THE DIFFERENCE BETWEEN KETAMINE AND PROPOFOL ADMINISTRATION TO INDUCE APOPTOSIS NEURODEGENERATION IN MICE CEREBRAL CORTEX
Copyright (c) 2019 Nameer Fadhel Gaeb
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Background: The ketamine and propofol stimulates neuroapoptosis in the mice brain if administration. The programmed cell death (apoptosis) follows regular growth of the central nervous system. The mechanisms that normalize neurons is submit to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors generate common apoptotic neurodegeneration in the developing mice brain, suggesting that excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal perseverance.
Objectives: This study aims to study the neurotoxic significance of either ketamine or propofol exposure on mice brain using immunohistochemical marker.
Methods: administration of ketamine or propofol intraperitonially at normal dose to mice and assessed the degree of neuroapoptosis (Programmed cell death) in frontal cortex of the brain areas following either saline or normal drug doses administration (ketamine or propofol). Each drug was administered as only one-time inject in dose range that would be measured anesthetic dose, and the brains were evaluated by immunohistochemical marker methods five hours following drug administration. Neuroapoptosis (Programmed cell death) was identified by Immunohistochemical antibodies to malondialdehyde (MDA). The ketamine or propofol produced a dose-dependent, statistically significant increase in the rate of neuroapoptosis (Programmed cell death).
Conclusion: mild administration of ketamine or propofol can trigger apoptotic neurodegeneration in the developing mice brain frontal cortex.