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dc.contributor.authorKoon, Alex C.
dc.contributor.authorBudnik, Vivian
dc.date2022-08-11T08:08:54.000
dc.date.accessioned2022-08-23T16:11:50Z
dc.date.available2022-08-23T16:11:50Z
dc.date.issued2012-05-02
dc.date.submitted2012-09-07
dc.identifier.citation<p>J Neurosci. 2012 May 2;32(18):6312-22. doi: 10.1523/JNEUROSCI.6517-11.2012. <a href="http://dx.doi.org/10.1523/JNEUROSCI.6517-11.2012" target="_blank">Link to article on publisher's site</a></p>
dc.identifier.issn1529-2401
dc.identifier.doi10.1523/JNEUROSCI.6517-11.2012
dc.identifier.pmid22553037
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33261
dc.description.abstractAdrenergic receptors and their ligands are important regulators of synaptic plasticity and metaplasticity, but the exact mechanisms underlying their action are still poorly understood. Octopamine, the invertebrate homolog of mammalian adrenaline or noradrenaline, plays important roles in modulating behavior and synaptic functions. We previously uncovered an octopaminergic positive-feedback mechanism to regulate structural synaptic plasticity during development and in response to starvation. Under this mechanism, activation of Octß2R autoreceptors by octopamine at octopaminergic neurons initiated a cAMP-dependent cascade that stimulated the development of new synaptic boutons at the Drosophila larval neuromuscular junction (NMJ). However, the regulatory mechanisms that served to brake such positive feedback were not known. Here, we report the presence of an alternative octopamine autoreceptor, Octß1R, with antagonistic functions on synaptic growth. Mutations in octß1r result in the overgrowth of both glutamatergic and octopaminergic NMJs, suggesting that Octß1R is a negative regulator of synaptic expansion. As Octß2R, Octß1R functioned in a cell-autonomous manner at presynaptic motorneurons. However, unlike Octß2R, which activated a cAMP pathway, Octß1R likely inhibited cAMP production through inhibitory Goα. Despite its inhibitory role, Octß1R was required for acute changes in synaptic structure in response to octopamine and for starvation-induced increase in locomotor speed. These results demonstrate the dual action of octopamine on synaptic growth and behavioral plasticity, and highlight the important role of inhibitory influences for normal responses to physiological stimuli.
dc.language.isoen_US
dc.publisherSociety for Neuroscience
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22553037&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1523/JNEUROSCI.6517-11.2012
dc.rights<p>Copyright © 2012 the authors. Publisher PDF posted as allowed by the publisher's author rights policy at http://www.jneurosci.org/site/misc/ifa_policies.xhtml#copyright. Copyright of all material published in The Journal of Neuroscience remains with the authors. The authors grant the Society for Neuroscience an exclusive license to publish their work for the first 6 months. After 6 months the work becomes available to the public to copy, distribute, or display under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license.</p>
dc.subjectAnimals; Drosophila; Neural Inhibition; Neuronal Plasticity; Neurons; Octopamine; Receptors, Biogenic Amine; Synapses; Synaptic Transmission
dc.subjectNeuroscience and Neurobiology
dc.titleInhibitory control of synaptic and behavioral plasticity by octopaminergic signaling
dc.typeJournal Article
dc.source.journaltitleThe Journal of neuroscience : the official journal of the Society for Neuroscience
dc.source.volume32
dc.source.issue18
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2813&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1794
dc.identifier.contextkey3302289
refterms.dateFOA2022-08-23T16:11:50Z
html.description.abstract<p>Adrenergic receptors and their ligands are important regulators of synaptic plasticity and metaplasticity, but the exact mechanisms underlying their action are still poorly understood. Octopamine, the invertebrate homolog of mammalian adrenaline or noradrenaline, plays important roles in modulating behavior and synaptic functions. We previously uncovered an octopaminergic positive-feedback mechanism to regulate structural synaptic plasticity during development and in response to starvation. Under this mechanism, activation of Octß2R autoreceptors by octopamine at octopaminergic neurons initiated a cAMP-dependent cascade that stimulated the development of new synaptic boutons at the Drosophila larval neuromuscular junction (NMJ). However, the regulatory mechanisms that served to brake such positive feedback were not known. Here, we report the presence of an alternative octopamine autoreceptor, Octß1R, with antagonistic functions on synaptic growth. Mutations in octß1r result in the overgrowth of both glutamatergic and octopaminergic NMJs, suggesting that Octß1R is a negative regulator of synaptic expansion. As Octß2R, Octß1R functioned in a cell-autonomous manner at presynaptic motorneurons. However, unlike Octß2R, which activated a cAMP pathway, Octß1R likely inhibited cAMP production through inhibitory Goα. Despite its inhibitory role, Octß1R was required for acute changes in synaptic structure in response to octopamine and for starvation-induced increase in locomotor speed. These results demonstrate the dual action of octopamine on synaptic growth and behavioral plasticity, and highlight the important role of inhibitory influences for normal responses to physiological stimuli.</p>
dc.identifier.submissionpathgsbs_sp/1794
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentBudnik Lab
dc.contributor.departmentNeurobiology
dc.source.pages6312-22
dc.contributor.studentAlex Koon
dc.description.thesisprogramNeuroscience


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