Animal models for human behavioral deficiencies during development.

Abstract

Often considered to be a subdiscipline of neurotoxicology, experimental behavioral teratology has difficulties to be acknowledged by its own right. Results obtained in the laboratory concerning purely behavioral effects induced by low level prenatal exposure to substances are often doubted to contain any relevance with respect to humans. This doubt is based on many debates going on in the numerous extrapolation steps between observed effects on animal behavior and human psychopathology. Taking the inverse path, extrapolation from a typical human behavioral syndrome (minimal brain dysfunction) to observations which can be made on laboratory animals, the following main debates are discussed: the psychology debate (behaviorism--perceptionism--cognitivism); the psychopathology debate (hyperactivity--attention deficit--tactile-kinesthetic perception deficiency--sensory integration deficits); the relevance debate (behavior is reprogrammable software--behavioral deficits may reflect undetectable hardware defects); the interpretation debate (behavioral teratogenicity is chemical imprinting--behavioral disturbances due to chemicals reflect neurotoxicity); the intelligence debate (IQ decrements--attention deficits); the developmental delay debate (the relevance of a delay in the behavioral development); the sensitivity debate (behavior is the most sensitive measure in toxicology--the brain redundancy and plasticity compensates subtle deficiencies); the statistics debate (gather as many behavioral variables as possible--stay simple and measure only one aspect of behavior); the regulation debate (behavioral teratology should be regulated in detail--tests should not be prescribed). It is attempted to find rational solutions for these debates which menace to jeopardize the very existence of behavioral teratology.