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Phrenicotomy alters expression of long term facilitation (LTF) in anesthetized rats
Author(s) -
Sandhu Milapjit Singh,
Reier Paul J,
Fregosi Ralph F,
Fuller David D
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.1010.15
Subject(s) - phrenic nerve , axotomy , intermittent hypoxia , hypoxia (environmental) , anesthesia , medicine , facilitation , motor neuron , respiratory system , neuroscience , central nervous system , chemistry , biology , disease , organic chemistry , oxygen , obstructive sleep apnea
Intermittent hypoxia (IH) can induce a persistent increase in phrenic motor output known as LTF. The cut, central end of the phrenic nerve is typically used to record phrenic motor output, but the impact of phrenicotomy (PhrX) on LTF has not been described. Both the removal of afferent inputs to phrenic motoneurons and alterations in motoneuron excitability secondary to axotomy could alter the motor output recorded from cut phrenic nerves. Accordingly, we tested the hypothesis that PhrX influences LTF following IH. Bilateral phrenic neurograms were recorded in anesthetized, ventilated and vagotomized male Sprague‐Dawley rats before (i.e. baseline), during and after 3, 5‐min bouts of isocapnic hypoxia (PaO2 = 30‐50mmHg) in phrenic intact (n=5) and PhrX rats (n=5). At 60 minutes post‐hypoxia, phrenic burst amplitude was significantly greater than baseline (i.e. LTF was present, p<0.05) in PhrX recordings (151±22% baseline) but not in phrenic intact recordings (109±10% baseline). These preliminary studies suggest that removal of phrenic afferents and/or axotomy‐induced changes in phrenic motoneuron excitability may play a role in LTF in anesthetized rats. Funding: NIH 1R01HD052682‐01A1 (DDF) and NIH RO1 NS054025 (PJR).