Excitotoxins: An Overview
The theme of this conference--excitotoxins (ET)--is a fascinating one that poses many intriguing research challenges and promises substantial rewards for the effort spent in pursuing these challenges. If we are right in suspecting that endogenous excitotoxins--glutamate (Glu), aspartate (Asp) and perhaps others--are the neurotransmitters released at the majority of excitatory synapses in the mammalian CNS, this is reason enough for our intrigue with these agents. If these transmitter candidates, which are distributed abundantly throughout the CNS, can attack and destroy central neurons, this suggests they might be involved in human neuropathological processes, a prospect that certainly enhances one’s level of interest. If by harnessing the powerful neurotoxic activities of ET, we can use them as tools to explore the magnificent organization and functions of the CNS, this is a splendid bonus for which we must indeed be grateful. But there are many gaps in our understanding of these agents, gaps which can only be filled by years of methodical research, but gaps which must be filled if we are to decipher the roles of ET in the physiology and pathology of the CNS and realize their full potential as tools in neuroscience research. In this overview on ET lesions, I will not attempt a comprehensive review of the burgeoning literature on ET--a task that would be impossible within the time constraints--but rather will focus on a few key issues which I consider fundamental to our understanding of these agents and the lesions they induce.
KeywordsKainic Acid Brain Damage Quinolinic Acid Distant Lesion Depolarization Block
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