In the early 1970's the clinical effects of human fetal alcohol exposure were described as Fetal Alcohol Syndrome (FAS). Mental retardation, visual deficits, and changes in muscle coordination and reflex actions are characteristics of FAS. Research has been focused on the effect FAS has on the neurons in the central nervous system (CNS). FAS has been shown to decrease neuron numbers and alter their migration pattern. Recently, research has also been studying the effect that FAS has on the glial cells which support neuron activity and myelinate axons. Limited research in animal models has shown that fetal alcohol exposure can delay maturation of these cells and alter myelination of axons. The goal of this proposal is to investigate the effect of developmental alcohol exposure on the superior colliculus (SC) which is important in relaying visual sensory input to motor areas for coordination of head and eye movements in reflex activity. To simulate an equivalent human exposure in an animal model, pregnant rat dams will be fed a diet containing alcohol. After birth, rat pups will be reared using an artificial rearing technique to expose them to alcohol during postnatal days 1-10. Animals will be sacrificed at different ages and tissues taken from the SC for study. Maturation of glial populations, myelin development, and axon terminals will be analyzed using a combination of techniques to include light and electron microscopy, morphometric analysis, immunohistochemistry, and axon terminal labeling. Potential findings could help explain some of the neurological dysfunctions involving visual motor coordination.
| Phillips, D E; Cummings, J D; Wall, K A (2000) Prenatal alcohol exposure decreases the number of nitric oxide synthase positive neurons in rat superior colliculus and periaqueductal gray. Alcohol 22:75-84 |
