Abstract
Acute toxic models of Huntington’s disease (HD) and Parkinson’s disease (PD) have been used extensively to study neuropathology and behavior in rodents and non-human primates, but not large animals. We have created an acute quinolinic acid (QA) model of HD in sheep (Ovis aries), first to investigate the clinical signs of ovine striatum pathology and second to assess the value of a veterinary neurological examination in the symptomology investigation. Sixteen sheep underwent two surgeries, four weeks apart, in which either QA or saline was infused into the left (unilateral) and then the right (bilateral) caudate nucleus. Neurological examinations were performed pre-surgically, two weeks after the unilateral surgery and eight weeks after the bilateral surgery. Examining veterinarians were blind to treatment group. Evidence of laterality and hind limb motor dysfunction was identified in the QA-lesioned sheep. The neurological examination identified clinical signs in two out of eight saline control sheep and four out of eight QA-lesioned sheep after the unilateral surgery and three out of eight saline control sheep and seven out of eight QA-lesioned sheep after the bilateral lesion surgery. There was no association between clinical profile and treatment group, or lesion size and location. While the neurological examination was moderately useful for identification of QA-lesioned sheep, it was not informative about lesion characteristics.
Original language | English |
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Pages (from-to) | 56-67 |
Number of pages | 12 |
Journal | Journal of Neurology and Experimental Neuroscience |
Volume | 5 |
Issue number | 2 |
DOIs | |
Publication status | Published - 6 Aug 2019 |
Externally published | Yes |
Bibliographical note
Copyright: ©2019 O’Connell et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC-BY ) (http://creativecommons.org/licenses/by/4.0/) which permits commercial use, including reproduction, adaptation, and distribution of the article provided the original author and source are credited.Keywords
- Basal ganglia
- Excitoxicity
- Putamen
- Ventral striatum
- Movement disorders
- Locomotion