Chapter 13 Neurotrauma/neurodegeneration and mitochondrial dysfunction

• Published in: Progress in Brain Research Vol. 137; pp. 171 - 176
• Main Authors: Frantseva, Marina, Perez Velazquez, Jose Luis, Tonkikh, Alexandre, Adamchik, Yana, Carlen, Peter L.
• Format: Book Chapter
• Language: English
• Published: Elsevier Science & Technology 2002
• ISBN: 9780444508171; 0444508171
• ISSN: 0079-6123; 1875-7855
• DOI: 10.1016/S0079-6123(02)37015-8

This chapter focuses on neurodegeneration and mitochondrial dysfunction. The chapter presents the in vitro model of ischemic injury, which consists of superfusing organotypic cultured hippocampal slices with glucose-free deoxygenated solution for 8 min. After an ischemic episode, free radicals are produced in pyramidal neurons mostly during reoxygenation and intracellular calcium levels increase in parallel to free radical generation. The chapter presents evidence for a prolonged mitochondrial depolarization, indicative of the mitochondrial permeability transition (MPT), during reperfusion in organotypic hippocampal neurons, by using two mitochondrial dyes: rhodamine 123 and JC-1. Mitochondrial dysfunction results from several converging deleterious mechanisms. Mitochondrial dysfunction also plays a major role in traumatic cell death. To date mitochondria have been little studied for their involvement in traumatic brain injury, but they could be an important therapeutic target for the early treatment and prevention of secondary brain and spinal cord damage.