Interaction between Kolliker-Fuse/A7 and the parafacial respiratory region on the control of respiratory regulation

Respiration is regulated by various types of neurons located in the pontine-medullary regions. The Ko center dot lliker-Fuse (KF)/A7 noradrenergic neurons play a role in modulating the inspiratory cycle by influencing the respiratory output. These neurons are interconnected and may also project to brainstem and spinal cord, potentially involved in regulating the post -inspiratory phase. In the present study, we hypothesize that the parafacial (pF) neurons, in conjunction with adrenergic mechanisms originating from the KF/A7 region, may provide the neurophysiological basis for breathing modulation. We conducted experiments using urethane -anesthetized, vagotomized, and artificially ventilated male Wistar rats. Injection of L -glutamate into the KF/A7 region resulted in inhibition of inspiratory activity, and a prolonged and high -amplitude genioglossal activity (GGEMG). Blockade of the alpha 1 adrenergic receptors (alpha 1-AR) or the ionotropic glutamatergic receptors in the pF region decrease the activity of the GGEMG without affecting inspiratory cessation. In contrast, blockade of alpha 2-AR in the pF region extended the duration of GG activity. Notably, the inspiratory and GGEMG activities induced by KF/A7 stimulation were completely blocked by bilateral blockade of glutamatergic receptors in the Bo center dot tzinger complex (Bo center dot tC). While our study found a limited role for alpha 1 and alpha 2 adrenergic receptors at the pF level in modulating the breathing response to KF/A7 stimulation, it became evident that Bo center dot tC neurons are responsible for the respiratory effects induced by KF/A7 stimulation.