Recovery of Sensorimotor Function After Distal Middle Cerebral Artery Photothrombotic Occlusion in Rats

Background and Purpose The purpose of the present study was to delineate the behavioral correlates of focal thrombotic occlusion of the distal middle cerebral artery in rats and to compare the pattern of deficits and subsequent recovery to that following proximal middle cerebral artery occlusion. Methods Ten Sprague-Dawley rats underwent photothrombotic occlusion of the distal middle cerebral artery with tandem occlusion of the common carotid arteries (dMCAO group); 10 animals served as operated controls. Beginning on postischemia day 2, animals were given a battery of five tests that assessed sensorimotor integration, attentional mechanisms, and muscle strength; testing continued twice weekly until day 30. Nine days of cognitive testing on the learning set of the water maze task were then given. Infarct volume and hemispheric atrophy were determined for each dMCAO animal. Results After ischemia, the dMCAO group exhibited significant behavioral deficits in posture reflex, ability to place a forelimb to various stimuli, limb adduction during rearing, and neglect of contralateral space. These deficits showed variable recovery rates. No deficits were observed in muscle strength or cognitive performance. The deficits and patterns of recovery were related to infarct location and to degree of hemisphere atrophy. Conclusions The present study suggests that a battery of tests is necessary to fully characterize the pattern of behavioral deficits after focal cerebral ischemia. Location of infarct damage and associated degree of hemispheric atrophy were important variables in determining behavioral outcome. The present results are compared with those of the more traditional model of electrocoagulation of the proximal middle cerebral artery.

[1]  C G Markgraf,et al.  Comparative Histopathologic Consequences of Photothrombotic Occlusion of the Distal Middle Cerebral Artery in Sprague‐Dawley and Wistar Rats , 1993, Stroke.

[2]  E. J. Green,et al.  Sensorimotor and cognitive consequences of middle cerebral artery occlusion in rats , 1992, Brain Research.

[3]  G. Clincke,et al.  Neocortical localization of tactile/proprioceptive limb placing reactions in the rat , 1992, Brain Research.

[4]  T. Jones,et al.  Functional subdivisions of the rat somatic sensorimotor cortex , 1990, Behavioural Brain Research.

[5]  M D Ginsberg,et al.  Rodent models of cerebral ischemia. , 1989, Stroke.

[6]  M. Borgers,et al.  Photochemical stroke model: flunarizine prevents sensorimotor deficits after neocortical infarcts in rats. , 1989, Stroke.

[7]  Y. Olsson,et al.  Neurologic and neuropathologic outcome after middle cerebral artery occlusion in rats. , 1989, Stroke.

[8]  R. Auer,et al.  Neurobehavioral deficit due to ischemic brain damage limited to half of the CA1 sector of the hippocampus , 1989, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[9]  S. Ohnishi,et al.  Interrelationship of brain edema, motor deficits, and memory impairment in rats exposed to focal ischemia. , 1989, Stroke.

[10]  M. Ginsberg,et al.  (S)‐Emopamil, a novel calcium channel blocker and serotonin S2 antagonist, markedly reduces infarct size following middle cerebral artery occlusion in the rat , 1988, Neurology.

[11]  W. Dietrich,et al.  Photochemically stimulated blood-borne factors induce blood-brain barrier alterations in rats. , 1988, Stroke.

[12]  A. Tamura,et al.  Behavioral changes after focal cerebral ischemia by left middle cerebral artery occlusion in rats , 1988, Brain Research.

[13]  L. Pitts,et al.  The therapeutic value of nimodipine in experimental focal cerebral ischemia. Neurological outcome and histopathological findings. , 1987, Journal of neurosurgery.

[14]  B. Kolb,et al.  Behavioural and anatomical studies of the posterior parietal cortex in the rat , 1987, Behavioural Brain Research.

[15]  T. Schallert,et al.  Recovery of function after brain damage: Severe and chronic disruption by diazepam , 1986, Brain Research.

[16]  E. Hogan,et al.  A model of focal ischemic stroke in the rat: reproducible extensive cortical infarction. , 1986, Stroke.

[17]  L. Pitts,et al.  Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. , 1986, Stroke.

[18]  Ian Q. Whishaw,et al.  Formation of a place learning-set by the rat: A new paradigm for neurobehavioral studies , 1985, Physiology & Behavior.

[19]  F. Bolgert,et al.  Pure Sensory Stroke Caused by a Small Cortical Infarct in the Middle Cerebral Artery Territory , 1984, Stroke.

[20]  G. Ettlinger,et al.  Subcortical neglect. , 1984, Neurology.

[21]  R. Sutherland,et al.  A comparison of the contributions of the frontal and parietal association cortex to spatial localization in rats. , 1983, Behavioral neuroscience.

[22]  義昭 田崎,et al.  Pure sensory strokeの臨床的検討 , 1982 .

[23]  R. Morris,et al.  Place navigation impaired in rats with hippocampal lesions , 1982, Nature.

[24]  T. Schallert,et al.  Rescuing neurons from trans-synaptic degeneration after brain damage: helpful, harmful, or neutral in recovery of function? , 1990, Canadian journal of psychology.

[25]  D B Hier,et al.  Caudate infarcts. , 1990, Archives of neurology.

[26]  Prof. Dr. Karl Zilles The Cortex of the Rat , 1985, Springer Berlin Heidelberg.