MERRYWEST, S.D.; SILLAR, K.T.; University of St Andrews: Noradrenergic control of cell properties and synaptic transmission during motor pattern generation.

In vertebrates, the amine noradrenaline (NA) can initiate, sustain and modulate rhythmic motor activity. We have examined the noradrenergic modulation of sensory inputs and resulting motor outputs in the intact CNS of Xenopus laevis tadpoles. NA slows swimming and reduces the rostro-caudal (RC-) delay in motor neuron firing. α₁– and α₂-adrenoreceptor activation mimics the noradrenergic slowing of swimming, whilst α₁-receptors also reduce RC-delays, suggesting the effects of NA are largely mediated via α-receptors. Strychnine reduces the effects of NA and α₁-receptors on frequency and RC-delays and the slowing of swimming by α₂-receptors, whilst blocking GABA_A receptors counteracts only the slowing of swimming by NA and α₂-receptor activation. Thus, α₁-receptors utilise only glycinergic inhibition to modulate swimming frequency and RC-delays, whilst α₂-receptors slow swimming via glycinergic and GABAergic pathways. NA and α-receptor activation enhances the GABAergic barrage following stimulation of the cement gland in embryos. In addition, NA pre-synaptically enhances the spontaneous release of GABA in quiescent periods between swimming. Similarly, NA and α₁-receptors facilitate the release of glycine. Both NA and α₁-receptors also enhance the probability of rebound firing in motor neurons, presumably via a direct effect on cell properties. This contributes to the reduced delays and maintenance of long swim cycle periods under NA. During another distinct behaviour, struggling, blocking α- and β-receptors reduces the burst frequency caudo-rostral delays. Often the firing pattern switches to become rostro-caudal, a characteristic of swimming rather than struggling. Thus, NA appears to prime, and can activate, the switch between these two behaviours.