Neurodegeneration of dopaminergic neurons in the central and peripheral nervous system arises due to several highly intricate neurotoxic mechanisms in specific neuronal pathways / tracts.  Among the various neurotoxic mechanisms, excitotoxicity has a great impact on the survival of the dopaminergic neurons. Most of the present neurotoxins primarily target tyrosine hydroxylase (synthesizing enzyme) to exert its dopaminergic neurotoxicity.  Since dopaminergic neurotoxicity is a multi-mechanistic complex endeavor, it will be appropriate to have a neurotoxin with multiple toxicodynamic effects.  Interestingly, kainic acid is an accepted and established epileptic excitatory neurotoxin which exerts its effect by primarily binding to kainate (glutamate) receptor to enhance excessive calcium influx, increase pro-oxidants generation, induce mitochondrial dysfunction and apoptosis or necrosis which triggers neurodegeneration leading to neuronal death. Currently, the dopaminergic neurotoxic potency of kainic acid as compared to the well-known dopaminergic neurotoxins are not clearly elucidated.  Hence, this study compared the dopaminergic neurotoxicity of kainic acid with various endogenous and exogenous neurotoxins using valid in vitro dopaminergic neuronal models. Our finding clearly indicates that as compared to the existing valid and scientifically accepted dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP⁺), kainic acid has significantly less dopaminergic neurotoxicity.  Consequently, kainic acid may be used as an adjuvant to enhance the dopaminergic neurotoxicity.  Further in vivo studies will be done in the future to investigate the potentiating / synergistic role of kainic acid on dopaminergic neurotoxicity.