Norepinephrine (NE) is a potent modulator of breathing that can increase/decrease respiratory activity by α1-/ α2-adrenergic receptors (AR) activation, respectively. The retrotrapezoid nucleus (RTN) is known to contribute to central chemoreception, inspiration and active expiration. Here we investigate the sources of catecholaminergic inputs to the RTN and identify respiratory effects produced by activation of ARs in this region. By injecting the retrograde tracer FluorGold into the RTN we identified back-labeled catecholaminergic neurons in the A7 region. In urethane-anesthetized, vagotomized and artificial ventilated male Wistar rats unilateral injection of NE or moxonidine (α2-ARagonist) blunted DiaEMG frequency and amplitude, without changing AbdEMG. Those inhibitory effects were reduced by pre-application of yohimbine (α2-AR antagonist) into the RTN. Conversely, unilateral RTN injection of phenylephrine (α1-AR agonist) increased DiaEMG amplitude, frequency and facilitated active expiration. This response was blocked by prior RTN injection of prazosin (α1-AR antagonist). Interestingly, RTN injection of propranolol (β-AR antagonist) had no effect on respiratory inhibition elicited by applications of NE into the RTN, however, the combined blockade of α2- and β-ARs (co-application of propranolol and yohimbine) revealed an α1-AR-dependent excitatory response to NE that resulted in increase in DiaEMG frequency and facilitation of active expiration. However, blockade of α1-, α2-, or β-ARs in the RTN had minimal effect on baseline respiratory activity, on central or peripheral chemoreflexes. These results suggest that NE signaling can modulate RTN chemoreceptor function; however, endogenous NE signaling does not contribute to baseline breathing or the ventilatory response to central or peripheral chemoreceptor activity in urethane-anesthetized rats.
- medulla oblongata
- adrenergic receptors
- in vivo
- Copyright © 2016, Journal of Neurophysiology