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 (Song and Poon, Respir. Physiol. Neurobiol., 165(1): [1][2][3][4][5][6][7][8] 2009). Here, we report that unilateral LPBN lesion by kainic acid in the same group of animals not only abolished normal T Eshortening 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