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Autoregulatory and paracrine control of synaptic and behavioral plasticity by octopaminergic signaling
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Autoregulatory and paracrine control of synaptic and behavioral plasticity by octopaminergic signaling
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Journal Article
Autoregulatory and paracrine control of synaptic and behavioral plasticity by octopaminergic signaling
2011
Overview
Hunger makes
Drosophila
larvae move faster in search of food. Koon and colleagues show that starvation increases the branching of octopaminergic motoneurons' axonal terminal arbors, driven by octopamine released from these same motoneurons. The increased locomotor activity of starved larvae requires octopaminergic signaling.
Adrenergic signaling has important roles in synaptic plasticity and metaplasticity. However, the underlying mechanisms of these functions remain poorly understood. We investigated the role of octopamine, the invertebrate counterpart of adrenaline and noradrenaline, in synaptic and behavioral plasticity in
Drosophila
. We found that an increase in locomotor speed induced by food deprivation was accompanied by an activity- and octopamine-dependent extension of octopaminergic arbors and that the formation and maintenance of these arbors required electrical activity. Growth of octopaminergic arbors was controlled by a cAMP- and CREB-dependent positive-feedback mechanism that required Octβ2R octopamine autoreceptors. Notably, this autoregulation was necessary for the locomotor response. In addition, octopamine neurons regulated the expansion of excitatory glutamatergic neuromuscular arbors through Octβ2Rs on glutamatergic motor neurons. Our results provide a mechanism for global regulation of excitatory synapses, presumably to maintain synaptic and behavioral plasticity in a dynamic range.
Publisher
Nature Publishing Group US,Nature Publishing Group
