Spinal and supraspinal functions of noradrenaline in the frog embryo: consequences for motor behaviour

The monoamine noradrenaline (NA) can initiate and/or modulate locomotion in a variety of vertebrates. Here we report that exogenous NA application can facilitate two completely different fictive behaviours in embryos of the common frog Rana temporaria, depending on whether spinal networks are connected to supraspinal centres. When the nervous system is intact, NA elicits a non-rhythmic coiling motor response, reminiscent of a spontaneous behaviour appropriate to drive hatching movements, but has only minor effects on evoked swimming activity. After the spinal cord has been severed from the brain, spontaneous coiling is no longer observed, nor can NA elicit it, but the amine can ‘release’ swimming rhythm generation in response to electrical skin stimulation. The rhythm is similar, but relatively inflexible when compared to fictive swimming recorded from intact animals. Our pharmacological tests indicate that α1-adrenoreceptors are involved in the permissive role of NA during spinalised rhythmic swimming and that the fictive coiling response to NA in intact animals involves descending inputs and the activation of β1-adrenoreceptors. Furthermore, the subtle effects of NA on evoked swimming in intact animals were mimicked by either α1- or α2-adrenoreceptor activation, reversibly decreasing motor burst durations and increasing their frequency. We discuss our results with reference to the known synergistic actions of NA with another aminergic neuromodulator, serotonin, and raise the possibility that these amines may actively regulate the release of one another during locomotion, in addition to their respective post-synaptic targets in the spinal cord

Smoke extracts and nicotine, but not tobacco extracts, potentiate firing and burst activity of Ventral Tegmental Area dopaminergic neurons in mice

International audienceNicotine prominently mediates the behavioral effects of tobacco consumption, either through smoking or when taking tobacco by snuff or chew. However, many studies question the exclusive role of nicotine in these effects. The use of preparations containing all the components of tobacco, such as tobacco and smoke extracts, may be more suitable than nicotine alone to investigate the behavioral effects of smoking and tobacco intake. In the present study, the electrophysiological effects of tobacco and smoke on ventral tegmental area dopamine (DA) neurons were examined in vivo in anesthetized wild-type (WT), ß2 nicotinic acetylcholine receptor (nAChR) knock-out (ß2-/-), α4-/- and α6-/- mice and compared to those of nicotine alone. In WT mice, smoke and nicotine had similar potentiating effects on DA cells activity, but the action of tobacco on neuronal firing was weak, and often inhibitory. In particular, nicotine triggered strong bursting activity, while no bursting activity was observed after tobacco extract administration. In ß2-/- mice, nicotine or extract elicited no modification of the firing patterns of DA cells, indicating that extract act predominantly through nAChRs. The differences between DA cells activation profiles induced by tobacco and nicotine alone observed in WT persited in α6-/- mice but not in α4-/- mice. These results would suggest that tobacco has lower addiction generating properties compared to either nicotine alone or smoke. The weak activation and prominent inhibition obtained with tobacco extracts suggest that tobacco contains compounds which counteract some of the activating effects of nicotine and promote inhibition on DA cell acting through α4ß2*-nAChRs. The nature of these compounds remains to be elucidated. It nevertheless confirms that nicotine is the main substance involved in the tobacco addiction-related activation of mesolimbic DA neurons