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Stimulating opioid μ‐receptors in the commissural subdivision of the nucleus tractus solitarius (cNTS) abolishes the carotid body‐mediated ventilatory response in anesthetized rats
Author(s) -
Zhang Zhenxiong,
Zhang Cancan,
Xu Fadi
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.621.20
Subject(s) - damgo , carotid body , hypoxic ventilatory response , microinjection , chemoreceptor , ventilation (architecture) , receptor , agonist , endocrinology , chemistry , medicine , anesthesia , peripheral chemoreceptors , control of respiration , pharmacology , respiratory system , opioid receptor , electrophysiology , mechanical engineering , engineering
Carotid chemoreceptors are essential in generating hypoxic ventilatory response (HVR) and their afferents primarily terminate in the cNTS. As the cNTS contains the highest expression of μ‐receptors in the brainstem, we tested whether activating cNTS μ‐receptors modulated the carotid body‐mediated HVR. In anesthetized and spontaneously breathing rats, cardiorespiratory activities and their responses to pure N 2 administered for 10 s were recorded before and after microinjection of μ‐receptor agonist, DAMGO (≈5 nl), into the cNTS. DAMGO concentration at 0.5 and 2.5 mM caused a similar increase in blood pressure (26% and 33%) and decrease in ventilation (13% and 11%) due to the depression of V T . The transient N 2 ‐induced ventilatory response was attenuated (64% reduction) by the low dose, and abolished by the high dose of DAMGO due to the impact on both V T and f responses. Similarly, the ventilatory responses to intra‐carotid delivery of NaCN (5 μg/50 μl) were eliminated after microinjection of the high dose of DAMGO into the cNTS. Our data suggest that cNTS opioids are capable of blocking the carotid chemoreceptor‐mediated ventilatory responses via acting on μ‐receptors that are likely located on the synapses where the second‐order neurons receive the inputs from the carotid chemoreceptors. (Supported by ALA RT‐83131‐N)