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Ketamine treatment affects hippocampal but not cortical mitochondrial function in prepubertal rats.

07:00 EST 13th February 2020 | BioPortfolio

Summary of "Ketamine treatment affects hippocampal but not cortical mitochondrial function in prepubertal rats."

Previous reports have shown that ketamine triggered apoptosis in immature developing brain involving mitochondrial mediated pathways. However, no data for ketamine effects on hippocampal and cortical mitochondrial function are available in pre-pubertal rats. Twenty-one days-old Sprague-Dawley rats received ketamine (40 mg/Kg i.p.) for 3 days and were sacrificed 24 hours after last injection. Hippocampal mitochondria from ketamine-treated rats showed decreased malate-glutamate state 4 and 3 respiratory rates and an inhibition in Complex I and IV activities. Hippocampal mitochondrial membrane depolarization and mitochondrial permeability transition induction were observed. This was not reflected in an increment of H O production probably due to increased Mn-SOD and catalase activities, 24 hours after treatment. Interestingly, increased H O production rates and cardiolipin oxidation were found in hippocampal mitochondria shortly after ketamine treatment (45 min). Unlike hippocampus, ketamine did not affect mitochondrial parameters in brain cortex, being this area less vulnerable to suffer ketamine-induced oxidative damage. Results provide evidences that exposure of pre-pubertal rats to ketamine leads to an induction of mitochondrial ROS generation at early stages of treatment, that was normalized by the triggering of antioxidant systems. Although hippocampal mitochondria from pre-pubertal rats were capable of respond to the oxidative stress, they remain partially dysfunctional.

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This article was published in the following journal.

Name: International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
ISSN: 1873-474X
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