DEVELOPMENTAL CONTROL OF THE DIAPHRAGM AND UPPER AIRWAYS

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Recent theories propose that there are several causes of Sudden Infant Death Syndrome (SIDS). One probable etiology is severe mixed and obstructive apnea during sleep. It has been proposed that this particular dysfunction results from a delayed development of the brainstem neurons controlling the patency of the upper airways relative to those neurons controlling the diaphragm. To test this hypothesis, there must be a fundamental data base on the normal development of the neurons controlling the upper airways and diaphgragm. This proposal will compare the time course of development of hypoglossal motoneurons innervating the genioglossus muscle of the tongue with that of the spinal motoneurons that innervate the diaphragm. The first project will investigate the normal development of phrenic motoneurons which innervate the diaphragm and compare these results to data from the adult. The second project will generate data on the genioglossal motoneuron in the adult for comparison with the same neurons at various developmental stages. The third project will describe the time course of development in the genioglossal motoneurons for comparisons with that of the phrenic motoneurons. These studies of hypoglossal motoneurons will yield important information on the development of neural control of the upper airways but may, in addition, reflect the more global state of development of other brainstem neurons which may generate respiratory rhythm or sleep states. The changes in anatomy and physiology of these two motoneuron populations will be compared at three different stages of early postnatal life. Various electrophysiological properties of the motoneurons will be determined by intracellular recording, and fine details of their cellular morphology will be revealed from histological analyses after intracellular staining with the enzyme, horseradish peroxidase (HRP). The physiologic properties of the motoneuron to be investigated to assess their maturity include the value of the resting membrane potential, amplitude of the overshoot of the action potential, duration of the after hyperpolarization, input resistance, rheobase, the conduction velocity of its axon and the presence of recurrent inhibition and/or electrical coupling. In a similar fashion, anatomical maturity will be evaluated by the eccentricity of the cell body, amount of membrane surface area, the number of dendrites projecting into various synaptic fields, complexity of the pattern of dendritic branching, number of dendritic spines and axonal collaterals.