Modulation of Nicotine-Associated Behaviour in Rats By μ-Opioid Signals from the Medial Prefrontal Cortex to the Nucleus Accumbens Shell.
10.1007/s12264-024-01230-1
- Author:
Feng ZHU
1
;
Hirosato KANDA
2
;
Hiroyuki NEYAMA
3
;
Yuping WU
3
;
Shigeki KATO
4
;
Di HU
3
;
Shaoqi DUAN
1
;
Koichi NOGUCHI
1
;
Yasuyoshi WATANABE
3
;
Kazuto KOBAYASHI
4
;
Yi DAI
5
;
Yilong CUI
6
Author Information
1. Department of Anatomy and Neuroscience, Hyogo Medical University, Nishinomiya, Hyogo, 663-8501, Japan.
2. School of Pharmacy, Hyogo Medical University, Kobe, Hyogo, 650-8530, Japan.
3. RIKEN Center for Biosystems Dynamics Research, Kobe, Hyogo, 650-0047, Japan.
4. Department of Molecular Genetics, Fukushima Medical University Institute of Biomedical Sciences, Fukushima, 960-1295, Japan.
5. Department of Anatomy and Neuroscience, Hyogo Medical University, Nishinomiya, Hyogo, 663-8501, Japan. ydai@hyo-med.ac.jp.
6. Department of Anatomy and Neuroscience, Hyogo Medical University, Nishinomiya, Hyogo, 663-8501, Japan. cuiyl@riken.jp.
- Publication Type:Journal Article
- Keywords:
Medial prefrontal cortex;
Nicotine-associated behaviour;
Nucleus accumbens shell;
Small-animal neuroimaging;
μ-Opioid receptor
- MeSH:
Animals;
Nucleus Accumbens/drug effects*;
Prefrontal Cortex/drug effects*;
Nicotine/pharmacology*;
Receptors, Opioid, mu/metabolism*;
Male;
Rats;
Rats, Sprague-Dawley;
Tobacco Use Disorder/metabolism*;
Neurons/drug effects*;
Neural Pathways/drug effects*
- From:
Neuroscience Bulletin
2024;40(12):1826-1842
- CountryChina
- Language:English
-
Abstract:
Nicotine addiction is a concern worldwide. Most mechanistic investigations are on nicotine substance dependence properties based on its pharmacological effects. However, no effective therapeutic treatment has been established. Nicotine addiction is reinforced by environments or habits. We demonstrate the neurobiological basis of the behavioural aspect of nicotine addiction. We utilized the conditioned place preference to establish nicotine-associated behavioural preferences (NABP) in rats. Brain-wide neuroimaging analysis revealed that the medial prefrontal cortex (mPFC) was activated and contributed to NABP. Chemogenetic manipulation of µ-opioid receptor positive (MOR+) neurons in the mPFC or the excitatory outflow to the nucleus accumbens shell (NAcShell) modulated the NABP. Electrophysiological recording confirmed that the MOR+ neurons directly regulate the mPFC-NAcShell circuit via GABAA receptors. Thus, the MOR+ neurons in the mPFC modulate the formation of behavioural aspects of nicotine addiction via direct excitatory innervation to the NAcShell, which may provide new insight for the development of effective therapeutic strategies.
