Related Experiment Video

Updated: Jul 4, 2026

A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats
04:11

A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats

Published on: November 6, 2018

Morphine withdrawal increases metabotropic glutamate 2/3 receptors expression in nucleus accumbens

Antonella M E Modafferi1, Marco Diana, Ferdinando Nicoletti

  • 1Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Rome, Italy.

Neuroreport
|June 4, 2008
PubMed

Insights

Chronic morphine withdrawal increases metabotropic glutamate (mGlu)2/3 receptors in the nucleus accumbens. This change in mGlu2/3 receptor expression may contribute to morphine withdrawal symptoms.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Opioid addiction is a major public health concern.
  • Understanding the neurobiological mechanisms of opioid withdrawal is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the impact of chronic morphine treatment and subsequent withdrawal on metabotropic glutamate receptor expression.
  • To determine the specific roles of mGlu1, mGlu5, and mGlu2/3 receptors in the nucleus accumbens and caudate putamen during morphine withdrawal.

Main Methods:

  • Rats underwent a 14-day escalating-dose morphine treatment.
  • Receptor density for mGlu1, mGlu5, and mGlu2/3 was assessed post-treatment and during withdrawal (1, 3, and 14 days).
  • Quantitative analysis of receptor expression in specific brain regions.

Main Results:

  • Metabotropic glutamate (mGlu)1 and mGlu5 receptor expression remained unchanged in both the nucleus accumbens and caudate putamen.
  • A significant increase in mGlu2/3 receptor expression was observed in the nucleus accumbens during withdrawal (days 1, 3, and 14).
  • No significant changes in mGlu2/3 receptor expression were found in the caudate putamen.

Conclusions:

  • Increased expression of mGlu2/3 receptors in the nucleus accumbens is a key neuroadaptive change during morphine withdrawal.
  • These findings suggest that mGlu2/3 receptors in the nucleus accumbens play a role in the manifestation of morphine withdrawal symptoms.
  • Targeting mGlu2/3 receptors could be a potential therapeutic strategy for managing opioid withdrawal.

More Related Videos

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence09:54

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence

Published on: March 8, 2020

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods09:29

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods

Published on: August 4, 2022

Related Concept Videos

Opioid Receptors: Overview01:22

Opioid Receptors: Overview

Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2, D-Pen5]-enkephalin or DPDPE for...
Analgesia and Pain Management01:25

Analgesia and Pain Management

Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
Opioid Analgesics: Synthetic and Semisynthetic Opioids01:15

Opioid Analgesics: Synthetic and Semisynthetic Opioids

Synthetic and semisynthetic opioids are pivotal in pain management and tackling opioid addiction. Semisynthetic opioids, including morphinans (morphine derivatives), oxycodone, oxymorphone, hydrocodone, and hydromorphone, have improved pharmacokinetic profiles compared to morphine. Additionally, heroin and 6-MAM (6-Monoacetylmorphine) show better CNS penetration than morphine due to heightened lipid solubility. Hydromorphone, a potent opioid, undergoes hepatic metabolism to form the active...
Drug Abuse and Addiction: Pharmacological Phenomena01:15

Drug Abuse and Addiction: Pharmacological Phenomena

Drug dependence, abuse, and addiction are complex phenomena that can precipitate various abnormal states. Physical dependence refers to a state of pharmacological adaptation to a drug. This adaptation often results in tolerance—a reduced response to the drug after repeated administrations. When the drug use is abruptly stopped, withdrawal symptoms occur due to the body's need to readjust from the pharmacologically induced imbalance. However, tolerance and withdrawal symptoms do not necessarily...
Opioid Analgesics: Morphine and Other Natural Cogeners01:20

Opioid Analgesics: Morphine and Other Natural Cogeners

Opioids are a class of drugs that mimic endogenous opioid peptides and act on opioid receptors, and help in pain relief. These compounds are classified as natural, synthetic, or semi-synthetic. Natural opioids, like morphine, codeine, and thebaine, are derived from the opium poppy plant (Papaver somniferum or Papaver album) and are termed opiates. Synthetic opioids are artificial, while semi-synthetic opioids combine natural and synthetic compounds. Morphine, a prototypical opioid, possesses a...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...