期刊
JOURNAL OF NEUROSCIENCE
卷 30, 期 37, 页码 12466-12473出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3141-10.2010
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资金
- The Wellcome Trust [079040]
- National Institute of Neurological Disorders and Stroke (NINDS)
- National Heart, Lung, and Blood Institute [HL 28066]
- Medical Research Council [G0600928]
- Royal Society
- MRC [G0600928] Funding Source: UKRI
- British Heart Foundation [RG/07/006/23634] Funding Source: researchfish
- Medical Research Council [G0600928] Funding Source: researchfish
Phox2b-expressing neurons of the retrotrapezoid nucleus (RTN), located in the ventrolateral brainstem, are sensitive to changes in PCO2/pH, have excitatory projections to the central respiratory rhythm/pattern generator, and their activation enhances central respiratory drive. Using in vivo (conscious and anesthetized rats) and in situ (arterially perfused rat brainstem-spinal cord preparations) models, we evaluated the functional significance of this neuronal population for both resting respiratory activity and the CO2-evoked respiratory responses by reversibly inhibiting these neurons using the insect peptide allatostatin following transduction with a lentiviral construct to express the G-protein-coupled Drosophila allatostatin receptor. Selective inhibition of the Phox2b-expressing neurons in the ventrolateral brainstem, including the RTN, using allatostatin was without effect on resting respiratory activity in conscious rats, but decreased the amplitude of the phrenic nerve discharge in anesthetized rats and the in situ rat preparations. Postinspiratory activity was also reduced in situ. In the absence or presence of the peripheral chemoreceptor input, inhibiting the Phox2b-expressing neurons during hypercapnia abolished the CO2-evoked abdominal expiratory activity in anesthetized rats and in situ preparations. Inspiratory responses evoked by rising levels of CO2 in the breathing air were also reduced in anesthetized rats with denervated carotid bodies and conscious rats with peripheral chemoreceptors intact (by 28% and 60%, respectively). These data indicate a crucial dependence of central expiratory drive upon Phox2b-expressing neurons of the ventrolateral brainstem and support the hypothesis that these neurons contribute in a significant manner to CO2-evoked increases of inspiratory activity.
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