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Modulation of temporal and spectral characteristics in phrenic nerve discharge by activation of NK1 receptors in arterially‐perfused adult rat
Author(s) -
Lin Robert,
Warren Kelly A,
Chen Xinnian,
Solomon Irene C
Publication year - 2007
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.21.5.a562
Subject(s) - phrenic nerve , perfusion , bursting , anesthesia , chemistry , medicine , respiratory system , endocrinology , biology , neuroscience
In the in vitro transverse medullary slice preparation from neonatal rodents, application of substance P (SP) increases inspiratory burst frequency as well as the incidence of augmented bursts. The effects of application of SP on inspiratory motor discharge in a more intact and mature in vitro preparation as well as on the intrinsic dynamics underlying inspiratory motor discharges remain to be determined. Therefore, we examined the effects of increasing doses of the long‐lasting SP analog [SAR 9 , Met(O 2 ) 11 ] (SP MET , 0.1–1.4 μM final concentration) on the temporal and spectral (including time‐frequency (TF)) characteristics of phrenic nerve discharge recorded from 6 arterially‐perfused decerebrate adult rat preparations. Since not all doses were examined in each experiment, statistical analyses were only performed for comparisons between baseline and perfusion with 0.2 μM SP MET (n=5). At this dose, an increase in burst frequency (~24%; P=0.076), mediated by small reductions in T I (from 780±89 to 727±102 ms; P=0.154) and T E (from 4.2±1.0 to 3.2±0.4 s; P=0.224), was observed. Perfusion with SP MET also modified spectral activity by increasing MFO power in a dose‐dependent manner and shifting the MFO peak to a slightly lower frequency and an earlier time point in the inspiratory burst; the effects on HFO activity were somewhat variable. Although additional experiments are needed, our preliminary findings suggest that SP affects inspiratory network excitability resulting in modulation of burst timing and inspiratory‐phase synchronization. Supported by NS045321 and NS049310

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