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Ketamine treatment affects hippocampal but not cortical mitochondrial function in prepubertal rats.
Czerniczyniec, Analía; Karadayian, Analía G; Bustamante, Juanita; Lores-Arnaiz, Silvia.
Afiliación
  • Czerniczyniec A; Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
  • Karadayian AG; Instituto de Bioquímica y Medicina Molecular (IBIMOL), CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina.
  • Bustamante J; Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
  • Lores-Arnaiz S; Instituto de Bioquímica y Medicina Molecular (IBIMOL), CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina.
Int J Dev Neurosci ; 80(3): 175-187, 2020 May.
Article en En | MEDLINE | ID: mdl-32053738
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 prepubertal rats. Twenty-one-day-old Sprague-Dawley rats received ketamine (40 mg/kg i.p.) for 3 days and were killed 24 hr after the 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 H2 O2 production probably due to increased Mn-SOD and catalase activities, 24 hr after treatment. Interestingly, increased H2 O2 production rates and cardiolipin oxidation were found in hippocampal mitochondria shortly after ketamine treatment (45 min). Unlike the hippocampus, ketamine did not affect mitochondrial parameters in the brain cortex, being the area less vulnerable to suffer ketamine-induced oxidative damage. Results provide evidences that exposure of prepubertal 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 prepubertal rats were capable of responding to the oxidative stress, they remain partially dysfunctional.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Corteza Cerebral / Estrés Oxidativo / Antagonistas de Aminoácidos Excitadores / Hipocampo / Ketamina / Mitocondrias Límite: Animals Idioma: En Revista: Int J Dev Neurosci Año: 2020 Tipo del documento: Article País de afiliación: Argentina Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Corteza Cerebral / Estrés Oxidativo / Antagonistas de Aminoácidos Excitadores / Hipocampo / Ketamina / Mitocondrias Límite: Animals Idioma: En Revista: Int J Dev Neurosci Año: 2020 Tipo del documento: Article País de afiliación: Argentina Pais de publicación: Estados Unidos