Figure 20.

Rats exposed to CIH have increased density of NE terminals in the ventromedial quadrant of the XII nucleus (top section) and increased endogenous excitatory drive to XII motoneurons mediated by α₁-adrenergic receptors (bottom section). (A1 and B1) Comparison of the appearance of NE-containing terminals in 100 × 100 μm images of the ventromedial quadrant of the XII nucleus in a rat exposed to CIH for 35 days (A1) and a sham-treated animal (B1). Also visible are several XII motoneurons retrogradely labeled from the base of the tongue (dark brown). (A2 and B2) Graphic renditions of all NE-containing terminals found in the images shown in A1 and B1. Red dots indicate terminals that were closely apposed to the somatic membrane of retrogradely labeled XII motoneurons (gray), whereas black dots represent the remaining NE terminals. (C) Average numbers of NE terminals (immunostained for dopamine-β-hydroxylase) counted in 24 matched for the anteroposterior level pairs of brain sections from eight pairs of CIH/sham-treated rats. (Panels A–C modified from Fig. 2 and 3 in Ref. 443 and republished with permission from the American Thoracic Society.) (D) Microinjections of the α₁-adrenergic receptor antagonist, prazosin (PZ), into the XII nucleus caused larger decrements of spontaneous XII nerve activity in anesthetized, paralyzed, and artificially ventilated rats that were earlier exposed to CIH for 35 days than in sham-treated animals. (E) Prazosin injections did not cause any changes of the central respiratory rate. (Panels D and E modified from Fig. 3 in Ref. 517 and republished with permission from the American Physiological Society.)