Sleep deprivation prior to transient global cerebral ischemia attenuates glial reaction in the rat hippocampal formation.
This study was aimed to ascertain the effect of sleep deprivation on subsequent cerebral ischemia in the rat hippocampal formation. Seven days after transient global cerebral ischemia induced by four-vessel occlusion method, most of the pyramidal cells in the hippocampal CA1 subfield underwent disruption and pyknosis as detected by cresyl violet staining. With OX-42, OX-18, OX-6 and ED1 immunohistochemistry, robust microglia/macrophage reactions were observed in the CA1 and dentate hilus. The majority of reactive microglia was rod-shaped, bushy or amoeboidic cells bearing hypertrophic processes. Astrocytes also displayed hypertrophic processes, whose immunostaining for glial fibrillary acidic protein was markedly enhanced. The ischemia-induced neuronal damage and glial reactions, however, were noticeably attenuated in rats subjected to pretreatment with sleep deprivation for five consecutive days. The most drastic effect was the diminution of OX-18, OX-6 and ED1 immunoreactivities, suggesting that the immune potentiality and/or phagocytosis of these cells was suppressed by prolonged sleep deprivation prior to ischemic insult. It is postulated that sleep deprivation may have a preconditioning influence on subsequent lethal cerebral ischemia. Hence, sleep deprivation may be considered as a therapeutic strategy in brain ischemic damage.
Hsu
Jee-Ching
JC
Department of Anesthesiology, Chang-Gung Memorial Hospital, Taipai, Taiwan. ctlan@csmu.edu.tw
Lee
Ying-Shiung
YS
Chang
Chen-Nen
CN
Ling
Eng-Ang
EA
Lan
Chyn-Tair
CT
D000818:Animals; D005260:Female; D006624:Hippocampus / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control*; D008297:Male; D009457:Neuroglia / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012892:Sleep Deprivation / Q000378:metabolism