Next Article in Journal
Transcriptome-Wide Identification of miRNA Targets under Nitrogen Deficiency in Populus tomentosa Using Degradome Sequencing
Next Article in Special Issue
Stromal Cell-Derived Factor-1α Plays a Crucial Role Based on Neuroprotective Role in Neonatal Brain Injury in Rats
Previous Article in Journal
In Vitro Proliferation and Anti-Apoptosis of the Papain-Generated Casein and Soy Protein Hydrolysates towards Osteoblastic Cells (hFOB1.19)
Previous Article in Special Issue
Association between Serum Soluble CD154 Levels and Mortality in Patients with Malignant Middle Cerebral Artery Infarction
Article Menu
Issue 6 (June) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2015, 16(6), 13921-13936; doi:10.3390/ijms160613921

Characterization of Behaviour and Remote Degeneration Following Thalamic Stroke in the Rat

1
Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada
2
Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario, London, ON N6A 5A5, Canada
*
Author to whom correspondence should be addressed.
Academic Editor: Chris Sobey
Received: 17 March 2015 / Revised: 18 May 2015 / Accepted: 11 June 2015 / Published: 17 June 2015
(This article belongs to the Special Issue The Immune System and Inflammation in Cerebral Ischemia)
View Full-Text   |   Download PDF [11386 KB, uploaded 17 June 2015]   |  

Abstract

Subcortical ischemic strokes are among the leading causes of cognitive impairment. Selective atrophy of remote brain regions connected to the infarct is thought to contribute to deterioration of cognitive functions. The mechanisms underlying this secondary degenerative process are incompletely understood, but are thought to include inflammation. We induce ischemia by unilateral injection of endothelin-I into the rat dorsomedial thalamic nucleus, which has defined reciprocal connections to the frontal cortex. We use a comprehensive test battery to probe for changes in behaviour, including executive functions. After a four-week recovery period, brain sections are stained with markers for degeneration, microglia, astrocytes and myelin. Degenerative processes are localized within the stroke core and along the full thalamocortical projection, which does not translate into measurable behavioural deficits. Significant microglia recruitment, astrogliosis or myelin loss along the axonal projection or within the frontal cortex cannot be detected. These findings indicate that critical effects of stroke-induced axonal degeneration may only be measurable beyond a threshold of stroke severity and/or follow a different time course. Further investigations are needed to clarify the impact of inflammation accompanying axonal degeneration on delayed remote atrophy after stroke. View Full-Text
Keywords: subcortical ischemia; axonal degeneration; inflammation; secondary damage; executive function; frontal cortex subcortical ischemia; axonal degeneration; inflammation; secondary damage; executive function; frontal cortex
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Weishaupt, N.; Riccio, P.; Dobbs, T.; Hachinski, V.C.; Whitehead, S.N. Characterization of Behaviour and Remote Degeneration Following Thalamic Stroke in the Rat. Int. J. Mol. Sci. 2015, 16, 13921-13936.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top