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Active expiration and sympathetic excitation during hypercapnia require glutamatergic neurotransmission in the retrotrapezoid nucleus
Author(s) -
Lemes Eduardo,
Zoccal Daniel
Publication year - 2016
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.30.1_supplement.757.7
Subject(s) - hypercapnia , glutamatergic , kynurenic acid , neurotransmission , central chemoreceptors , medicine , glutamate receptor , anesthesia , chemoreceptor , expiration , ionotropic effect , neuroscience , endocrinology , chemistry , respiratory system , receptor , biology
Animals exposed to hypercapnia exhibit increases in sympathetic and expiratory motor activities that are depend on, at least in part, the activation of glutamatergic neurons in the retrotrapezoid nucleus (RTN). The generation of active expiratory pattern requires the expiratory neurons of the parafacial respiratory group (pFRG), which are anatomically co‐localized with the RTN neurons. Herein we explored the hypothesis that antagonism of glutamate receptors in the RTN/pFRG prevents the emergence of active expiration and reduces the sympathoexcitation induced by hypercapnia. Microinjections of kynurenic acid (KYN, antagonist of glutamate ionotropic receptor, 100mM, 50 nL) were performed bilaterally in the RTN of arterially‐perfused decerebrated in situ preparations of Holtzman rats (60–70 g) during the exposure to hypercapnia (8% CO 2 ) and the changes in the thoracic sympathetic (tSN), abdominal (AbN) and phrenic nerve (PN) activities were evaluated. Hypercapnia elevated tSN, PN and AbN activities of the in situ preparations (n=7). KYN microinjections in the RTN during hypercapnia reduced the sympathetic‐excitation (ΔtSN: 158±25 vs 80 ± 11%, P<0.05) and greatly attenuated the AbN response (ΔAbN: 41±13 vs 16±3%, P<0.001), but not changed the reflex increase in PN activity. Also, KYN in the RTN during hypercapnia further reduced the inspiratory time (ΔTi: −0.06±0.05 vs −0.13±0.05 s, P<0.05) and the perfusion pressure (ΔPP: −12±1 vs −20±3 mmHg, P<0.05). The results indicate that glutamatergic neurotransmission in the RTN is required for processing of the sympathetic‐excitatory and the generation of active expiratory pattern in response to hypercapnia. Support or Funding Information Support by FAPESP (2013/17251‐6), NIH (1R01AT008632‐01).