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(American Journal of Pathology. 2001;158:2145-2151.)
© 2001 American Society for Investigative Pathology

Regular Article

Hibernation, a Model of Neuroprotection

Fang Zhou*, Xiongwei Zhu{dagger}, Rudy J. Castellani{dagger}, Raphaela Stimmelmayr*, George Perry{dagger}, Mark A. Smith{dagger} and Kelly L. Drew*

From the Institute of Arctic Biology and Department of Chemistry and Biochemistry,*
University of Alaska Fairbanks, Fairbanks, Alaska; and the Institute of Pathology,{dagger}
Case Western Reserve University, Cleveland, Ohio

Hibernation, a natural model of tolerance to cerebral ischemia, represents a state of pronounced fluctuation in cerebral blood flow where no brain damage occurs. Numerous neuroprotective aspects may contribute in concert to such tolerance. The purpose of this study was to determine whether hibernating brain tissue is tolerant to penetrating brain injury modeled by insertion of microdialysis probes. Guide cannulae were surgically implanted in striatum of Arctic ground squirrels before any of the animals began to hibernate. Microdialysis probes were then inserted in some animals after they entered hibernation and in others while they remained euthermic. The brain tissue from hibernating and euthermic animals was examined 3 days after implantation of microdialysis probes. Tissue response, indicated by examination of hematoxylin and eosin-stained tissue sections and immunocytochemical identification of activated microglia, astrocytes, and hemeoxygenase-1 immunoreactivity, was dramatically attenuated around probe tracks in hibernating animals compared to euthermic controls. No difference in tissue response around guide cannulae was observed between groups. Further study of the mechanisms underlying neuroprotective aspects of hibernation may lead to novel therapeutic strategies for stroke and traumatic brain injury.




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