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
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GPR4 mediates CO2 chemosensitivity in mice; leaves open translation to human respiratory control.
GPR4 and TASK-2 are distinct, parallel, and essential central mediators of respiratory chemosensitivity in mice.
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.