Neuronal plasticity after ischemic preconditioning and TIA-like preconditioning ischemic periods.
Transient ischemic attacks (TIAs) have recently become the center of attention since they are thought to share some characteristics with experimental ischemic preconditioning (IPC). This phenomenon describes the situation that a brief, per se harmless, cerebral ischemic period renders the brain resistant to a subsequent severe and normally damaging ischemia. Preconditioning (PC) is not restricted to the brain but also occurs in other organs. Furthermore, apart from a short ischemia, the PC event may comprise nearly any noxious stimulus which, however, must not exceed the threshold to tissue damage. In the last two decades, our knowledge concerning the underlying molecular basis of PC has substantially grown and there is hope to potentially imitate the induction of an endogenous neuroprotective state in patients with a high risk of cerebral ischemia. While, at present, there is virtually no neuropathological data on changes after TIAs or TIA-like PC ischemic periods in human brains, the following review will briefly summarize the current knowledge of plastic neuronal changes after PC in animal models, still awaiting their detection in the human brain.
Sommer
Clemens
C
Department of Neuropathology, Mainz University Medical Center, Langenbeckstrasse 1, 55131, Mainz, Germany. sommer@neuropatho.klinik.uni-mainz.de
D000818:Animals; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000473:pathology* / Q000503:physiopathology; D019194:Ischemic Preconditioning / Q000379:methods; D009473:Neuronal Plasticity; D009474:Neurons / Q000473:pathology; D013997:Time Factors