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June 11, 2015ScienceOpen Access

Regulation of breathing by CO 2 requires the proton-activated receptor GPR4 in retrotrapezoid nucleus neurons

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Population

Mice (specifically focusing on retrotrapezoid nucleus neurons)

Comparison

Genetic deletion of GPR4, reintroduction of… vs Wild-type/control state

Design

Preclinical

Key result

Genetic deletion of GPR4 in mouse retrotrapezoid nucleus neurons disrupted acidosis-dependent activation and blunted ventilatory responses to CO2, which were restored by GPR4 reintroduction.

Authors

NKNatasha N. KumarAVAna VelićJSJorge Soliz

Discussion

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Overview

GPR4 mediates CO2 chemosensitivity in mice; leaves open translation to human respiratory control.

Structured PICO

P
Population
Mice (specifically focusing on retrotrapezoid nucleus neurons)
I
Intervention
Genetic deletion of GPR4, reintroduction of GPR4, and additional elimination of TASK-2
C
Comparator
Wild-type/control state
O
Outcome
Ventilatory response to CO2 and acidosis-dependent activation of RTN neuronssurrogate

GPR4 and TASK-2 are distinct, parallel, and essential central mediators of respiratory chemosensitivity in mice.

Cite This Study

Kumar et al. (2015) studied Respiratory chemosensitivity. Genetic deletion and reintroduction of GPR4 was evaluated on Ventilatory responses to CO2 and acidosis-dependent activation of RTN neurons. Genetic deletion of GPR4 in mouse retrotrapezoid nucleus neurons disrupted acidosis-dependent activation and blunted ventilatory responses to CO2, which were restored by GPR4 reintroduction.

synapsesocial.com/papers/6aa87a6eed57a7b7cb59fd21https://doi.org/10.1126/science.aaa0922
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