The Difference Between Ketamine and Propofol Administration to Induce Apoptosis Neurodegeneration in Mice Cerebral Cortex

Abstract

Background:Theketamineand propofol stimulatesneuroapoptosisin the mice brain if administration. The  programmed  cell  death  (apoptosis) followsregulargrowthof  the  central  nervous  system. The mechanisms  that normalizeneurons issubmitto  apoptosis  are poorlyunderstood.  Blockade  of  N-methyl-D-aspartate (NMDA) glutamate receptors generatecommonapoptotic neurodegeneration in the developingmice brain,  suggesting  that  excitatory  neurotransmitter  glutamate,  acting  at  NMDA receptors, controls neuronal perseverance. Objectives: This study aims to studythe neurotoxic significanceofeitherketamineor propofolexposure on mice brain using immunohistochemical marker.Methods:administration of ketamine orpropofol intraperitoniallyatnormal dosetomice and assessedthe degreeof  neuroapoptosis(Programmed  cell  death)in frontal cortex  of  thebrain areasfollowingeither saline or normal drugdosesadministration(ketamine or propofol).Each drug was administered as onlyone-time inject  in dose  range  that  would  be measuredanestheticdose,  and  the  brains  were evaluatedby immunohistochemical   markermethods fivehoursfollowing   drug administration. Neuroapoptosis (Programmed  cell  death)was identifiedby Immunohistochemical  antibodies  to malondialdehyde (MDA). Theketamine or propofolproduceda dose-dependent, statistically significant increase in the rate of neuroapoptosis(Programmed cell death). Conclusion: mildadministrationofketamine  orpropofolcan  trigger  apoptotic neurodegeneration  in the developing mice brainfrontal cortex