Nonocclusive common carotid artery thrombosis in the rat results in reversible sensorimotor and cognitive behavioral deficits

N. E. Alexis, W. Dalton Dietrich, E. J. Green, R. Prado, B. D. Watson, M. De Ryck

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Background and Purpose: Microemboli released during transient ischemic attack, stroke, and cardiac surgery are thought to cause a variety of functional deficits in humans. The purpose of this study was to characterize the type and extent of neurobehavioral deficits present after photochemically induced common carotid artery thrombosis (CCAT), a thromboembolic model of stroke in the rat that results in a platelet emboli shower. Methods: Thirty- two male Wistar rats were assigned to four groups, Groups 1 (n=8) and 3 (n=8) were long-term (6-week survival) and short-term (2-week survival) experimental groups subjected to right CCAT with the use of the photochemical technique. Groups 2 (n=8) and 4 (n=8) served as sham-operated controls for each experimental group. A battery of behavioral tests was applied daily beginning 24 hours after thrombosis: this consisted of elicited forelimb placing, postural reflex, beam balance, beam walking, and open field activity. Cognitive testing with a water maze task was performed on post- CCAT days 30 to 33 for groups 1 and 2 and on post-CCAT day 2 for groups 3 and 4. Ten-micrometer coronal brain sections were stained wit hematoxylin and eosin, and infarct location and frequency were determined. Results: Significant sensorimotor deficits were observed, which recovered within 2 weeks after CCAT. The data that follow are derived by combining the two experimental groups and comparing these with the two sham groups. The following tests showed significant effects after CCAT: contralateral elicited forelimb placing, ipsilateral elicited forelimb placing, beam balance, and beam walking score. Cognitive dysfunction was seen acutely (group 3 animals) at 2 days after CCAT: Morris water maze length and latency to target were significantly greater in the experimental group. No deficits were seen in postural reflex, open field activity, or delayed cognitive testing. Histopathological assessment revealed small infarcts in 11 of 16 thrombosed rats. However, a strong relationship between neurobehavioral deficits and infarct location was not consistently demonstrated. Conclusions: CCAT produces consistent sensorimotor and cognitive behavioral deficits that recover within 2 weeks of injury. Behavioral outcome was not necessarily associated with overt histopathological damage, suggesting that reversible injury mechanisms, both vascular and neuronal, may be partly responsible for the temporary loss of function. These data strengthen the role of CCAT as a clinically relevant model of thromboembolic stroke.

Original languageEnglish
Pages (from-to)2338-2346
Number of pages9
JournalStroke
Volume26
Issue number12
StatePublished - Jan 1 1995

Fingerprint

Carotid Artery Thrombosis
Forelimb
Stroke
Walking
Reflex
Thrombosis
Wit and Humor
Survival
Water
Transient Ischemic Attack
Wounds and Injuries
Hematoxylin
Eosine Yellowish-(YS)
Embolism
Thoracic Surgery
Blood Vessels
Wistar Rats
Blood Platelets

Keywords

  • behavior, animal
  • cerebral ischemia
  • cognition
  • rats
  • stroke

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

Nonocclusive common carotid artery thrombosis in the rat results in reversible sensorimotor and cognitive behavioral deficits. / Alexis, N. E.; Dalton Dietrich, W.; Green, E. J.; Prado, R.; Watson, B. D.; De Ryck, M.

In: Stroke, Vol. 26, No. 12, 01.01.1995, p. 2338-2346.

Research output: Contribution to journalArticle

Alexis, N. E. ; Dalton Dietrich, W. ; Green, E. J. ; Prado, R. ; Watson, B. D. ; De Ryck, M. / Nonocclusive common carotid artery thrombosis in the rat results in reversible sensorimotor and cognitive behavioral deficits. In: Stroke. 1995 ; Vol. 26, No. 12. pp. 2338-2346.
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AU - De Ryck, M.

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N2 - Background and Purpose: Microemboli released during transient ischemic attack, stroke, and cardiac surgery are thought to cause a variety of functional deficits in humans. The purpose of this study was to characterize the type and extent of neurobehavioral deficits present after photochemically induced common carotid artery thrombosis (CCAT), a thromboembolic model of stroke in the rat that results in a platelet emboli shower. Methods: Thirty- two male Wistar rats were assigned to four groups, Groups 1 (n=8) and 3 (n=8) were long-term (6-week survival) and short-term (2-week survival) experimental groups subjected to right CCAT with the use of the photochemical technique. Groups 2 (n=8) and 4 (n=8) served as sham-operated controls for each experimental group. A battery of behavioral tests was applied daily beginning 24 hours after thrombosis: this consisted of elicited forelimb placing, postural reflex, beam balance, beam walking, and open field activity. Cognitive testing with a water maze task was performed on post- CCAT days 30 to 33 for groups 1 and 2 and on post-CCAT day 2 for groups 3 and 4. Ten-micrometer coronal brain sections were stained wit hematoxylin and eosin, and infarct location and frequency were determined. Results: Significant sensorimotor deficits were observed, which recovered within 2 weeks after CCAT. The data that follow are derived by combining the two experimental groups and comparing these with the two sham groups. The following tests showed significant effects after CCAT: contralateral elicited forelimb placing, ipsilateral elicited forelimb placing, beam balance, and beam walking score. Cognitive dysfunction was seen acutely (group 3 animals) at 2 days after CCAT: Morris water maze length and latency to target were significantly greater in the experimental group. No deficits were seen in postural reflex, open field activity, or delayed cognitive testing. Histopathological assessment revealed small infarcts in 11 of 16 thrombosed rats. However, a strong relationship between neurobehavioral deficits and infarct location was not consistently demonstrated. Conclusions: CCAT produces consistent sensorimotor and cognitive behavioral deficits that recover within 2 weeks of injury. Behavioral outcome was not necessarily associated with overt histopathological damage, suggesting that reversible injury mechanisms, both vascular and neuronal, may be partly responsible for the temporary loss of function. These data strengthen the role of CCAT as a clinically relevant model of thromboembolic stroke.

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