Changes in the expression levels of semaphorin 3A (SEMA3A) in an in vivo model of acute excitotoxicity

Abstract

The nervous system is undoubtedly one of the most important and complex tissue systems that exist in the animal body. It is involved in controlling and coordinating the body at multitudinous levels. At the cellular level, the neurons along with neuroglia function in a choreographed manner to transmit information across synapses using neurotransmitters. Glutamate is one of the major excitatory neurotransmitters which is involved in synaptic plasticity and excitotoxicity. During excitotoxicity, over stimulation of the glutamate receptor, N-methyl-D-aspartate receptor (NMDAR) results in influx of lethal doses of Ca2+. Semaphorins (SEMA) are a class of transmembrane proteins that are secreted upon processing and are involved in the development of nervous system and axonal guidance. SEMA and associated proteins function by inducing cell death and has been found to be associated with various neurodegenerative diseases in the adult brain (Quintremil et al., 2018).In this study, we have analyzed the changes in the expression level of SEMA3A in cortical tissue samples obtained from an in vivo acute excitotoxicity model, created by injecting saline and NMDA (40 μg/Kg body weight) via intracerebroventricular (ICV) route into the left and right lateral ventricles respectively (Kumar et al.,2019). No significant change in the expression ofSEMA3A protein was observed30 mins after NMDA treatment. This study indicates that the level ofSEMA3A may not be affected during an acute excitotoxic event.