The effect of ischemic preconditioning on hippocampal mitochondria
Field:	Disorders of the nervous system
Authors:	Rytter, Anna Mattiasson, Gustav Wieloch, Tadeusz
Address of presenting author:	Experimental Brain Research Wallenberg Neuroscience Center 221 85 LUND, Sweden
E-mail:	Anna.Rytter@expbr.lu.se
Phone:	046-2220613
Fax:	046-2220615
Text of abstract:	Aim: Brains that have been exposed to a short period of sub-lethal ischemia are resistant to damage caused by a subsequent period of ischemia. The mechanisms whereby ischemic tolerance is achieved are yet poorly understood, but may be linked to the regulation of signals/events normally involved in cell injury. Mitochondria have a pivotal role in ischemic cell death, and therefore we examined how preconditioning affected mitochondrial physiology. Methods: Ischemic tolerance was induced by three minutes of bilateral carotid artery occlusion. Rat hippocampal mitochondria were isolated 48 hours after preconditioning ischemia/sham operation. Mitochondrial calcium uptake was measured using calcium green, and respiratory activity as oxygen consumption. Mitochondrial membrane potential, swelling and production of reactive oxygen species were analyzed by flow cytometry. Mitochondria from preconditioned brains took up less calcium than non-treated mitochondria, and also released it quicker. Preliminary data showed no change in respiratory activity after preconditioning. We have previously shown that preconditioning leads to a transient activation of pathological cell signalling, which may activate negative feedback loops leading to downregulation of lethal signalling. As cellular calcium homeostasis is a key regulator of many cell signalling cascades it is possible that the change in calcium uptake capabilities induced by preconditioning is involved in the regulation of detrimental cell signalling.
Keywords:	ischemia, preconditioning, mitochondria

Created 2000-03-15