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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Physical Therapy, Marquette University, Milwaukee, WI, USA
3 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Zablocki V.A. Medical Center, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: hodgesmr{at}mcw.edu.
The major objective of this study was to gain insight into whether under physiologic conditions medullary raphe-area neurons influence breathing through CO2/H+ chemoreceptors and/or through a postulated, non-chemoreceptor modulatory influence. Microtubules were chronically implanted into the raphe of adult goats (n=13), and breathing at rest (awake and asleep), during exercise, as well as CO2 sensitivity were assessed repeatedly before and after sequential injections of the neurotoxins saporin conjugated to substance p (SP-SAP, neurokinin-1 receptor (NK1R)-specific) and ibotenic acid (IA, non-specific glutamate receptor excitotoxin). In all goats, microtubule implantation alone resulted in altered breathing periods, manifested as central or obstructive apneas, and fractionated breathing. The frequency and characteristics of the altered breathing periods were not subsequently affected by injections of the neurotoxins (P > 0.05). Three to seven days after SP-SAP or subsequent IA injection, CO2 sensitivity was reduced (P < 0.05) 23.8% and 26.8% respectively but CO2 sensitivity returned to pre-injection control values >7 days post-injection. However, there was no hypoventilation at rest (awake, NREM or REM sleep) or during exercise after these injections (P > 0.05). The neurotoxin injections resulted in neuronal death >3 times greater than microtubule implantation alone, and reduced (P < 0.05) both TPOH+ (36%) and NK1R+ (35%) neurons at the site of injection. We conclude that both NK1R- and GluR-expressing neurons in the medullary raphe nuclei influence CO2 sensitivity apparently through CO2/H+ chemoreception, but the altered breathing periods appear unrelated to CO2 chemoreception and thus are likely due to non-chemoreceptor-related neuromodulation of ventilatory control mechanisms.
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