Apoptotic Process Induced by Oxaliplatin in Rat Hippocampus Causes Memory Impairment

Male 0301 basic medicine Copper Sulfate Organoplatinum Compounds Physiological Cells Intraventricular Antidotes Antineoplastic Agents Apoptosis Hippocampus Absorption Injections Cell Line Antineoplastic Agent Random Allocation 03 medical and health sciences Hippocampu Cognition 0302 clinical medicine Avoidance Learning Animals Intraperitoneal Cells, Cultured Injections, Intraventricular Neurons Behavior Memory Disorders Cultured Behavior, Animal Animal Absorption, Physiological; Animals; Antidotes; Antineoplastic Agents; Apoptosis; Avoidance Learning; Behavior, Animal; Cell Line; Cells, Cultured; Cognition; Copper Sulfate; Exploratory Behavior; Hippocampus; Injections, Intraperitoneal; Injections, Intraventricular; Male; Memory Disorders; Neurons; Organoplatinum Compounds; Oxaliplatin; Random Allocation; Rats; Social Learning Organoplatinum Compound Apoptosi Neuron Social Learning Absorption, Physiological Oxaliplatin Medicine (all); Toxicology; Pharmacology Antidote Exploratory Behavior Rat Injections, Intraperitoneal Memory Disorder
DOI: 10.1111/bcpt.12629 Publication Date: 2016-06-06T15:08:49Z
ABSTRACT
AbstractAspects of memory involved in cognitive mechanisms were investigated in rat after oxaliplatin (OX) chemotherapy using animal behavioural assessment of passive avoidance and social learning paradigms, which are both hippocampus‐sensitive. Rodents, previously subjected to 2‐week OX treatment, showed passive avoidance and social learning impairment and apoptotic processes in the hippocampus. Apoptosis rate significantly increased in cultured hippocampal cells exposed to OX at increasing doses, and this effect was dose‐dependent. Ex vivo experiments showed that cell damage and apoptosis were blocked in the hippocampus from OX rats cotreated with copper sulphate (CS) which precludes OX transport inside the cell. In vivo, passive avoidance and social learning impairment could not be observed in OX rats co‐administered with CS. Thus, a site of action of OX treatment on memory impairment appears to be located at the hippocampus. These findings strongly support that cellular damage induced by OX in rodent hippocampus underlies the weakening of some memory functions.
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