Respiratory neurons mediating the Breuer-Hering reflex prolongation of expiration in rat

Afferent input from pulmonary stretch receptors is important in the control of the timing of inspiratory and expiratory phases of the respiratory cycle. The current study was undertaken to identify neurons within a column of respiratory neurons in the ventrolateral medulla (termed the ventral respiratory group, VRG) that, when activated by lung inflation, produce the Breuer-Hering (BH) reflex in which lung inflation causes inspiratory termination and expiratory prolongation. Intracellular recordings of VRG neurons revealed three groups of inspiratory (I) and two groups of expiratory (E) neurons similar to previous descriptions: I-augmenting (I-Aug), I- decrementing (I-Dec), I-plateau (I-All), E-augmenting (E-Aug), and E- decrementing (E-Dec) neurons. Low-intensity, low-frequency stimulation of a vagus nerve elicited paucisynaptic EPSPs in E-Dec, I-Aug, and I-All neurons that could be divided into two groups on the basis of latency (2.8 ± 0.1 msec, n = 10; 4.0 ± 0.1 msec, n = 17). IPSPs were elicited in I-Aug and I- All neurons (4.8 ± 0.1 msec, n = 12). However, only E-Dec neurons were depolarized when the BH reflex was activated by lung inflation (7.5 cm H₂O) or mimicked by vagus nerve stimulation (50 Hz). All other neurons were hyperpolarized and ceased firing during BH reflexmediated expiratory prolongation. A subset of E-Dec neurons (termed E-Dec(early)) discharged before inspiratory termination and could contribute to inspiratory termination. The findings are consistent with the hypothesis that a group of E-Dec neurons receives a paucisynaptic (probably disynaptic) input from pulmonary afferents and, in turn, inhibits inspiratory neurons, thereby lengthening expiration.