DEVELOPMENTAL CONTROL OF THE DIAPHRAGM AND UPPER AIRWAYS

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.