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 Experiment Videos

Neuropathologic changes in the gerbil brain after chronic hypoperfusion

T Kudo1, M Takeda, S Tanimukai

  • 1Department of Neuropsychiatry, Osaka University Medical School, Japan.

Stroke
|February 1, 1993
PubMed
Summary
This summary is machine-generated.

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

Encephalomyocarditis (EMC) virus-induced myocarditis by different virus variants and mouse strains.

The Journal of veterinary medical science·1992
Same author

Purification and characterization of a possible protooncogene fyn product, p59fyn, from a rat brain particulate fraction.

Journal of biochemistry·1992
Same author

Tyraminelike action of succinylcholine in the isolated, blood-perfused canine atrium.

Anesthesia and analgesia·1992
Same author

Assembly regulatory domain of glial fibrillary acidic protein. A single phosphorylation diminishes its assembly-accelerating property.

The Journal of biological chemistry·1992
Same author

Mechanism of PGE2-induced cell swelling in distal nephron segments.

The American journal of physiology·1992
Same author

O2- scavenging activity of lignins, tannins and PSK.

Anticancer research·1992
Same journal

Defining the Therapeutic Ceiling of Endovascular Thrombectomy in Large-Core Stroke: Beyond the Limits of ASPECTS.

Stroke·2026
Same journal

Adjunctive Normobaric Hyperoxia With Endovascular Thrombectomy for Acute Stroke at 6 to 24 Hours: A Phase IIb Randomized Trial.

Stroke·2026
Same journal

Management of Patients at Risk of Ischemic Stroke With Left Ventricular Systolic Dysfunction in the Absence of Intracardiac Thrombus: A Scientific Statement From the American Heart Association.

Stroke·2026
Same journal

Update on Rehabilitation After Stroke: Global Changes and the Continued Importance of Therapy Intensity, Dose, and Timing.

Stroke·2026
Same journal

ENTF Neuromodulation Yields Reduced Disability After Stroke: An Individual Participant-Level Data Meta-Analysis.

Stroke·2026
Same journal

Menopause and Its Implications for Stroke in Women.

Stroke·2026
See all related articles

Chronic cerebral hypoperfusion in gerbils alters brain cytoskeletal proteins, affecting neurons and glial cells. These changes in microtubule-associated protein 2, neurofilament, and glial fibrillary acidic protein suggest a role in neuronal death.

Area of Science:

  • Neuroscience
  • Pathology
  • Cerebrovascular Research

Background:

  • Chronic cerebral hypoperfusion is a significant factor in neurodegenerative diseases.
  • Understanding pathological changes in brain cytoskeletal proteins is crucial.

Purpose of the Study:

  • To develop and utilize an animal model to study brain cytoskeletal protein alterations during chronic hypoperfusion.
  • To elucidate the specific changes in neuronal and glial cytoskeletal proteins.

Main Methods:

  • A novel coiled clip method was used to induce non-occlusive stenosis in the carotid arteries of Mongolian gerbils.
  • Animals underwent behavioral testing (passive avoidance paradigm) to assess learning ability.
  • Neuropathological examination was performed on gerbils after 12 weeks.

Related Experiment Videos

Main Results:

  • Cerebral hypoperfusion led to ventricular dilatation, cortical atrophy, and white matter rarefaction.
  • Diminished immunoreactivity for microtubule-associated protein 2 indicated dendritic changes in neurons.
  • Increased neurofilament 200K protein staining suggested axonal alterations, while increased glial fibrillary acidic protein indicated glial cell activation.

Conclusions:

  • Alterations in cytoskeletal proteins (MAP2, neurofilaments, GFAP) are observed in dendrites, axons, and glial cells.
  • These cytoskeletal changes are implicated in neuronal death under chronic hypoperfusion conditions.
  • The animal model effectively demonstrates the neuropathological consequences of reduced cerebral blood flow.