Octopamine immunoreactivity in the fruit fly <i>Drosophila melanogaster</i>

Monastirioti, Maria; Gorczyca, Michael; Rapus, Jürgen; Eckert, Manfred; White, K. Andrew; Budnik, Vivian

doi:10.1002/cne.903560210

Cited by 184 publications

(186 citation statements)

References 59 publications

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“…The presence of exuberant ectopic synapses could reflect efforts by neurons to compensate for the loss of synapses to enhance glutamatergic synaptic transmission. However, we do not favor the idea that formation of ectopic synapses is a result of developmental compensation because 1) ectopic type I boutons are not always found in dennervated muscles; and 2) octopamine, which is the major neurotransmitter in type II synapses (Monastirioti et al, 1995), inhibits glutamate-mediated synaptic potentials instead of enhancing them (Nishikawa and Kidokoro, 1999). Alternatively, these ectopic synapses might result from a defect in either synaptic targeting or nerve sprouting.…”

Section: Flamingo Is Crucial For Both Target Selection and Synaptogenmentioning

confidence: 63%

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

Bao

Berlanga

Xue

et al. 2007

Molecular and Cellular Neuroscience

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The formation of synaptic connections with target cells and maintenance of axons are highly regulated and crucial for neuronal function. The atypical cadherin and G-protein-coupled receptor Flamingo and its orthologs in amphibians and mammals have been shown to regulate cell polarity, dendritic and axonal growth, and neural tube closure. However, the role of Flamingo in synapse formation and function and in axonal health remains poorly understood. Here we show that fmi mutations cause a significant increase in the number of ectopic synapses on muscles and result in the formation of novel en passant synapses along axons, and unique presynaptic varicosities, including active zones, within axons. fmi mutations also cause defective synaptic responses in a small subset of muscles, an agedependent loss of muscle innervation and a drastic degeneration of axons in 3 rd instar larvae without an apparent loss of neurons. Neuronal expression of Flamingo rescues all of these synaptic and axonal defects and larval lethality. Based on these observations, we propose that Flamingo is required in neurons for synaptic target selection, synaptogenesis, the survival of axons and synapses, and adult viability. These findings shed new light on a possible role for Flamingo in progressive neurodegenerative diseases.

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Section: Flamingo Is Crucial For Both Target Selection and Synaptogenmentioning

confidence: 63%

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

Bao

Berlanga

Xue

et al. 2007

Molecular and Cellular Neuroscience

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“…Like DLG, GTX was enriched postsynaptically at glutamatergic type I boutons ( Fig. 1G-J ) but absent from type II [octopamine-containing (Monastirioti et al, 1995)] and type III [peptide-containing in muscle 12 ] boutons (data not shown). Like DLG, GTX immunoreactivity was enriched at type Ib boutons, less prominent at type Is boutons (data not shown), and decreased at sites of bouton budding arrow).…”

Section: Dlg Is Required For Proper Synaptic Localization Of Gtxmentioning

confidence: 99%

Postsynaptic Membrane Addition Depends on the Discs-Large-Interacting t-SNARE Gtaxin

Gorczyca¹,

Ashley²,

Speese³

et al. 2007

J. Neurosci.

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Targeted membrane addition is a hallmark of many cellular functions. In the nervous system, modification of synaptic membrane size has a major impact on synaptic function. However, because of the complex shape of neurons and the need to target membrane addition to very small andpolarizedsynapticcompartments,thisprocessispoorlyunderstood.Here,weshowthatGtaxin(GTX),aDrosophilat-SNARE(target-soluble N-ethylmaleimide-sensitive factor attachment protein receptor), is required for expansion of postsynaptic membranes during new synapse formation. Mutations in gtx lead to drastic reductions in postsynaptic membrane surface, whereas gtx upregulation results in the formation of complex membrane structures at ectopic sites. Postsynaptic GTX activity depends on its direct interaction with Discs-Large (DLG), a multidomain scaffolding protein of the PSD-95 (postsynaptic density protein-95) family with key roles in cell polarity and formation of cellular junctions as well as synaptic protein anchoring and trafficking. We show that DLG selectively determines the postsynaptic distribution of GTX to type I, but not to type II or type III boutons on the same cell, thereby defining sites of membrane addition to this unique set of glutamatergic synapses. We provide a mechanistic explanation for selective targeted membrane expansion at specific synaptic junctions.

