Exogenous nitric oxide causes collapse of retinal ganglion cell axonal growth cones in vitro

Renterı́a, René C.; Constantine‐Paton, Martha

doi:10.1002/(sici)1097-4695(199604)29:4<415::aid-neu1>3.3.co;2-d

Cited by 28 publications

(46 citation statements)

References 36 publications

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“…Gibbs and Truman (1998) have shown that blockade of NOS activity in Drosophila leads to disorganization of the projection of photoreceptor axons into the optic lobe. Since NO has been demonstrated to mediate growth cone collapse (Hess et al, 1993;Rentería and Constantine-Paton, 1995), it has been suggested that an NO "stop signal" may subserve the maintenance of initial contacts between ingrowing axons and their postsynaptic targets. An analogous situation might exist in the developing spinal cord because the establishment of patterned afferent input into motor neurons from segmental interneuronal and suprasegmental sources in early postnatal life is coincident with the period of major remodeling of the motor neuron dendritic tree (Curfs et al, 1993;Núñez-Abades et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

The Role of Nitric Oxide and NMDA Receptors in the Development of Motor Neuron Dendrites

Inglis¹,

Furia²,

Zuckerman³

et al. 1998

J. Neurosci.

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Nitric oxide (NO) has been implicated in the establishment of precise synaptic connectivity throughout the neuroaxis in several species. To determine the contribution of NO to NMDA receptor-dependent dendritic growth in motor neurons, we administered the NMDA antagonist MK-801 to wild-type mice and neuronal nitric oxide synthase (nNOS) knock-out mice between postnatal days 7 and 14. Compared to saline-treated wild-type animals the number of dendritic bifurcations was significantly reduced in nNOS knock-out animals and MK-801-treated wildtype animals. There was no significant difference in dendritic bifurcation between MK-801-treated wild-type, MK-801-treated nNOS knock-out, and saline-treated nNOS knock-out animals, suggesting that nNOS knock-out and NMDA receptor block had similar effects. The path of the longest dendrite and the number of primary dendrites was the same in all treatment groups, indicating an effect specific to bifurcation. Sholl analysis revealed that differences in bifurcation numbers occurred between 160 and 320 m from the cell body, the distance at which second, third, and fourth order dendrites are most prevalent. Dendrite order analyses confirmed a significant reduction in numbers, but not lengths, of third and fourth order dendrites in nNOS knock-out and drug-treatment groups. Finally, immunohistochemical examination of the developing spinal cord indicated that NMDA receptors and nNOS are colocalized within interneurons surrounding the motor neuron pool. These results support the view that at least part of NMDA receptordependent arborization of motor neuron dendrites is mediated by the local production of NO within the developing spinal cord.

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Section: Discussionmentioning

confidence: 99%

The Role of Nitric Oxide and NMDA Receptors in the Development of Motor Neuron Dendrites

Inglis¹,

Furia²,

Zuckerman³

et al. 1998

J. Neurosci.

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“…A number of pharmacological studies support the premise that NO regulates development of vertebrate and invertebrate axons (Hess et al, 1993;Roskams et al, 1994;Cramer et al, 1996;Rentería and Constantine-Paton, 1996;Hindley et al, 1997;Gibbs and Truman, 1998;Ernst et al, 1999Ernst et al, , 2000Van Wagenen et al, 1999;Cogen and Cohen-Cory, 2000;Seidel and Bicker, 2000;Van Wagenen and Rehder, 2001;Yamazaki et al, 2001Yamazaki et al, , 2006He et al, 2002;Trimm and Rehder, 2004;Rehder, 2005, 2007). Moreover, there is direct molecular evidence that NOS isoforms are required for development of mouse retinal axons: Double knock-out of NOS1 and NOS3, the two constitutively active NOS isoforms in mammals, disrupts retinocollicular axon refinement (Mize et al, 1998;Wu et al, 2000a,b).…”

Section: Introductionmentioning

confidence: 95%

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Bradley¹,

Tossell²,

Lockley³

et al. 2010

J. Neurosci.

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Nitric oxide (NO) is a signaling molecule that is synthesized in a range of tissues by the NO synthases (NOSs). In the immature nervous system, the neuronal isoform of NOS (NOS1) is often expressed during periods of axon outgrowth and elaboration. However, there is little direct molecular evidence to suggest that NOS1 influences these processes. Here we address the functional role of NOS1 during in vivo zebrafish locomotor circuit development. We show that NOS1 is expressed in a population of interneurons that lie close to nascent motoneurons of the spinal cord. To determine how this protein regulates spinal network assembly, we perturbed NOS1 expression in vivo with antisense morpholino oligonucleotides. This treatment dramatically increased the number of axon collaterals formed by motoneuron axons, an effect mimicked by pharmacological inhibition of the NO/cGMP signaling pathway. In contrast, exogenous elevation of NO/cGMP levels suppressed motor axon branching. These effects were not accompanied by a change in motoneuron number, suggesting that NOS1 does not regulate motoneuron differentiation. Finally we show that perturbation of NO signaling affects the ontogeny of locomotor performance. Our findings provide evidence that NOS1 is a key regulator of motor axon ontogeny in the developing vertebrate spinal cord.

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“…Early production of NO may a¡ect immediate events after damage. For example, NO may cause growth cones to collapse (Hess et al 1993;Rentera & Constantine-Paton 1995). In the pruning of damaged axons that takes place before axonal outgrowth and regeneration (Muller 1984), NO may also be involved through a similar mechanism.…”

Section: (C) Regulation Of Injury-induced Enos-like Proteinmentioning

confidence: 99%

Injury–induced expression of endothelial nitric oxide synthase by glial and microglial cells in the leech central nervous system within minutes after injury

Shafer

Chen

Kumar

et al. 1998

Proc. R. Soc. Lond. B

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It is known that nitric oxide (NO) is produced by injured tissues of the mammalian central nervous system (CNS) within days of injury. The aim of the present experiments was to determine the cellular synthesis of NO in the CNS immediately after injury, using the CNS of the leech which is capable of synapse regeneration, as a step towards understanding the role of NO in nerve repair. We report that within minutes after crushing the nerve cord of the leech, the region of damage stained histochemically for NADPH diaphorase, which is indicative of nitric oxide synthase (NOS) activity, and was immunoreactive for endothelial NOS (eNOS). On immunoblots of leech CNS extract, the same antibody detected a band with a relative molecular mass of 140 000, which is approximately the size of vertebrate eNOS. Cells expressing eNOS immunoreactivity as a result of injury were identi¢ed after freezing nerve cords, a procedure that produced less tissue distortion than mechanical crushing. Immunoreactive cells included connective glia and some microglia. Calmodulin was necessary for the eNOS immunoreactivity: it was blocked by calmodulin antagonist W7 (25 mM), but not by similar concentrations of the less potent calmodulin antagonist W12. Thus in the leech CNS, in which axon and synapse regeneration is successful, an increase in NOS activity at lesions appears to be among the earliest responses to injury and may be important for repair of axons.

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Exogenous nitric oxide causes collapse of retinal ganglion cell axonal growth cones in vitro

Cited by 28 publications

References 36 publications

The Role of Nitric Oxide and NMDA Receptors in the Development of Motor Neuron Dendrites

The Role of Nitric Oxide and NMDA Receptors in the Development of Motor Neuron Dendrites

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Injury–induced expression of endothelial nitric oxide synthase by glial and microglial cells in the leech central nervous system within minutes after injury

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