Role of Collapsin-Response Mediator Protein 2 in the Development of Epileptic Seizures in Clinics and Experimental Models

Abstract

Problems of the engagement of collapsin-response mediator protein 2 (CRMP2) in the induction of epileptic seizures and the interrelationship between epileptic activity and the back-remodeling process in brain neurons were examined. The first part of the study was carried out in clinics. Chronic patients of both sexes (pre-puberty age) formed the patient group (n = 20), whereas 15 healthy persons of the same age served as the control group. The blood samples were taken from the patients within the free-of- seizure timeframe, and the platelets and serum were saved. The levels of CRMP2 and βIII tubulin were evaluated in the patient platelets, and the levels of natural anti-CRMP2 autoantibody and nerve growth factor (NGF) were evaluated in the serum samples with an indirect ELISA test. Downregulation of CRMP2 and βIII tubulin in the platelets, sharp downregulation of natural anti-CRMP2 autoantibody, and upregulation of NGF in the serum samples were revealed. In the second (experimental) series, epileptic seizures were induced in the Chinchilla male rabbits through penicillin microapplication into the basolateral portion of the amygdala. Microapplication of CRMP2 into the brain lateral ventricle 4–5 min later provided termination of epileptic seizures. The effect of the intracerebral administration of polyclonal anti-CRMP2 antibody to stress-tolerant Wistar male rats on their tolerance to audiogenic stress (90–120 dB, 3 min) was also examined. Antibody administration did not decrease the tolerance of the stress-tolerant rats to audiogenic stress and did not elicit epileptic seizures in them. The results obtained give grounds to formulate a conclusion on the negative relationship between the CRMP2 level and both the induction of epileptic seizures and the process of back remodeling in the brain neurons.