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“…Octopamine, the homolog of norepinephrine in Drosophila, controls many behaviors by activating central G protein-coupled receptors that induce adenylyl cyclase activation and intracellular Ca 2+ release (4,5). Octopamine is also in NMJ boutons at muscles 12 and 13 and can have complex effects at adjacent muscle 6 and 7 NMJs: octopamine inhibits phasic transmission and facilitates tonic release induced by K + , with the latter effect requiring cAMP-dependent protein kinase (PKA) (6)(7)(8). Drosophila motoneurons also contain neuropeptides, which are released in response to nerve stimulation, depolarization, and developmental cues (9)(10)(11)(12)(13).…”

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confidence: 99%

Synaptic neuropeptide release induced by octopamine without Ca ²⁺ entry into the nerve terminal

Shakiryanova

Zettel

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Synaptic release of neurotransmitters is evoked by activity-dependent Ca 2+ entry into the nerve terminal. However, here it is shown that robust synaptic neuropeptide release from Drosophila motoneurons is evoked in the absence of extracellular Ca 2+ by octopamine, the arthropod homolog to norepinephrine. Genetic and pharmacology experiments demonstrate that this surprising peptidergic transmission requires cAMP-dependent protein kinase, with only a minor contribution of exchange protein activated by cAMP (epac). Octopamine-evoked neuropeptide release also requires endoplasmic reticulum Ca 2+ mobilization by the ryanodine receptor and the inositol trisphosphate receptor. Hence, rather than relying exclusively on activity-dependent Ca 2+ entry into the nerve terminal, a behaviorally important neuromodulator uses synergistic cAMP-dependent protein kinase and endoplasmic reticulum Ca 2+ signaling to induce synaptic neuropeptide release.N euromodulators induce presynaptic signaling to regulate fast neurotransmission triggered by activity-induced Ca 2+ entry into the nerve terminal. Neuromodulators also influence the very low rate of spontaneous quantal release of classical transmitters. However, because spontaneous release is functionally relevant only in specialized cases (1), neuromodulators are not believed to typically induce physiologically significant release in the absence of extracellular Ca 2+ . Studies of endocrine cells suggest that release of peptides packaged in large dense-core vesicles (LDCVs) also requires Ca 2+ entry because of the rarity of spontaneous LDCV fusion and the inefficient permeation of peptides through the LDCV-fusion pore (2, 3). However, because it is difficult to measure peptide release at intact synapses, a much more limited dataset supports the conclusion that Ca 2+ influx into the nerve terminal is absolutely required for peptidergic transmission. Thus, it remains unclear how neuromodulators control synaptic neuropeptide release.With this background in mind, we set out to study regulation of neuropeptide release at the Drosophila neuromuscular junction (NMJ) by octopamine-induced cAMP signaling. Octopamine, the homolog of norepinephrine in Drosophila, controls many behaviors by activating central G protein-coupled receptors that induce adenylyl cyclase activation and intracellular Ca 2+ release (4, 5).

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Octopamine immunoreactivity in the fruit fly Drosophila melanogaster

Cited by 184 publications

References 59 publications

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

Postsynaptic Membrane Addition Depends on the Discs-Large-Interacting t-SNARE Gtaxin

Synaptic neuropeptide release induced by octopamine without Ca ²⁺ entry into the nerve terminal

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Octopamine immunoreactivity in the fruit fly Drosophila melanogaster

Cited by 184 publications

References 59 publications

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

The atypical cadherin flamingo regulates synaptogenesis and helps prevent axonal and synaptic degeneration in Drosophila

Postsynaptic Membrane Addition Depends on the Discs-Large-Interacting t-SNARE Gtaxin

Synaptic neuropeptide release induced by octopamine without Ca 2+ entry into the nerve terminal

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Synaptic neuropeptide release induced by octopamine without Ca ²⁺ entry into the nerve terminal