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Hypoxia silences retrotrapezoid nucleus respiratory chemoreceptors via alkalosis
#MMPMID25589748
Basting TM
; Burke PG
; Kanbar R
; Viar KE
; Stornetta DS
; Stornetta RL
; Guyenet PG
J Neurosci
2015[Jan]; 35
(2
): 527-43
PMID25589748
show ga
In conscious mammals, hypoxia or hypercapnia stimulates breathing while
theoretically exerting opposite effects on central respiratory chemoreceptors
(CRCs). We tested this theory by examining how hypoxia and hypercapnia change the
activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex
integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly
silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby
C1 neurons with Arch (PRSx8-ArchT-EYFP-LVV) and measured the cardiorespiratory
consequences of Arch activation (10 s) in conscious rats during normoxia,
hypoxia, or hyperoxia. RTN photoinhibition reduced breathing equally during
non-REM sleep and quiet wake. Compared with normoxia, the breathing frequency
reduction (?f(R)) was larger in hyperoxia (65% FiO2), smaller in 15% FiO2, and
absent in 12% FiO2. Tidal volume changes (?V(T)) followed the same trend. The
effect of hypoxia on ?f(R) was not arousal-dependent but was reversed by
reacidifying the blood (acetazolamide; 3% FiCO2). ?f(R) was highly correlated
with arterial pH up to arterial pH (pHa) 7.5 with no frequency inhibition
occurring above pHa 7.53. Blood pressure was minimally reduced suggesting that C1
neurons were very modestly inhibited. In conclusion, RTN neurons regulate eupneic
breathing about equally during both sleep and wake. RTN neurons are the first
putative CRCs demonstrably silenced by hypocapnic hypoxia in conscious mammals.
RTN neurons are silent above pHa 7.5 and increasingly active below this value.
During hyperoxia, RTN activation maintains breathing despite the inactivity of
the carotid bodies. Finally, during hypocapnic hypoxia, carotid body stimulation
increases breathing frequency via pathways that bypass RTN.
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