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Effects of the AT₁ Receptor Antagonist L-158,809 on Microglia and Neurogenesis after Fractionated Whole-Brain Irradiation
Kelly R. Conner, Valerie S. Payne, M. Elizabeth Forbes, Mike E. Robbins and David R. Riddle
Vol. 173, No. 1 (Jan., 2010), pp. 49-61
Published by: Radiation Research Society
Stable URL: http://www.jstor.org/stable/40539814
Page Count: 13
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Cognitive dysfunction develops in approximately 50% of patients who receive fractionated whole-brain irradiation and survive 6 months or more. The mechanisms underlying these deficits are unknown. A recent study demonstrated that treatment with the angiotensin II type 1 receptor antagonist (AT₁ RA) L-158,809 before, during and after fractionated wholebrain irradiation prevents or ameliorates radiation-induced cognitive deficits in adult rats. Given that (1) AT, RAs may function as anti-inflammatory drugs, (2) inflammation is thought to contribute to radiation injury, and (3) radiation-induced inflammation alters progenitor cell populations, we tested whether the cognitive benefits of L-158,809 treatment were associated with amelioration of the sustained neuroinflammation and changes in neurogenesis that are induced by fractionated whole-brain irradiation. In rats examined 28 and 54 weeks after irradiation, L-158,809 treatment did not alter the effects of radiation on the number and activation of microglia in the perirhinal cortex and hippocampus, nor did it prevent the radiation-induced decrease in proliferating cells and immature neurons in the hippocampus. These findings suggest that L-158,809 does not prevent or ameliorate radiation-induced cognitive deficits by modulation of chronic inflammatory mechanisms, but rather may reduce radiation-induced changes that occur earlier in the postirradiation period and that lead to Cognitive dysfunction.
Radiation Research © 2010 Radiation Research Society