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

Glial Cells01:04

Glial Cells

Overview
Nervous Tissue: Glial Cells01:31

Nervous Tissue: Glial Cells

Glia, or neuroglia, are vital support cells that assist neurons in their functions. The term "glia" originates from the Greek word for "glue," reflecting their role in holding the nervous system together. These cells can be categorized into six types: four in the central nervous system (CNS) and two in the peripheral nervous system (PNS).
The CNS glial cell includes the astrocytes, the oligodendrocytes, the microglia, and the ependymal cells.
Astrocytes are star-shaped glial cells that interact...
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

You might also read

Related Articles

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

Sort by
Same author

Mouse offspring exposed to preeclampsia/eclampsia-like symptoms exhibit cerebral hypoperfusion and mild cognitive impairment at 2 mo of age.

American journal of physiology. Heart and circulatory physiology·2026
Same author

Considering Litter Effects in Preclinical Research: Evidence from E17.5 Acid-Sensing Ion Channel 2a Knockout Mice Exposed to Acute Seizures.

Brain sciences·2025
Same author

Increased hippocampal cannabinoid 1 receptor expression is associated with protection from severe seizures in pregnant mice with reduced uterine perfusion pressure.

Journal of neuroscience research·2023
Same author

Retinal Venule Coverage by Pericytes Decreases in Multiparous Mice in a Time-Dependent Manner Post-Delivery.

International journal of molecular sciences·2023
Same author

Protocol to Study West Nile Virus Infection in Brain Slices In Vitro.

Methods in molecular biology (Clifton, N.J.)·2022
Same author

Increased seizure sensitivity in pregnant mice with genetic knockdown of acid sensing ion channel 2a is associated with impaired hippocampal inflammatory response.

Frontiers in physiology·2022

Related Experiment Video

Updated: Jun 17, 2026

Growth Assays to Assess Polyglutamine Toxicity in Yeast
09:06

Growth Assays to Assess Polyglutamine Toxicity in Yeast

Published on: March 5, 2012

Glial response to polyglutamine-mediated stress.

Parminder J S Vig1, Qingmei Shao, Maripar E Lopez

  • 1Department of Neurology, University of Mississippi Medical Center, Jackson, Mississippi 39216.

Bioscience Hypotheses
|January 5, 2010
PubMed
Summary

Intercellular miscommunication, not just intracellular changes, may drive neurodegeneration in CAG repeat disorders. Focusing on neuron-glia interactions offers new therapeutic avenues for these conditions.

More Related Videos

Caenorhabditis elegans as a Model System for Discovering Bioactive Compounds Against Polyglutamine-Mediated Neurotoxicity
08:16

Caenorhabditis elegans as a Model System for Discovering Bioactive Compounds Against Polyglutamine-Mediated Neurotoxicity

Published on: September 21, 2021

Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
09:33

Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules

Published on: May 12, 2017

Related Experiment Videos

Last Updated: Jun 17, 2026

Growth Assays to Assess Polyglutamine Toxicity in Yeast
09:06

Growth Assays to Assess Polyglutamine Toxicity in Yeast

Published on: March 5, 2012

Caenorhabditis elegans as a Model System for Discovering Bioactive Compounds Against Polyglutamine-Mediated Neurotoxicity
08:16

Caenorhabditis elegans as a Model System for Discovering Bioactive Compounds Against Polyglutamine-Mediated Neurotoxicity

Published on: September 21, 2021

Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
09:33

Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules

Published on: May 12, 2017

Area of Science:

  • Neurobiology
  • Neurodegenerative Diseases
  • Cellular Biology

Background:

  • Trinucleotide (CAG) repeat disorders stem from expanded polyglutamine tracts in proteins.
  • The precise mechanisms of polyglutamine-induced neurodegeneration remain unclear.
  • Emerging evidence points to intercellular miscommunication as a factor in CAG repeat disorder pathogenesis.

Purpose of the Study:

  • To hypothesize that impaired cell-cell interactions, specifically glia-neuron communication, are critical in neurodegeneration.
  • To propose that failures in intercellular signaling have more severe consequences than intracellular alterations.
  • To highlight the importance of bidirectional neuron-glia communication for normal neural function.

Main Methods:

  • This study is primarily theoretical, based on current evidence and forming a hypothesis.
  • It reviews existing literature on polyglutamine diseases and intercellular signaling.
  • It focuses on the conceptual framework of glia-neuron interactions in neurodegeneration.

Main Results:

  • The hypothesis posits that the failure of cell:cell interactions significantly contributes to neurodegeneration.
  • It suggests that disruptions in neuron-glia communication are a key pathogenic mechanism.
  • Altered intracellular biology alone may be less consequential than impaired intercellular signaling.

Conclusions:

  • Bidirectional communication between neurons and glia is essential for their development and function.
  • Understanding intercellular signaling pathways (e.g., glial factors, cell adhesion molecules) is crucial.
  • Targeting these intercellular mechanisms presents potential therapeutic strategies for CAG repeat disorders.