Abstract

Active expiration is essential for increasing pulmonary ventilation during high chemical drive (hypercapnia). Several studies demonstrated that the lateral aspect of the parafacial (pFL) region, which contains expiratory neurons, drives abdominal muscles during active expiration in response to hypercapnia. However, the electrophysiological properties and synaptic mechanisms determining the activity of pFL expiratory neurons and the specific conditions for their emergence are not fully understood. Therefore, using whole-cell electrophysiology and single-cell qRT-PCR techniques, we evaluated the intrinsic electrophysiological properties, the phenotype, and the respiratory-related synaptic inputs to the pFL expiratory neurons, as well as the mechanisms for the expression of their expiratory activity under conditions of hypercapnia induced active expiration in in situ preparations of juvenile rats. We also evaluated whether these neurons possess intrinsic CO 2 /[H + ] sensitivity. All recorded pFL expiratory neurons were glutamatergic. In normocapnia, GABAergic and glycinergic inhibition during inspiration and expiration suppressed the activity of excitatory pFL expiratory neurons. In hypercapnia, these neurons escape glycinergic inhibition and generate burst discharges at the end of expiration. Post-inhibitory rebound, Ca V 3.2 isoform of T-type Ca 2+ channels, and intracellular [Ca 2+ ] contribute to their expiratory activity. Hypercapnia/hypocapnia or acidosis/alkalosis did not affect the activity of pFL expiratory neurons, indicating that these neurons do not possess intrinsic CO2 and pH sensitivity. Additionally, ion channels/receptors (TASK or GPR4) related to CO 2 /[H + ] sensitivity were not expressed by pFL expiratory neurons. In conclusion, the intrinsic electrophysiological properties and post-synaptic disinhibition of glutamatergic neurons both play essential roles in generating the expiratory oscillations in the pFL region during hypercapnia in rats. FAPESP and CNPq This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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