The authors’ previous paper Koon et al. (2011) presented in JC in March last year, demonstrated structural changes in octopaminergic synaptic terminals in response to starvation. These changes induce an increase in locomotion. Underlying the structural change is the activation of a positive-feedback mechanism, in which octopamine release, presumably by type II octopaminergic synaptic boutons, activates octopamine autoreceptors Octß2R. In turn, Octß2R turns on a cAMP- and CREB-dependent signaling cascade at octopaminergic neurons, which induces synaptic expansion.
In their new paper (May 2012), they report the presence of an alternative octopamine autoreceptor Octß1R. That receptor has opposed functions on synaptic growth. Mutations in octß1r result in the overgrowth of both glutamatergic and octopaminergic neuromuscular junctions (NMJs). Octß1R is suggested to function in a cell-autonomous manner at presynaptic motorneurons (like Octß2R) and likely inhibits cAMP production through inhibitory Go (unlike Octß2R). Octß1R is required for acute changes in synaptic structure in response to octopamine and for starvation-induced increase in locomotor speed (like Octß2R). Any paracrine stimulation of type I boutons’ growth as it was found for the Octß2R is not mentioned for Octß1R.
This paper shows a antagonistic action of one neurotransmitter on synaptic growth depending on the receptor it is binding to.
Koon, A., & Budnik, V. (2012). Inhibitory Control of Synaptic and Behavioral Plasticity by Octopaminergic Signaling Journal of Neuroscience, 32 (18), 6312-6322 DOI: 10.1523/JNEUROSCI.6517-11.2012
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