Ketamine treatment affects hippocampal but not cortical mitochondrial function in prepubertal rats
| Autor: | Silvia Lores-Arnaiz, Analía G. Karadayian, Analía Czerniczyniec, Juanita Bustamante |
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| Rok vydání: | 2019 |
| Předmět: |
Mitochondrial ROS
Male medicine.medical_specialty Malates Hippocampus Glutamic Acid Apoptosis Mitochondrion Hippocampal formation medicine.disease_cause Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Oxygen Consumption Developmental Neuroscience Internal medicine medicine Cardiolipin Animals Ketamine 030304 developmental biology Cerebral Cortex Membrane Potential Mitochondrial 0303 health sciences Chemistry Superoxide Dismutase Catalase Mitochondria Rats Oxidative Stress Endocrinology Mitochondrial permeability transition pore Excitatory Amino Acid Antagonists 030217 neurology & neurosurgery Oxidative stress Developmental Biology medicine.drug Signal Transduction |
| Zdroj: | International journal of developmental neuroscience : the official journal of the International Society for Developmental NeuroscienceREFERENCES. 80(3) |
| ISSN: | 1873-474X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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