Facilitated recovery from postischemic suppression of protein synthesis in the gerbil brain with ischemic tolerance.
Preconditioning of the gerbil brain with a 2-min period of sublethal ischemia followed by 4 days of reperfusion protects against neuronal damage following a subsequent 3-min period of ischemia, which normally destroys pyramidal neurons in the CA1 region of the hippocampus. To clarify the role of protein synthesis in this ischemic tolerance phenomenon, we performed an autoradiographic analysis with [14C]leucine at 4 h, 24 h, and 48 h after 3 min of ischemia with and without preconditioning. General protein synthesis in the CA1 region was severely suppressed after 4 h in both groups. The protein synthesis in CA1 partially recovered after 24 h and fully recovered after 48 h in animals with preconditioning, but never recovered in animals without preconditioning. Protein synthesis in the neocortex and the striatum was suppressed in the early reperfusion periods only in animals without preconditioning. The results show that the ischemic tolerance is closely related to the facilitated recovery from suppressed protein synthesis in the brain after ischemia.
Kato
H
H
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Kogure
K
K
Nakata
N
N
Araki
T
T
Itoyama
Y
Y
D000222:Adaptation, Physiological; D000818:Animals; D001345:Autoradiography; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology*; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism; D007930:Leucine / Q000378:metabolism; D008297:Male; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D015424:Reperfusion; D013997:Time Factors
D009419:Nerve Tissue Proteins; D007930:Leucine