracellular DA in the NAc. In contrast, Shati/Nat8l-mPFC overexpression did not alter METH-induced hyperlocomotion. This study demonstrates that Shati/Nat8l in the mPFC attenuates METH reward-seeking behaviour but not the psychomotor activity of METH.
Identifiants
pubmed: 30950164
doi: 10.1111/adb.12749
pmc: PMC7187255
doi:
Substances chimiques
Central Nervous System Stimulants
0
Receptors, Metabotropic Glutamate
0
metabotropic glutamate receptor 3
0
Glutamic Acid
3KX376GY7L
Methamphetamine
44RAL3456C
Acetyltransferases
EC 2.3.1.-
Shati protein, mouse
EC 2.3.1.-
Dopamine
VTD58H1Z2X
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12749Informations de copyright
© 2019 Society for the Study of Addiction.
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