Lateral parabrachial nucleus mediates shortening of expiration and increase of inspiratory drive during hypercapnia.

We have previously shown that unilateral or bilateral lesions of the lateral parabrachial nucleus (LPBN) in anesthetized, vagotomized rats markedly and selectively attenuate the shortening of expiratory duration (T(E)) during hypoxia without appreciably affecting all other hypoxic response components. Here, we report that unilateral LPBN lesion by kainic acid in the same group of animals not only abolished normal T(E)-shortening during central chemoreceptors activation by hyperoxic hypercapnia, but led to paradoxical T(E)-prolongation and corresponding decrease of respiratory frequency. Furthermore, LPBN lesion significantly attenuated the increase in phrenic activity during hyperoxic hypercapnia, without appreciably affecting the corresponding shortening of inspiratory duration (T(I)). These findings provide the first evidence indicating that central chemoafferent inputs are organized in parallel and segregated pathways that separately modulate inspiratory drive, T(I), and T(E) in conjunction with similar parallel and segregated central processing of peripheral chemoafferent inputs reported previously [Young, D.L., Eldridge, F.L., Poon, C.S., 2003. Integration-differentiation and gating of carotid afferent traffic that shapes the respiratory pattern. J. Appl. Physiol. 94, 1213-1229].