Power spectral analysis of hypoglossal nerve activity during intermittent hypoxia-induced long-term facilitation in mice.

Published

Journal Article

Power spectral analyses of electrical signals from respiratory nerves reveal prominent oscillations above the primary rate of breathing. Acute exposure to intermittent hypoxia can induce a form of neuroplasticity known as long-term facilitation (LTF), in which inspiratory burst amplitude is persistently elevated. Most evidence indicates that the mechanisms of LTF are postsynaptic and also that high-frequency oscillations within the power spectrum show coherence across different respiratory nerves. Since the most logical interpretation of this coherence is that a shared presynaptic mechanism is responsible, we hypothesized that high-frequency spectral content would be unchanged during LTF. Recordings of inspiratory hypoglossal (XII) activity were made from anesthetized, vagotomized, and ventilated 129/SVE mice. When arterial O2 saturation (SaO2) was maintained >96%, the XII power spectrum and burst amplitude were unchanged for 90 min. Three, 1-min hypoxic episodes (SaO2 = 50 ± 10%), however, caused a persistent (>60 min) and robust (>400% baseline) increase in burst amplitude. Spectral analyses revealed a rightward shift of the signal content during LTF, with sustained increases in content above ∼125 Hz following intermittent hypoxia and reductions in power at lower frequencies. Changes in the spectral content during LTF were qualitatively similar to what occurred during the acute hypoxic response. We conclude that high-frequency content increases during XII LTF in this experimental preparation; this may indicate that intermittent hypoxia-induced plasticity in the premotor network contributes to expression of XII LTF.

Full Text

Duke Authors

Cited Authors

  • ElMallah, MK; Stanley, DA; Lee, K-Z; Turner, SMF; Streeter, KA; Baekey, DM; Fuller, DD

Published Date

  • March 2016

Published In

Volume / Issue

  • 115 / 3

Start / End Page

  • 1372 - 1380

PubMed ID

  • 26683067

Pubmed Central ID

  • 26683067

Electronic International Standard Serial Number (EISSN)

  • 1522-1598

Digital Object Identifier (DOI)

  • 10.1152/jn.00479.2015

Language

  • eng

Conference Location

  • United States