Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Ligand-gated Ion Channels01:19

Ligand-gated Ion Channels

Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...
Peripherally and Centrally Acting Muscle Relaxants: A Comparison01:09

Peripherally and Centrally Acting Muscle Relaxants: A Comparison

Skeletal muscle relaxants can target the central nervous system [CNS] to reduce muscle tension or act directly at the neuromuscular junction to induce temporary paralysis. These two classes of muscle relaxants are called centrally acting muscle relaxants and peripherally acting muscle relaxants. They differ in their action, mechanism, administration route, and clinical uses.
Centrally acting muscle relaxants can be further divided into spasmolytic and antispasmodic drugs. Spasmolytic drugs,...

You might also read

Related Articles

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

Sort by
Same author

Integrative In Silico and In Vivo Analysis of Banhasasim-Tang for Irritable Bowel Syndrome: Mechanistic Insights into Inflammation-Related Pathways.

Pharmaceuticals (Basel, Switzerland)·2025
Same author

Warburg-like Metabolic Reprogramming in Endometriosis: From Molecular Mechanisms to Therapeutic Approaches.

Pharmaceuticals (Basel, Switzerland)·2025
Same author

Discovery of a novel alpha isoform of the long-known enzyme LDHA provides new insights into cancer research.

The FEBS journal·2025
Same author

Effects of Repeated Exposure to Ambient Cold on the Development of Inflammatory Pain in a Rat Model of Knee Arthritis.

Life (Basel, Switzerland)·2024
Same author

New Insights into the Acupuncture Point Microenvironment.

Journal of acupuncture and meridian studies·2024
Same author

Targeting pyruvate dehydrogenase kinase 1 overcomes EGFR C797S mutation-driven osimertinib resistance in non-small cell lung cancer.

Experimental & molecular medicine·2024

Related Experiment Video

Updated: Jun 27, 2026

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
07:09

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Published on: July 16, 2014

49.2K

Electroacupuncture Alleviates Neuropathic Pain by Inhibiting Spinal CCL2-Driven Microglial Activation.

Vishnumolakala Sindhuri1, Min-Jae Koo1, Seung Heon Jeon2

  • 1Research Institute for Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea.

International Journal of Molecular Sciences
|September 27, 2025
PubMed
Summary

Electroacupuncture (EA) alleviates neuropathic pain by downregulating spinal CCL2/CCR2 signaling and reducing microglial activation. This mechanism is crucial for EA

Keywords:
acupuncturechemokine receptorchronic paininflammatory cytokinesmicroglia

More Related Videos

Author Spotlight: Unveiling the Therapeutic Effects of FSN Treatment – Bridging Research and Clinical Applications in Neuropathic Pain
08:20

Author Spotlight: Unveiling the Therapeutic Effects of FSN Treatment – Bridging Research and Clinical Applications in Neuropathic Pain

Published on: June 30, 2023

2.7K
Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn
07:12

Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn

Published on: May 23, 2025

523

Related Experiment Videos

Last Updated: Jun 27, 2026

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
07:09

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Published on: July 16, 2014

49.2K
Author Spotlight: Unveiling the Therapeutic Effects of FSN Treatment – Bridging Research and Clinical Applications in Neuropathic Pain
08:20

Author Spotlight: Unveiling the Therapeutic Effects of FSN Treatment – Bridging Research and Clinical Applications in Neuropathic Pain

Published on: June 30, 2023

2.7K
Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn
07:12

Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn

Published on: May 23, 2025

523

Area of Science:

  • Neuroscience
  • Pain Research
  • Integrative Medicine

Background:

  • Neuropathic pain mechanisms are complex and incompletely understood.
  • Electroacupuncture (EA) shows promise for pain relief but requires mechanistic clarification.
  • Spinal chemokine signaling and microglial activation are implicated in pain pathways.

Purpose of the Study:

  • To investigate if EA modulates CCL2/CCR2 signaling and microglial activation for neuropathic pain relief.
  • To elucidate the molecular mechanisms underlying EA's analgesic effects in a rat model.
  • To establish the causal role of CCL2/CCR2 signaling in EA-mediated analgesia.

Main Methods:

  • Neuropathic pain induced via L5 spinal nerve ligation in rats.
  • EA applied to acupoints ST36 and GB34; behavioral pain assessments conducted.
  • Western blot and immunofluorescence used to quantify spinal CCL2, CCR2, Iba1, IL-1β, and TNF-α.
  • Recombinant CCL2 administered intrathecally to assess its effect on EA analgesia.

Main Results:

  • EA significantly reduced mechanical allodynia and thermal hyperalgesia.
  • EA treatment decreased spinal expression of CCL2, CCR2, Iba1, IL-1β, and TNF-α.
  • Intrathecal CCL2 administration reversed EA's analgesic effects, confirming pathway necessity.

Conclusions:

  • EA exerts analgesic effects by downregulating the spinal CCL2/CCR2 pathway.
  • EA inhibits microglial activation, contributing to its pain-relieving properties.
  • Spinal chemokine signaling is a critical target for EA-mediated neuropathic pain relief.