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
AUTHORS (6)
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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