The adult abdominal neuromuscular junction of <i>Drosophila</i>: A model for synaptic plasticity

Hebbar, Sarita; Hall, Rachel E.; Demski, Sarah A.; Subramanian, Aswati; Fernandes, Joyce J.

doi:10.1002/neu.20279

Cited by 27 publications

(38 citation statements)

References 47 publications

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“…By co-labeling with the neuronal marker 22C10, we found that the ventral muscles in segment A2 are robustly innervated by Hb9-Gal4 expressing neurons, as previously reported (Fig. 5I) (Hebbar et al, 2006). However, in segment A3 Hb9-Gal4 expressing neurons make a much smaller contribution to the ventral muscle innervation (Fig.…”

Section: Resultssupporting

confidence: 88%

“…The Hb9 homeodomain protein is another marker of motor neurons. Some of the ventrally projecting motor neurons express Hb9 (Broihier and Skeath, 2002; Hebbar et al, 2006). …”

Section: Resultsmentioning

confidence: 99%

“…To further examine the contribution of Hb9 expressing neurons to ventral abdominal muscle innervation, we examined filet preps from wild type and grim rpr mutant animals with Hb9-Gal4 UAS-mCD8-GFP (Broihier and Skeath, 2002; Hebbar et al, 2006). By co-labeling with the neuronal marker 22C10, we found that the ventral muscles in segment A2 are robustly innervated by Hb9-Gal4 expressing neurons, as previously reported (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The repetitive and simple organization of the abdominal muscles provides a particularly tractable model for examining alterations in adult myogenesis (Hebbar et al, 2006). The tissue is accessible in both pupae and adults, and extensive studies have described the normal development of these muscles (Bate et al, 1991; Currie and Bate, 1995; Dutta et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Cell death regulates muscle fiber number

Sarkissian

Arya

Gyonjyan

et al. 2016

Developmental Biology

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Cell death can have both cell autonomous and non-autonomous roles in normal development. Previous studies have shown that the central cell death regulators grim and reaper are required for the developmentally important elimination of stem cells and neurons in the developing central nervous system (CNS). Here we show that cell death in the nervous system is also required for normal muscle development. In the absence of grim and reaper, there is an increase in the number of fibers in the ventral abdominal muscles in the Drosophila adult. This phenotype can be partially recapitulated by inhibition of cell death specifically in the CNS, indicating a non-autonomous role for neuronal death in limiting muscle fiber number. We also show that FGFs produced in the cell death defective nervous system are required for the increase in muscle fiber number. Cell death in the muscle lineage during pupal stages also plays a role in specifying fiber number. Our work suggests that FGFs from the CNS act as a survival signal for muscle FCs. Thus, proper muscle fiber specification requires cell death in both the nervous system and in the developing muscle itself.

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Section: Resultssupporting

confidence: 88%

“…The Hb9 homeodomain protein is another marker of motor neurons. Some of the ventrally projecting motor neurons express Hb9 (Broihier and Skeath, 2002; Hebbar et al, 2006). …”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cell death regulates muscle fiber number

Sarkissian

Arya

Gyonjyan

et al. 2016

Developmental Biology

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“…A genetically induced reduction of FasII affects the morphology of adult NMJs by reducing the area, but not the size of individual synaptic boutons. Conversely, a genetically encoded increase of FasII results in increased numbers of boutons and presynaptic area (Hebbar et al 2006).…”

Section: Cams In Nmj Plasticitymentioning

confidence: 99%

Cell Adhesion Molecules at the Drosophila Neuromuscular Junction

Carrero-Martínez

Chiba

2009

The Sticky Synapse

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PrefaceThe molecular mechanisms, which are responsible for the functional differences between the various types of neuronal synapses, have become one of the central themes of modern neurobiology. It is becoming increasingly clear that a misregulation of synaptogenesis and synaptic remodeling and dysfunctional neuronal synapses are at the heart of several human diseases, both neurological disorders and psychiatric conditions. As synapses present specialized cellular junctions between neurons and their target cells, it may not come as a surprise that neural cell adhesion molecules (CAMs) are of special importance for the genesis and the maintenance of synaptic connections. Genes encoding adhesive molecules make up a significant portion of the human genome, and neural CAMs even have been postulated to be a major factor in the evolution of the human brain. These are just some of the many reasons why we thought a book on neural CAMs and their role in establishing and maintaining neuronal synapses would be highly appropriate for summarizing our current state of knowledge. Without question, over the near future, additional adhesive proteins will join the ranks of synaptic CAMs and our knowledge, and how these molecules enable neurons and their targets to communicate effectively will grow. We hope that this book will provide a comprehensive and timely synopsis of the role of CAMs at synaptic connections and will encourage other researchers to join this exciting field of neuroscience, which has the promise not only to yield new insights into the functioning of our brain but also to shed light on some devastating human diseases. Abstract A major goal in neuroscience is the understanding of organizational principles underlying cellular communication and the ensuing molecular integrations that lead to a functional nervous system. The establishment of neuromuscular connections (junctions) is a complex process that requires enumerable cellular and molecular interactions. There are many known and well-characterized molecular events involved in every aspect of neuromuscular junction (NMJ) formation. For instance, at the presynaptic side the motoneuron must differentiate, polarize, undergo dendrogenesis and axogenesis, and extend its processes out to the muscle field. This requires axon guidance, pathfinding, and finally synaptogenesis. At the postsynaptic side, the muscle cell must differentiate and find its correct place in the embryonic body plan to receive motor axons. There are many molecules known to play essential roles during each step in these self-organizational processes. Genetic and biochemical studies have identified molecules that facilitate accurate synaptic target recognitions, as well as those responsible for pre-and postsynaptic specializations. Cell adhesion molecules (CAMs) are known to play an essential role in establishing the NMJ. In this chapter, we begin by exploring Drosophila and its NMJ as a model system for glutamatergic synapses in the mammalian central nervous system. We continue by discussing sele...

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Aging Drosophila melanogaster display altered pre‐ and postsynaptic ultrastructure at adult neuromuscular junctions

Wagner

Laugks

Heckmann

et al. 2015

J of Comparative Neurology

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Although age-related changes in synaptic plasticity are an important focus within neuroscience, little is known about ultrastructural changes of synaptic morphology during aging. Here we report how aging affects synaptic ultrastructure by using fluorescence and electron microscopy at the adult Drosophila neuromuscular junction (NMJ) of ventral abdominal muscles. Mainly four striking morphological changes of aging NMJs were revealed. 1) Bouton size increases with proportionally rising number of active zones (AZs). 2) Synaptic vesicle density at AZs is increased in old flies. 3) Late endosomes, cisternae, and multivesicular bodies accumulate in the presynaptic terminal, and vesicles accumulate between membranes of the terminal bouton and the subsynaptic reticulum. 4) The electron-dense pre- and postsynaptic apposition is expanded in aging NMJs, which is accompanied by an expansion of the postsynaptic glutamate receptor fields. These findings suggest that aging is possibly accompanied by impaired synaptic vesicle release and recycling and a potentially compensatory expansion of AZs and postsynaptic densities.

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The adult abdominal neuromuscular junction of Drosophila: A model for synaptic plasticity

Cited by 27 publications

References 47 publications

Cell death regulates muscle fiber number

Cell death regulates muscle fiber number

Cell Adhesion Molecules at the Drosophila Neuromuscular Junction

Aging Drosophila melanogaster display altered pre‐ and postsynaptic ultrastructure at adult neuromuscular junctions

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