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Brain pacemaker cells appear essential for gasping
Feb 13, 2006, 05:20, Reviewed by: Dr. Priya Saxena
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"Our findings are exciting they demonstrate that emergency breathing, or gasping, is regulated by different mechanisms than those for normal breathing. This result explains why gasping is such a powerful mechanism for autoresuscitation.."
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By University of Bristol,
The mystery of cot death may be explained by new research published online in Nature Neuroscience today [Sunday 12 February 2006].
A failure to 'gasp' has long been proposed as the basis for sudden infant death syndrome, or cot death. A team at the University of Bristol has discovered a subset of cells in the brain that have the ability to self-generate nervous impulses, which appear essential for gasping. These cells have been termed 'pacemakers'.
Professor Julian Paton who heads up the research team at Bristol University said: "Our studies resolve a 15-year long controversy by showing that pacemaker cells in the brain appear responsible for gasping but not normal breathing. Importantly, cot death has been proposed to result from a failure of autoresuscitation and gasping."
Using a unique experimental set-up developed in Bristol, Paton combined forces with two other world leaders in respiration � Dr. Jeffrey Smith (NIH, USA) and Professor Walter St.-John (Dartmouth, USA) � to discover how gasping works. They found that many different types of brain cells are essential for normal breathing, but only a small subset of these is required for gasping or autoresuscitation.
If normal breathing should stop, this backup system is activated to induce gasping. This restores oxygen supplies and kick-starts the heart beat so that normal breathing can resume.
"A very important aspect of this work is that we have discovered a mechanism within the brain that allows autoresuscitation of both breathing and the heart beat to come about when oxygen levels are critically low," said Dr. Smith.
Paton and colleagues found that these pacemaking cells were dependent upon a unique protein that forms a tiny hole or pore within the membrane of the cells. When oxygen levels are low this pore opens wider to allow the passage of sodium ions into the cell and provides a way in which gasping can occur automatically.
The team showed that when this pore was blocked it eliminated pacemaking and the ability to gasp. Consequently, the heart would fail and death would be inevitable. This raises the intriguing possibility that a genetic defect in this special protein found in pacemaking cells could prevent gasping.
St.-John commented: "Our findings are exciting they demonstrate that emergency breathing, or gasping, is regulated by different mechanisms than those for normal breathing. This result explains why gasping is such a powerful mechanism for autoresuscitation.." 
- Nature Neuroscience [Sunday 12 February 2006]
www.bristol.ac.uk
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