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Chemoreflex sympatho‐excitation in the working heart‐brainstem preparation (WHBP) of rat was not affected by the antagonism of glutamate receptors in the commissural nucleus tractus solitarius (NTS).
Author(s) -
Braga Valdir A.,
Machado Benedito H.
Publication year - 2006
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.20.4.a363-b
Subject(s) - microinjections , microinjection , kynurenic acid , chemistry , glutamate receptor , medicine , endocrinology , glutamatergic , rostral ventrolateral medulla , receptor , medulla oblongata , central nervous system
The changes in thoracic sympathetic nerve activity (tSNA), heart rate (HR) and frequency of phrenic nerve discharge (PND) in response to chemoreflex activation before and after bilateral microinjections of glutamate receptor antagonists into the NTS were evaluated in the WHBP. Microinjections of kynurenic acid (KYN, 250 mM), MCPG (100 mM) or KYN plus MCPG into the NTS were performed in 3 different groups. Microinjections of KYN (54±3 vs 51±2 %, n=11), MCPG (48±5 vs 54±5 %, n=7) or KYN plus MCPG (57±6 vs 55±3 %, n=5) into the NTS did not affect the increase in the tSNA elicited by chemoreflex activation. The increase in the frequency of the PND in response to chemoreflex activation was also not affected by microinjections of glutamate receptor antagonists: KYN (0.68±0.03 vs 0.76±0.05 Hz), MCPG (0.60±0.03 vs 0.61±0.03 Hz) and KYN plus MCPG (0.62±0.03 vs 0.62±0.02 Hz). The bradycardic response to chemoreflex activation was significantly reduced at 2 (−220±16 vs −50±6 bpm) and 10 min (−220±16 vs −65±9 bpm) after microinjection of KYN and was abolished at 2 (−192±14 vs −2±1 bpm) and 10 min (−192±14 vs −4±2 bpm) after microinjections of KYN plus MCPG into the NTS. These data support the hypothesis that the neurotransmission of the sympatho‐excitatory and respiratory components of the chemoreflex in the NTS involves neurotransmitters other than L‐glutamate and also the concept that the parasympathetic component of this reflex is mediated by L‐glutamate. Supported by CNPq and FAPESP.