Neurons in a Subregion of the Medial Parabrachial Nucleus (mPBN) Attenuate the Gain of the Hering‐Breuer (H‐B) Reflex

Abstract

This study provides new evidence showing that a subregion of the mPBN, which plays a key role in the control of breathing frequency (1), also attenuates the H‐B expiratory facilitatory reflex. Experiments were performed in decerebrate, vagotomized dogs during isocapnic hyperoxia. Phase durations TI and TE were obtained from the phrenic neurogram(PNG). A small concentric bipolar electrode was used to microstimulate the mPBN subregion. Lung inflations and/or weak electrical stimulation of a desheathed cervical vagus nerve were used to activate the slowly adapting pulmonary stretch receptors (PSRs) to produce the H‐B reflex. Pulse‐train PSR stimulation at various frequencies (Fs) were delivered during the E‐phase of test cycles separated by several non‐stimulated control cycles. During every other PSR test cycle, pulse‐train stimulation of the pontine subregion at a predetermined frequency was concurrently delivered to determine its effect on the PSR‐induced increase in TE (e.g., fig A). The effect of the pontine stimulus in the absence of the PSR input was also measured. Plots of TE vs. PSR step Fs have the shape of an increasing exponential function. The effect of the pontine input was a proportional reduction in TE at each of the PSR step Fs, and was shown as an attenuated curve in the TE‐Fs plots (fig B). The relationship between the reduction in the H‐B reflex and the pontine stimulus frequency was linear over the range of 0 to 20 Hz, with a maximum attenuation of the H‐B reflex to ~20% of control (no pontine stimulus) produced by pontine stimulus frequencies in the 20–40 Hz range. These findings suggest that as inputs from the pontine subregion increase breathing frequency, this region concurrently attenuates the H‐B expiratory facilitatory reflex. This mechanism counteracts the PSR‐induced increase in TE, which reduces breathing frequency.Support or Funding InformationSupported by VA grant 2 I01BX000721‐07This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.