Sensory experience during perinatal development is necessary for proper structuring of the nervous system. Unknown, however, is the degree to which proprioceptive information is required for the normal development of spinal pattern generators. One way to gain understanding of the role of sensory feedback during embryogenesis is to selectively alter or remove particular modalities, e.g., proprioception. High doses of B6 cause selective loss of proprioceptive neurons in adult mammals, including humans, resulting in ataxia. The investigator's preliminary data show that embryonic administration of B6 in chick alters embryonic and post- hatch movements. However, the neurological effects of B6 toxicity in embryonic and neonatal animals has not been described. The specific goal of this proposal is to determine whether embryonic B6 treatment results in specific loss of proprioceptive sensory inputs. The investigators will use physiological and anatomical methods to determine: 1) whether embryonic B6 treatment results in preferential loss of proprioceptive neurons, and 2) whether B6 alters the reflex pathways involved in proprioceptive feedback. B6 could become a powerful tool in assessing the requirements for sensory information during ontogeny. The chick is an ideal system for such developmental studies because its bipedal mode of locomotion is similar to humans as well as providing easy accessibility of the embryos at all developmental stages.
| Sharp, A A; Fedorovich, Y (2015) Teratogenic effects of pyridoxine on the spinal cord and dorsal root ganglia of embryonic chickens. Neuroscience 289:233-41 |
