Nov. 14, 2000 CHAMPAIGN, Ill. - Studies at the University of Illinois have identified a specific brain pathway in which neurons activate in times of low oxygen (hypoxia) and trigger increased breathing.
The findings of the research - based on studies of electrical currents in rat brains - have led the scientists to postulate that many newborns don't have enough neurons to respond sufficiently to hypoxia. Such a deficit in response capability, they say, possibly is a factor in sudden infant death syndrome, which each year claims the lives of 3,000 babies under a year old in the United States.
"It is not fully understood why newborns, whether they are humans, rats, cats, dogs or whatever, do not have a maintained response to low oxygen," said Tony G. Waldrop, a professor of molecular and integrative physiology. "My lab has shown that neurons in some of the brain areas involved in the control of breathing are inherently sensitive to low oxygen. This sensitivity increases over developmental time. Newborn animals have far fewer neurons that respond to hypoxia than do adults.
"It may be that babies prone to SIDS do not have the same level of ability of typical newborns," he said. "Maturation of these cells may be at lower levels in these babies."
In a study to be published in the November Journal of Neurophysiology, Waldrop and colleagues will describe the activity of sodium currents - electrical streams of ions or group of atoms - involved in neuron communication in the caudal hypothalamus and the ventrolateral medulla of rat brains.
In times of hypoxia in adult brains, they found, there is "a significant increase in the persistent sodium current," which is most likely the primary mechanism for the activation of neurons that help to regulate cardiorespiratory activity. Such a reaction, however, was not seen in rats less than 12 days old, suggesting that the brain pathway in neonatal rats may not be sufficiently developed to respond.
The research was a part of the doctoral dissertation of Eric M. Horn, now a neurosurgery resident at the Barrow Neurological Institute in Phoenix. Waldrop is the UI vice chancellor for research and a professor in the UI College of Medicine at Urbana-Champaign. Their research was funded by grants from the National Heart, Lung, and Blood Institute and the American Heart Association.
Horn, Waldrop and Jeffery M. Kramer, a postdoctoral fellow in molecular and integrative physiology, elaborated on the possibility of oxygen-sensing neurons, based on brain-slice studies, in a paper in Respiration Physiology in 1997. In the October issue of Neuroscience, Waldrop and Horn reported that in live, conscious rats, the neurons activate and generate a protein called Fos when exposed to periods of hypoxia.
"We were able to take single neurons in the brains of these animals and go in and use glass pipettes to record the electrical currents of these cells as they communicate," Waldrop said. "This work has clearly shown that sodium ions mediate the neuronal response to low oxygen."
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