Abstract
The gain of the HBEF is controlled by neurons in the medial parabrachial (PB) region (1). However, the mechanism is unknown. Responses of E decrementing (Edec) neurons to inputs from slowly adapting pulmonary stretch receptors (PSRs) suggest that they may mediate the HBEF reflex (2). This study analyzed the responses of E‐neurons in the pre‐Bötzinger/Bötzinger (preBC/BC) region to inputs from both the PSRs and PB neurons in a decerebrate vagotomized dog model. Neurons were recorded with a 16‐electrode probe. Weak electrical stimulation (~100 μA & 100 μs duration) of the central end of a desheathed cervical vagus nerve was used to activate PSR afferents and a concentric bipolar microelectrode was used to activate the PB region neurons. Post‐stimulus time histograms triggered by stimulus sync pulses (10 Hz for 10 min) were used to detect the presence of synaptic inputs to E‐neurons by either or both of these inputs. Cycle‐triggered histograms triggered from the phrenic neurogram (PNG) were used to analyze induced‐changes in average discharge (Fn) patterns. The data from this study and a previous study (2) show that the decrementing rate of ~all Edec neurons decreases and the discharge duration increases with the PSR‐induced increases in expiratory duration (TE). About 60% (11/18) of the Edec neurons received an inhibitory input from the PB region (3). CTHs show that concurrent PB and PSR stimulation depress the PSR‐mediated increase in TE and depress Edec discharge patterns (e.g., see figure). This finding suggests that gain modulation of the HBEF reflex by the PB region may be mediated by inhibitory inputs to Edec neurons in the preBC/BC region.Support or Funding InformationSupported by VA grant 2 I01BX000721‐08 (Zuperku) & R01GM112960‐01A1 (Stucke)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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