Effects of persistent sodium current blockade in respiratory circuits depend on the pharmacological mechanism of action and network dynamics
Fig 12
Characterization of the intact respiratory network behavior.
(A) Identification of INaP and/or network dependent regimes of pre-I population bursting as a function of tonic excitatory drive (gTonic). Effect of post-I inhibition strength and gTonic on (B) post-inspiratory phase hyperpolarization, (C) hNaP dynamic range, and (D) the peak inspiratory phase INaP in the pre-I population. Notice that the INaP level is strongly affected by the magnitude of post-I inhibition and gTonic. Strong post-I inhibition increases the magnitude of post-inspiratory phase hyperpolarization, which decreases INaP inactivation and increases the peak INaP. In contrast, strong gTonic decreases post-inspiratory phase hyperpolarization, which increases INaP inactivation and decreases the peak INaP. Dashed lines in C indicate the dynamic range of hNaP in the isolated pre-I population under baseline conditions used in Fig 7.