The objective of this study was to evaluate effects of baclofen, a γ-aminobutyric acid type B (GABAB) receptor agonist, injected into the nucleus of the solitary tract, on the Hering-Breuer inspiratory-inhibitory (Ti-inhibitory) and deflation reflexes in urethan-anesthetized adult Wistar rats ( n = 7). The Ti-inhibitory reflex was estimated from changes in peak amplitude of the integrated diaphragmatic electromyogram and inspiratory time (Ti) provoked by airway occlusion at end expiration. The deflation reflex was evaluated from changes in Ti and expiration (Te) of the first two breaths (Ti-1, Te-1 and Ti-2, Te-2) immediately after a decrease in tracheal pressure (Ptr). Under control conditions, airway occlusion at end-Te prolonged Ti (66 ± 5%; mean ± SE) and the following Te (54 ± 11%). Decreases in Ptr, from −2 to −5 cmH2O, evoked an increase in Ti and shortening of Te of both breaths. Both effects were Ptr dependent, and Ti-1 and Te-1 differed from Ti-2 and Te-2, suggesting a rapid adaptation to the stimulus. At Ptr of −5 cmH2O, Ti-1 and Ti-2 increased by 30 ± 2 and 43 ± 6%, respectively, and Te-1 and Te-2 decreased by 53 ± 4 and 33 ± 7%, respectively. During unloaded breathing, 60 pmol baclofen prolonged Ti by 120 ± 11% and left Te unaffected. Baclofen abolished vagally mediated changes in Te. On the other hand, the Ti increases caused by either airway occlusion (24 ± 8%) or Ptr of −5 cmH2O (Ti-1; 16 ± 5%) were still significant, but Ti-1 and Ti-2 were not different. A GABAB receptor antagonist, CGP-35348 (2.8 nmol), reversed these effects of baclofen. These results imply that stimulation of GABAB receptors attenuates but does abolish vagally mediated control of Ti. The difference in effects of baclofen on the central and vagal control of Ti and Te suggests different distribution of GABAB receptors in neuronal networks controlling each of these respiratory phases.
Dendritic Assembly of Heteromeric γ-Aminobutyric Acid Type B Receptor Subunits in Hippocampal Neurons