Nitric oxide synthase activity is required for postsynaptic differentiation of the embryonic neuromuscular junction

Schwarte, Russell C.; Godfrey, Earl W.

doi:10.1016/j.ydbio.2004.06.003

Cited by 16 publications

(15 citation statements)

References 63 publications

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“…al., 2004). NO is thought to play an important role during synapse formation in a number of systems (Truman et al, 1996;Cramer et al, 1998;Schwarte and Godfrey, 2004;Sunico et al, 2005;Zhang et al, 2005) and is required for the rapid formation of new presynaptic processes (Nikonenko et al, 2003) and clusters of both presynaptic and postsynaptic proteins (Wang et al, 2005) during long-lasting potentiation in hippocampal neurons. In preliminary experiments, we observed a similar increase in clusters of presynaptic proteins during conditioning in the siphon-withdrawal preparation (I. Antonov, I. Antonova, and R. D. Hawkins, unpublished observations).…”

Section: Role Of No In the Le Membrane Property-independent Process Omentioning

confidence: 99%

Role of Nitric Oxide in Classical Conditioning of Siphon Withdrawal inAplysia

Antonov

Ha²,

Antonova³

et al. 2007

J. Neurosci.

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Nitric oxide (NO) is thought to be involved in several forms of learning in vivo and synaptic plasticity in vitro, but very little is known about the role of NO during physiological forms of plasticity that occur during learning. We addressed that question in a simplified preparation of the Aplysia siphon-withdrawal reflex. We first used in situ hybridization to show that the identified L29 facilitator neurons express NO synthase. Furthermore, exogenous NO produced facilitation of sensory-motor neuron EPSPs, and an inhibitor of NO synthase or an NO scavenger blocked behavioral conditioning. Application of the scavenger to the ganglion or injection into a sensory neuron blocked facilitation of the EPSP and changes in the sensory-neuron membrane properties during conditioning. Injection of the scavenger into the motor neuron reduced facilitation without affecting sensory neuron membrane properties, and injection of an inhibitor of NO synthase had no effect. Postsynaptic injection of an inhibitor of exocytosis had effects similar to injection of the scavenger. However, changes in the shape of the EPSP during conditioning were not consistent with postsynaptic AMPA-like receptor insertion but were mimicked by presynaptic spike broadening. These results suggest that NO makes an important contribution during conditioning and acts directly in both the sensory and motor neurons to affect different processes of facilitation at the synapses between them. In addition, they suggest that NO does not come from either the sensory or motor neurons but rather comes from another source, perhaps the L29 interneurons.

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Section: Role Of No In the Le Membrane Property-independent Process Omentioning

confidence: 99%

Role of Nitric Oxide in Classical Conditioning of Siphon Withdrawal inAplysia

Antonov

Ha²,

Antonova³

et al. 2007

J. Neurosci.

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“…In addition to calcium, two other diffusible second messengers, nitric oxide (NO) and cAMP, may also be involved in AChR clustering and dispersal. Nitric oxide synthase (NOS) localizes at NMJs, inhibition of NO production reduces agrin-induced AChR clustering in muscle cells and at NMJs, and NO donors enhance AChR clustering (119,120). And, in the case of cAMP, regulatory subunit of effector protein kinase A and an A-kinase anchoring protein (AKAP) localize at the NMJ (121).…”

Section: Intracellular Second Messengersmentioning

confidence: 99%

Molecular regulation of postsynaptic differentiation at the neuromuscular junction

Madhavan

Peng

2005

IUBMB Life (International Union of Biochemistry and Molecular B

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SummaryThe neuromuscular junction (NMJ) is a synapse that develops between a motor neuron and a muscle fiber. A defining feature of NMJ development in vertebrates is the re-distribution of muscle acetylcholine (ACh) receptors (AChRs) following innervation, which generates highdensity AChR clusters at the postsynaptic membrane and disperses aneural AChR clusters formed in muscle before innervation. This process in vivo requires MuSK, a muscle-specific receptor tyrosine kinase that triggers AChR re-distribution when activated; rapsyn, a muscle protein that binds and clusters AChRs; agrin, a nervesecreted heparan-sulfate proteoglycan that activates MuSK; and ACh, a neurotransmitter that stimulates muscle and also disperses aneural AChR clusters. Moreover, in cultured muscle cells, several additional muscle-and nerve-derived molecules induce, mediate or participate in AChR clustering and dispersal. In this review we discuss how regulation of AChR re-distribution by multiple factors ensures aggregation of AChRs exclusively at NMJs.

