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Electrophysiological properties of RVLM pre‐sympathetic neurons modulated by the respiratory network in rats (875.11)
Author(s) -
Moraes Davi,
Silva Melina,
Bonagamba Leni,
Mecawi André,
Zoccal Daniel,
AntunesRodrigues José,
Varanda Wamberto,
Machado Benedito
Publication year - 2014
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.28.1_supplement.875.11
Subject(s) - rostral ventrolateral medulla , electrophysiology , respiratory system , excitatory postsynaptic potential , neuroscience , patch clamp , bursting , medicine , chemistry , inhibitory postsynaptic potential , biology , medulla oblongata , central nervous system
The respiratory pattern generator modulates the sympathetic outflow which strength is enhanced by hypoxia. This coupling is due to the respiratory‐modulated pre‐sympathetic neurons in the RVLM, but the underlining electrophysiological mechanisms remain unclear. For a better understanding of the central generation of respiratory‐sympathetic coupling, we combined immunofluorescence, single cell qRT‐PCR and whole cell patch clamp recordings of the pre‐sympathetic neurons in in situ preparations from normal and rats submitted to chronic intermittent hypoxia (CIH). Our results show that the spinally projected C1‐ and non‐C1 respiratory‐modulated pre‐sympathetic neurons (inspiratory‐modulated: 22; post‐I‐modulated: 23; inspiratory‐inhibited: 11; non‐modulated: 20) present distinct electrophysiological properties, synaptic inputs and expression of ionic currents, albeit all neurons presented iNaP‐dependent intrinsic pacemaker after synaptic blockade. Only the non‐C1 post‐I‐modulated neurons presented enhanced excitatory synaptic inputs from the respiratory network after CIH (n=14), which may contribute to the increased sympathetic activity observed in CIH rats. We conclude that the different respiratory‐modulated pre‐sympathetic neurons contribute to the central generation of respiratory‐sympathetic coupling and in response to the challenges produced by CIH may contribute to respiratory‐related increase in the sympathetic activity and hypertension observed in this experimental model. Grant Funding Source : Supported by CAPES and FAPESP

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