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CNS & Neurological Disorders - Drug Targets


ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

Stress-Induced Oxidative Changes in Brain

Author(s): Jose L. M. Madrigal, Borja Garcia-Bueno, Javier R. Caso, Beatriz G. Perez-Nievas and Juan C. Leza

Volume 5 , Issue 5 , 2006

Page: [561 - 568] Pages: 8

DOI: 10.2174/187152706778559327

Price: $65


Numerous systems and organs are affected by stress. In this review we will focus on the effects in brain. Some of the most impressive effects of the stress in brain are the atrophy of hippocampal dendrites or even the reduction of the hippocampal size observed in brains from subjects exposed to severe or chronic stress. Obviously, before reaching this point of damage there are many other processes taking place in the stressed CNS. The release of glucocorticoids is one of the first features of the stress response. Glucocorticoids can result in neurotoxicity through different mechanisms, including modifications in the energy metabolism or via an increase in excitatory amino acids such as glutamate in the extracellular space. Glutamate can induce neuronal excitotoxicity. This sequence of events leads to the activation of TNFα convertase (TACE) and TNFα release in brain of rats subjected to restraint stress. One of the multiple effects exerted by this cytokine is to initiate the translocation of the transcription factor NFκB to neuronal nuclei. NFκB activation results in the induction of iNOS and COX2, two enzymes responsible for a great portion of the neurological damage produced in models of stress.

Keywords: ACTH, superoxide dismutase, NMDA, cytokines, transcription factor family, NOS isoenzyme

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