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“…Whilst we cannot exclude the possibility that pharmacological treatment at earlier time points may influence fascicular synaptogenesis, the observation that NOS1 is first expressed within the spinal cord at around 30 hpf [41] strongly suggests that NO has no physiological role during initial stages of neuromuscular development which begins at ∼ 17 hpf [54]. Thus, unlike amphibian and avian species, where NO affects aneural ACh receptor cluster assembly [2]–[5], the earliest stages of zebrafish NMJ development are unlikely to be NO-dependent.…”

Section: Discussionmentioning

confidence: 91%

“…During this study the following drugs were used: diethylenetriamine/nitric oxide adduct (DETA-NO, 250–500 µM, Sigma), N ω-Nitro-L-arginine methyl ester hydrochloride (L-NAME, 500 µM-1 mM, Sigma), 8-(4-Chlorophenylthio)-guanosine 3′, 5′-cyclic monophosphate sodium salt (8-pCPT-cGMP, 500–750 µM, Sigma), 1 H-[1], [2], [4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 500 µM, Ascent Scientific), tetrodotoxin (TTX, 1 µM, Ascent Scientific), (+)-tubocurarine hydrochloride (tubocurarine, 3 µM, Sigma), formamide (2 M, Sigma) and 18-β-glycyrrhetinic acid (18βGA, 100 µM, Sigma).…”

Section: Methodsmentioning

confidence: 99%

“…The NOS1 isozyme is expressed in neuronal tissue, often during periods of growth cone extension and synapse formation [1], [12]–[23] and can influence both synapse assembly [24]–[37] and maintenance [6], [8], [38], [39]. Recent evidence also suggests NO has developmental effects on the developing neuromuscular junction (NMJ): in Xenopus and chick embryos chronic NO treatment promotes acetylcholine (ACh) receptor clustering [2]–[5]. In addition, acute exposure to NO donors depresses spontaneous and evoked synaptic transmission at the NMJ of developing amphibians [40], an effect which may contribute to activity-dependent maturation of neuromuscular synapses.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Nitric Oxide on Neuromuscular Properties of Developing Zebrafish Embryos

2014

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Nitric oxide is a bioactive signalling molecule that is known to affect a wide range of neurodevelopmental processes. However, its functional relevance to neuromuscular development is not fully understood. Here we have examined developmental roles of nitric oxide during formation and maturation of neuromuscular contacts in zebrafish. Using histochemical approaches we show that elevating nitric oxide levels reduces the number of neuromuscular synapses within the axial swimming muscles whilst inhibition of nitric oxide biosynthesis has the opposite effect. We further show that nitric oxide signalling does not change synapse density, suggesting that the observed effects are a consequence of previously reported changes in motor axon branch formation. Moreover, we have used in vivo patch clamp electrophysiology to examine the effects of nitric oxide on physiological maturation of zebrafish neuromuscular junctions. We show that developmental exposure to nitric oxide affects the kinetics of spontaneous miniature end plate currents and impacts the neuromuscular drive for locomotion. Taken together, our findings implicate nitrergic signalling in the regulation of zebrafish neuromuscular development and locomotor maturation.

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Nitric oxide synthase activity is required for postsynaptic differentiation of the embryonic neuromuscular junction

Cited by 16 publications

References 63 publications

Role of Nitric Oxide in Classical Conditioning of Siphon Withdrawal inAplysia

Role of Nitric Oxide in Classical Conditioning of Siphon Withdrawal inAplysia

Molecular regulation of postsynaptic differentiation at the neuromuscular junction

Effects of Nitric Oxide on Neuromuscular Properties of Developing Zebrafish Embryos

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