Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Opioid Receptors: Overview

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 Management

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

A Mechanistic Approach to the Development of Gene Therapy for Chronic Pain.

International review of cell and molecular biology·2016

Same author

Reappraisal of bovril as a source of arginine in the arginine stimulation test for growth hormone deficiency.

The Medical journal of Malaysia·2015

Same author

β-arrestin protects neurons by mediating endogenous opioid arrest of inflammatory microglia.

Cell death and differentiation·2013

Same author

Acute renal failure and posterior reversible encephalopathy syndrome following multiple wasp stings: a case report.

The Medical journal of Malaysia·2012

Same author

Intrathecal delivery of a mutant micro-opioid receptor activated by naloxone as a possible antinociceptive paradigm.

The Journal of pharmacology and experimental therapeutics·2010

Same author

Organization of synaptic junction proteins.

Neurochemistry international·2010

Search research articles

Related Experiment Video

Updated: Jul 11, 2026

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection

Published on: September 2, 2014

Characterization of [3H]morphine binding to interleukin-1-activated thymocytes.

S Roy¹, B L Ge, H H Loh

¹Department of Pharmacology, University of Minnesota Medical School, Minneapolis.

The Journal of Pharmacology and Experimental Therapeutics

|November 1, 1992

Summary

Researchers identified novel [3H]morphine binding sites on thymocytes, distinct from brain opioid receptors. These sites may regulate interleukin-1-induced T-cell proliferation, suggesting a new immunomodulatory mechanism.

More Related Videos

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

Published on: March 14, 2016

Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay

Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay

Published on: September 7, 2018

Related Experiment Videos

Last Updated: Jul 11, 2026

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection

Published on: September 2, 2014

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

Published on: March 14, 2016

Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay

Characterization of Thymus-dependent and Thymus-independent Immunoglobulin Isotype Responses in Mice Using Enzyme-linked Immunosorbent Assay

Published on: September 7, 2018

Area of Science:

Immunology
Neuroscience
Pharmacology

Background:

Interleukin-1 (IL-1) stimulates thymocyte proliferation.
Previously observed [3H]morphine binding sites on thymocytes during IL-1-induced proliferation.

Purpose of the Study:

Characterize the nature of [3H]morphine binding sites on thymocytes.
Compare these sites to classical opioid receptors.
Investigate the potential role of these sites in T-cell regulation.

Main Methods:

Characterization of [3H]morphine binding sites on thymocyte membranes.
Assessing binding affinity, capacity, stereoselectivity, and ion dependency.
Enzymatic treatment of membranes (proteinase K/E, phospholipase A2, trypsin).
Flow cytometry to identify cell subsets (CD4+ T-cells).

Main Results:

Binding sites exhibit lack of stereoselectivity and relatively low affinity (Kd = 50 nM) with high capacity (Bmax = 3 pmol/mg protein).
Binding is inhibited by specific ions (Ca++, Mg++, Mn++, Cl-) and enzymatic treatments (proteinase K/E, phospholipase A2).
Sites are predominantly found on CD4+ T-cells and prefer opioid alkaloids over peptides.
These sites differ significantly from classical brain opioid receptors.

Conclusions:

The identified [3H]morphine binding sites on thymocytes are distinct from central nervous system opioid receptors.
These novel binding sites may play a role in modulating IL-1-induced thymocyte proliferation.
Potential negative feedback mechanism on T-cell proliferation mediated by these sites in vivo.