Janczewski WA, McKay LC, Feldman JL (2004) Decreased number of sighs and post-sigh apneas indicates neuronal degeneration within the preBötzinger complex. Neuroscience 2004 Abstracts 424.10. Society for Neuroscience, San Diego, CA.
Summary: Sighs, also known as augmented or deep breaths, are inspiratory efforts of increased tidal volume, duration and biphasic shape. Sighs occur periodically in most mammals and are present throughout life, even in utero. Some sighs are followed by a post-sigh apnea lasting longer than 2 average respiratory periods. In adult rats, the number of sighs per hour [sigh index (SI)] is ~20. When we injected 0.2 pmol of substance P (SP) into the preBötzinger Complex, SI increased to >100, suggesting that activation of preBötzinger Complex NK1 receptor expressing (NK1R) neurons produces sighs. We hypothesized that degeneration of preBötzinger Complex NK1R neurons would decrease SI and eliminate post-sigh apneas. We injected the toxin saporin conjugated to SP bilaterally into the preBötzinger Complex to selectively destroy NK1R neurons. The number of ablated NK1R neurons increased from days 2-6 postinjection. In all rats at days 2-3, SI dropped below 5 and all post-sigh apneas were eliminated. In one group of rats (n=6), an ataxic breathing pattern developed, resulting from >90% NK1R cell loss. In these rats, all sighs were eliminated from days 3-4 postinjection. A second group of rats (n=5) maintained a eupneic breathing pattern. They were observed for two months postinjection and did not recover the preinjection sigh pattern. Their NK1R cell loss was <80% after two months, but must have been smaller at day 2 postinjection when their sigh pattern changed. We hypothesize that a modest (<< 80%) decrease in the number of NK1R neurons within the preBötzinger Complex, due to a toxin here but otherwise due to aging or neurodegenerative processes, may explain the decrease in SI seen with age in humans. We postulate that a marked decrease in the number of sighs and post-sigh apneas is an early symptom of neurodegeneration within the preBötzinger Complex.
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