Alpha-adrenoreceptor activation modulates swimming via glycinergic and GABAergic inhibitory pathways in Xenopus laevis tadpoles

Abstract

This study focuses upon the network pathways underlying the adrenoreceptor-mediated modulation of fictive swimming in the immobilized Xenopus laevis tadpole. As shown recently, noradrenaline (NA) increases cycle periods while simultaneously reducing the rostrocaudal delay in head-to-tail firing and the duration of swimming episodes. Furthermore, both swimming frequency and duration are reduced by selective pharmacological activation of α1- and/or α2-adrenoreceptors, while α1-receptor activation also reduces rostrocaudal delays. We show that NA could still modulate aspects of swimming after blocking either glycine or GABAA receptors with strychnine and bicuculline, respectively. Furthermore, after prior application of NA, strychnine could counteract noradrenergic effects on cycle periods and rostrocaudal delays, while bicuculline could counteract effects on cycle periods, suggesting that these two fast inhibitory pathways are both involved in the NA modulation of swimming. In addition, blocking glycine receptors reduced the effects of α1-receptors on cycle periods and delays, while blocking GABAA receptors had no effect. Blocking either glycine or GABAA receptors, however, lessened the reduction in swimming frequency by α2-receptors. In addition, pre-application of bicuculline prevented a reduction in episode durations by NA, α1- and α2-receptors. Our findings suggest that the noradrenergic modulation of Xenopus swimming is mediated via α-adrenoreceptors interacting with both glycinergic and GABAergic inhibitory pathways. Both α1- and α2-receptor activation influences the GABAergic pathway controlling the duration of swimming episodes and is involved in the glycinergic modulation of the swimming rhythm and its longitudinal co-ordination, with α2-receptors additionally affecting swimming frequency through GABAergic pathways.