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Selective lesion of retrotrapezoid Phox2b‐expressing neurons attenuates the central chemoreflex in conscious rats
Author(s) -
Takakura Ana C,
Ragioto Danielle T,
Moreira Thiago S,
Colombari Eduardo
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.847.6
In the present study we ask whether the destruction of a type of pH‐sensitive interneuron that expresses the transcription factor Phox2b and is non‐catecholaminergic (Phox2b+TH‐) could affect breathing in conscious rats. We showed that RTN contains around 2000 Phox2b+TH‐ cells. Bilateral injections of SSP‐SAP into RTN destroyed Phox2b+TH‐ neurons but spared facial motoneurons, catecholaminergic and serotonergic neurons and the ventral respiratory column caudal to the facial motor nucleus. Bilateral inhibition of RTN neurons with SSP‐SAP (0.6 ng/30 nl) reduced resting ventilation (1029±142, vs. saline: 1663±137 ml/min/kg) and the increase in ventilation produced by hypercapnia (10% CO2) (2916±162, vs. saline: 3736±243 ml/min/kg). SSP‐SAP into the RTN did not affect the changes in MAP and heart rate produced by hypercapnia. In anesthetized rats with bilateral lesions of around 80% of the Phox2b+TH‐ neurons, acute activation of the Botzinger or the preBotzinger complex with NMDA (5 pmol/50 nl) elicited normal PND. In conclusion, the destruction of the Phox2b+TH‐ neurons is a plausible cause of the respiratory deficits caused by injection of SSP‐SAP into RTN. Our results also suggest that RTN neurons activate facilitatory mechanisms important to the control of ventilation in resting or hypercapnic conditions in conscious rats. Financial support: FAPESP