Melatonin Regulates Neuronal Synaptic Plasticity in the Supramammillary Nucleus and Attenuates Methamphetamine‐Induced Conditioned Place Preference and Sensitization in Mice

ABSTRACT Methamphetamine (METH) is an addictive drug that threatens human health. The supramammillary nucleus (SuM) and its neural circuits play key roles in the regulation of spatial memory retrieval, and hippocampal contextual or social memory. Melatonin (MLT), a pineal hormone, can regulate hypot...

Full description

Saved in:
Bibliographic Details
Published in:Journal of pineal research 2024-09, Vol.76 (6), p.e13006-n/a
Main Authors: Ren, Qingyu, Han, Weikai, Yue, Yanan, Tang, Yaqi, Yue, Qingwei, Comai, Stefano, Sun, Jinhao
Format: Article
Language:English
Subjects:
addiction
Animals
Hypothalamus, Posterior - drug effects
Hypothalamus, Posterior - metabolism
Male
melatonin
Melatonin - pharmacology
methamphetamine
Methamphetamine - pharmacology
Mice
Mice, Inbred C57BL
Neuronal Plasticity - drug effects
supramammillary nucleus
synaptic plasticity
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:ABSTRACT Methamphetamine (METH) is an addictive drug that threatens human health. The supramammillary nucleus (SuM) and its neural circuits play key roles in the regulation of spatial memory retrieval, and hippocampal contextual or social memory. Melatonin (MLT), a pineal hormone, can regulate hypothalamic‐neurohypophysial activity. Our previous study showed that MLT attenuates METH‐induced locomotor sensitization. However, whether MLT regulates SuM function and participates in METH‐induced contextual memory retrieval remains unclear. Using a mouse model of METH‐conditioned place preference (CPP) and sensitization, we found that METH activated c‐Fos expression and elevated calcium (Ca²⁺) levels in SuM neurons. Chemogenetic inhibition of SuM attenuates CPP and sensitization. Pretreatment with MLT decreased c‐Fos expression and Ca2+ levels in the SuM and reversed METH‐induced addictive behavior, effects that were blocked with the selective MT2 receptors antagonist 4P‐PDOT and the MT1 receptors antagonist S26131. Furthermore, MLT reduced SuM synaptic plasticity, glutamate (Glu) release, and neuronal oscillations caused by METH, which were blocked by 4P‐PDOT. In conclusion, our data revealed that MLT regulates neuronal synaptic plasticity in the SuM, likely through the MLT receptors (MTs), and plays a role in modulating METH‐addictive behavior.
ISSN:0742-3098
1600-079X
1600-079X
DOI:10.1111/jpi.13006