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

You might also read

Related Articles

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

Sort by
Same author

Wake-active brainstem GABA neurons signal sleep pressure by upregulating AMPA receptors to drive recovery sleep.

Current biology : CB·2026
Same author

Prime editing of a pathogenic <i>Scn1a</i> allele ameliorates seizure phenotypes in a GEFS<sup>+</sup> mouse model.

Science translational medicine·2026
Same author

Glycine transport inhibitors for the treatment of chronic pain conditions: the time is ripe for clinical evaluation!

Frontiers in molecular neuroscience·2026
Same author

Descending inhibitory rostral ventromedial medulla neurons cause widespread antinociception and contribute to the pain-inhibits-pain phenomenon.

Nature communications·2026
Same author

GABAergic Gbx1 neurons of the superficial dorsal horn are critical elements of a spinal circuit for stress-induced analgesia.

Neuron·2026
Same author

Dissociating role of Bassoon in glutamatergic and dopaminergic neurons in alcohol-related behaviour and affective state in mice.

British journal of pharmacology·2026

Related Experiment Video

Updated: Sep 23, 2025

The Spared Nerve Injury SNI Model of Induced Mechanical Allodynia in Mice
07:44

The Spared Nerve Injury SNI Model of Induced Mechanical Allodynia in Mice

Published on: August 18, 2011

63.9K

Nociception in the Glycine Receptor Deficient Mutant Mouse Spastic.

Teja Wolfgang Groemer1, Antoine Triller2, Hanns Ulrich Zeilhofer3

  • 1Institut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Frontiers in Molecular Neuroscience
|May 13, 2022
PubMed
Summary

Glycine receptors (GlyRs) are vital for spinal cord inhibition. A mutation in the GlyR beta subunit gene (Glrb) in spastic mice alters pain behaviors, indicating GlyRs

Keywords:
glycine receptorglycinergic inhibitionnociceptionpainspasticsynaptic clustering

More Related Videos

Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice
04:34

Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice

Published on: January 25, 2022

5.4K
In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration
06:35

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration

Published on: June 15, 2018

19.7K

Related Experiment Videos

Last Updated: Sep 23, 2025

The Spared Nerve Injury SNI Model of Induced Mechanical Allodynia in Mice
07:44

The Spared Nerve Injury SNI Model of Induced Mechanical Allodynia in Mice

Published on: August 18, 2011

63.9K
Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice
04:34

Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice

Published on: January 25, 2022

5.4K
In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration
06:35

In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration

Published on: June 15, 2018

19.7K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Glycine receptors (GlyRs) mediate fast inhibitory neurotransmission in the mammalian spinal cord, regulating sensory and motor functions.
  • Mutations in GlyR genes cause hyperekplexia, a disorder marked by muscle stiffness and exaggerated startle reflexes.
  • The spastic (spa) mouse model, with a mutation in the GlyR beta subunit gene (Glrb), exhibits reduced GlyR numbers.

Purpose of the Study:

  • To investigate pain-related behaviors and GlyR expression in the spinal cord of the spastic (spa) mouse mutant.
  • To understand how Glrb mutations affect GlyR localization and function in sensory processing.

Main Methods:

  • Analysis of pain-related behaviors in homozygous Glrb(spa)/Glrb(spa) mice using thermal, chemical (formalin test), and mechanical stimuli.
  • Immunohistochemical staining of spinal cord sections to assess GlyRα subunit expression and localization.
  • Quantification of GlyRα subunit transcripts in the dorsal horn.

Main Results:

  • Homozygous spastic mice showed reduced licking time and increased flinching in the formalin test, indicating altered chemically induced pain.
  • Mechanically induced nocifensive behavior was decreased, but allodynia following inflammation was comparable to wild-type mice.
  • Spinal cord staining revealed a significant reduction in clustered GlyRα subunits at synaptic sites, despite unchanged transcript levels for some variants.

Conclusions:

  • Loss of functional GlyRβ subunits and synaptic GlyRs differentially impacts sensory processing based on stimulus type.
  • The Glrb mutation in spastic mice disrupts GlyR clustering and alters pain perception.
  • These findings highlight the critical role of GlyRs in modulating pain pathways in the spinal cord.