Is plasticity within the retrotrapezoid nucleus responsible for the recovery of the ge="true" class="math-equation-image">g>

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• 作者：Tyler M. Basting ; Chikara Abe ; Kenneth E. Viar ; Ruth L. Stornetta ; Patrice G. Guyenet
• 刊名：The Journal of Physiology
• 出版年：2016
• 出版时间：15 June 2016
• 年：2016
• 卷：594
• 期：12
• 页码：3371-3390
• 全文大小：992.5KB
• ISSN：1469-7793

文摘

Carotid body denervation (CBD) causes hypoventilation and increases the arterial ge="true" class="math-equation-image">g/1998/Math/MathML">g/1998/Math/MathML">PCO2 set-point; these effects eventually subside. The hypoventilation is attributed to reduced CB afferent activity and the ge="true" class="math-equation-image">g/1998/Math/MathML">g/1998/Math/MathML">PCO2 set-point recovery to CNS plasticity. In the present study, we investigated whether the retrotrapezoid nucleus (RTN), a group of non-catecholaminergic Phox2b-expressing central respiratory chemoreceptors (CCRs), is the site of such plasticity. We evaluated the contribution of the RTN to breathing frequency (F_R), tidal volume (V_T) and minute volume (V_E) by inhibiting this nucleus optogenetically for 10 s (archaerhodopsinT3.0) in unanaesthetized rats breathing various levels of O₂ and/or CO₂. The measurements were made in seven rats before and 6–7 days after CBD and were repeated in seven sham-operated rats. Seven days post-CBD, blood gases and ventilation in 21% O₂ were normal, whereas the hypoxic ventilatory reflex was still depressed (95.3%) and hypoxia no longer evoked sighs. Sham surgery had no effect. In normoxia or hypoxia, RTN inhibition produced a more sustained hypopnoea post-CBD than before; in hyperoxia, the responses were identical. Post-CBD, RTN inhibition reduced F_R and V_E in proportion to arterial pH or ge="true" class="math-equation-image">g/1998/Math/MathML">g/1998/Math/MathML">PCO2 (ΔV_E: 3.3 ± 1.5% resting V_E/0.01 pHa). In these rats, 20.7 ± 8.9% of RTN neurons expressed archaerhodopsinT3.0. Hypercapnia (3–6% FiCO₂) increased F_R and V_T in CBD rats (n = 4). In conclusion, RTN regulates F_R and V_E in a pH-dependent manner after CBD, consistent with its postulated CCR function. RTN inhibition produces a more sustained hypopnoea after CBD than before, although this change may simply result from the loss of the fast feedback action of the CBs.