Locomotor and passive avoidance deficits following occlusion of the middle cerebral artery.
The characterization of sensory, motor and cognitive dysfunctions following occlusion of the middle cerebral artery (MCA) is prerequisite to investigations of treatment intervention in animal models of ischemia. Different strategies are used to induce ischemia, but the focal, transient occlusion of the MCA has been reported to result in neuropathology most similar to that seen in clinical cerebral ischemia. If the MCA occlusion technique results in a stroke animal model, then the behavioral impairments inherent in stroke should be manifested in this model. The present study provides a further characterization of behavioral alterations associated with MCA occlusion. Sprague-Dawley rats underwent temporal occlusion of the right MCA, and at 1 mo and 2 mo postischemia, were subsequently tested in passive avoidance behavior, motor coordination, asymmetrical motor behavior, neurological functioning, nocturnal spontaneous and amphetamine-induced locomotor activity, and haloperidol-induced catalepsy. Results revealed that ischemic rats showed long-term impairments in sensory, motor and cognitive functions. The discrepancy with other studies reporting temporal MCA-induced behavioral deficits may be due to techniques used to induce ischemia and consequent CNS damage, differences in time period of testing (i.e., immediate vs. later postischemia, nighttime vs. daytime), number of test-retests over the course of the experiment, and age of the animals. The mechanism involved in the MCA-induced behavioral changes may be represented by loss of dopamine receptors on striatal neurons. Histological analysis revealed damage limited to the lateral aspect of the striatum. These behavioral and anatomical data support MCA occlusion as a model of ischemia, and elucidate important factors that should be controlled for in characterizing the MCA-induced neuropathological alterations.
Borlongan
C V
CV
Department of Surgery, University of South Florida College of Medicine, Tampa 33612, USA.
Cahill
D W
DW
Sanberg
P R
PR
D000110:Acetylcholinesterase / Q000378:metabolism; D000661:Amphetamine / Q000494:pharmacology; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000033:anatomy & histology / Q000201:enzymology; D002375:Catalepsy / Q000139:chemically induced / Q000523:psychology; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D002536:Cerebral Arteries / Q000502:physiology*; D003071:Cognition / Q000187:drug effects / Q000502:physiology; D018492:Dopamine Antagonists / Q000494:pharmacology; D006220:Haloperidol; D006651:Histocytochemistry; D002546:Ischemic Attack, Transient / Q000201:enzymology / Q000523:psychology*; D008568:Memory / Q000502:physiology; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D004856:Postural Balance / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley
D000697:Central Nervous System Stimulants; D018492:Dopamine Antagonists; D000661:Amphetamine; D000110:Acetylcholinesterase; D006220:Haloperidol