Memory, synaptic plasticity and neurotoxins.

Abstract

Most neurotoxins induce serious impairments in cognitive or intellectual functioning; therefore, the ability of the individual to learn and remember forms a critical component of neurotoxin assessment. In depth investigations of neurotoxin-induced cognitive deficits have assisted in pinpointing the neural site of toxin activity. However, specific impairments in learning and memory can depend on the developmental stage at which the individual is exposed to the toxin, and certain neurotoxins show cognitive lifespan selectivity. There appears to be a basic sequence of events underlying neural development and information storage, and neurotoxins may disrupt this neuronal sequel critical for the storage or expression of "ancestral" or "environmental" memories. Certain primary rules govern the orderly development of the nervous system; these rules or mechanisms allow the expression of "ancestral memories" concerning neuronal differentiation and primitive behaviors. Following birth, these same mechanisms have been retained in a less robust form to allow learning and information storage, or the retention of "environmental memories." Neurotoxins which disrupt learning and memory capacities appear to interfere in this basic sequence of events, with the specific outcome depending on when during lifespan development the neurotoxin intervenes.