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Chronic intermittent hypoxia alters the respiratory and autonomic responses to activation of glutamate receptors in the caudal NTS of juvenile rats
Author(s) -
Zoccal Daniel B,
Machado Benedito H
Publication year - 2009
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.23.1_supplement.957.4
Subject(s) - glutamatergic , endocrinology , medicine , brainstem , vagus nerve , hypoxia (environmental) , respiratory system , glutamate receptor , control of respiration , chemistry , receptor , anesthesia , stimulation , organic chemistry , oxygen
Alterations in glutamatergic mechanisms in the caudal NTS (cNTS) were evaluated after chronic intermittent hypoxia (CIH) exposure. Using the in situ working heart‐brainstem preparation we recorded the changes in phrenic (PNA), cervical vagus (cVN) and thoracic sympathetic (tSNA) nerve activities evoked by microinjections of different concentrations of L‐glutamate (L‐glu: 25, 50 and 250 mM) into cNTS of juvenile Wistar rats submitted to CIH (6% O 2 for 40 s every 9 min, 8 h/day) for 10 days and of control rats. L‐glu into cNTS of CIH (n=10) and control (n=7) rats produced an increase in post‐inspiratory vagal activity and sympathoexcitation. The cVN responses was smaller in CIH rats than in controls at the all concentrations tested (P<0.05), while the tSNA response was higher in CIH only at the higher concentration of L‐glu microinjected (53±9 vs 27±2 %, P<0.05). Besides, L‐glu into cNTS evoked significant reductions in the frequency of PNA in the control but not in the CIH group (P<0.05). The higher sympathoexcitation and the blunted apnea in response to L‐glu into cNTS of CIH juvenile rats suggest that glutamatergic mechanisms in or downstream to cNTS are altered after CIH exposure. Further studies are required to verify the involvement of these alterations in the autonomic and respiratory dysfunctions observed after CIH. Supported by FAPESP and CNPq.