| Autor: |
Moreira, Thiago S., Mulkey, Daniel K., Takakura, Ana C. |
| Předmět: |
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| Zdroj: |
Experimental Physiology; Nov2024, Vol. 109 Issue 11, p1837-1843, 7p |
| Abstrakt: |
At least four mechanisms have been proposed to elucidate how neurons in the retrotrapezoid (RTN) region sense changes in CO2/H+ to regulate breathing (i.e., function as respiratory chemosensors). These mechanisms include: (1) intrinsic neuronal sensitivity to H+ mediated by TASK‐2 and GPR4; (2) paracrine activation of RTN neurons by CO2‐responsive astrocytes (via a purinergic mechanism); (3) enhanced excitatory synaptic input or disinhibition; and (4) CO2‐induced vascular contraction. Although blood flow can influence tissue CO2/H+ levels, there is limited understanding of how control of vascular tone in central CO2 chemosensitive regions might contribute to respiratory output. In this review, we focus on recent evidence that CO2/H+‐induced purinergic‐dependent vasoconstriction in the ventral parafacial region near RTN neurons supports respiratory chemoreception. This mechanism appears to be unique to the ventral parafacial region and opposite to other brain regions, including medullary chemosensor regions, where CO2/H+ elicits vasodilatation. We speculate that this mechanism helps to maintain CO2/H+ levels in the vicinity of RTN neurons, thereby maintaining the drive to breathe. Important next steps include determining whether disruption of CO2/H+ vascular reactivity contributes to or can be targeted to improve breathing problems in disease states, such as Parkinson's disease. What is the topic of this review?The homeostatic mechanism that controls breathing in response to changes in CO2/H+ is exquisitely sensitive, with convergent roles proposed for chemosensory brainstem neurons in the retrotrapezoid nucleus (RTN), their supporting glial cells and the vasculature.What advances does it highlight?We focus on recent evidence that CO2/H+‐induced purinergic‐dependent vasoconstriction in the RTN region supports respiratory chemoreception. This mechanism appears to be unique to the RTN and opposite to other medullary chemosensor regions, where CO2/H+ elicits vasodilatation. We speculate that this mechanism helps to maintain CO2/H+ levels in the vicinity of RTN neurons, thereby maintaining the drive to breathe. [ABSTRACT FROM AUTHOR] |
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