Chapter 10 The role of nitric oxide in development of the patch—cluster system and retinocollicular pathways in the rodent superior colliculus

Mize, R. Ranney; Wu, Hope H.; Cork, R. John; Scheiner, C.A.

doi:10.1016/s0079-6123(08)63205-7

Cited by 39 publications

(37 citation statements)

References 85 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similar repressive effects of NO have been reported to occur in Helisoma buccal ganglia (Van Wagenen et al, 1999;Trimm and Rehder, 2004), vertebrate sensory (Hess et al, 1993;Ernst et al, 2000;He et al, 2002), vertebrate retinal (Rentería and Constantine-Paton, 1996;Mize et al, 1998;Ernst et al, 2000;Wu et al, 2000a,b), and insect retinal (Gibbs and Truman, 1998) axons, but not in cultured PC12 cells (Hindley et al, 1997;Wright et al, 1998;Yamazaki et al, 2001Yamazaki et al, , 2006, or insect enteric/antennal pioneer neurons (Hindley et al, 1997;Seidel and Bicker, 2000;Haase and Bicker, 2003), where NO has trophic actions.…”

Section: Endogenous No and Motor Axon Branchingsupporting

confidence: 64%

“…The NOS1 AMO phenotype most closely resembles the exuberant retinocollicular axon branch phenotype induced in NOS1/NOS3 double knock-out mice (Mize et al, 1998;Wu et al, 2000a,b). In these animals, refinement of supernumerary synaptic connections is disrupted.…”

Section: Endogenous No and Motor Axon Branchingmentioning

confidence: 81%

“…Moreover, there is direct molecular evidence that NOS isozymes are required for retinal axon remodeling (Mize et al, 1998;Wu et al, 2000a,b). However, the role of NOS isoforms in other CNS regions has remained ambiguous.…”

Section: Nos1 As a Regulator Of Axon Development In Vivomentioning

confidence: 99%

“…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). However, it is currently not known whether NOS proteins have axonogenic functions in other CNS regions, despite their widespread expression.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Bradley¹,

Tossell²,

Lockley³

et al. 2010

J. Neurosci.

View full text Add to dashboard Cite

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.

show abstract

Section: Endogenous No and Motor Axon Branchingsupporting

confidence: 64%

Section: Endogenous No and Motor Axon Branchingmentioning

confidence: 81%

Section: Nos1 As a Regulator Of Axon Development In Vivomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Bradley¹,

Tossell²,

Lockley³

et al. 2010

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…For example, in chickens, the elimination of the ipsilateral retinotectal projections is partially dependent on the NO synthesized in the tectum opticum (14). Furthermore, several studies on rodents have suggested that NO might be involved in the topographic establishment of the ipsilateral retinotectal projections (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

Expression of neuronal nitric oxide synthase in the developing superficial layers of the rat superior colliculus

Giraldi-Guimarães

Bittencourt-Navarrete

Mendez-Otero

2004

Braz J Med Biol Res

View full text Add to dashboard Cite

We investigated the level of expression of neuronal nitric oxide synthase (nNOS) in the retinorecipient layers of the rat superior colliculus during early postnatal development. Male and female Lister rats ranging in age between the day of birth (P0) and the fourth postnatal week were used in the present study. Two biochemical methods were used, i.e., in vitro measurement of NOS specific activity by the conversion of [ 3 H]-arginine to [ 3 H]-citrulline, and analysis of Western blotting immunoreactive bands from superior colliculus homogenates. As revealed by Western blotting, very weak immunoreactive bands were observed as early as P0-2, and their intensity increased progressively at least until P21. The analysis of specific activity of NOS showed similar results. There was a progressive increase in enzymatic activity until near the end of the second postnatal week, and a nonsignificant tendency to an increase until the end of the third week was also observed. Thus, these results indicated an increase in the amount of nNOS during the first weeks after birth. Our results confirm and extend previous reports using histochemistry for NADPH-diaphorase and immunocytochemistry for nNOS, which showed a progressive increase in the number of stained cells in the superficial layers during the first two postnatal weeks, reaching an adult pattern at the end of the third week. Furthermore, our results suggested that nNOS is present in an active form in the rat superior colliculus during the period of refinement of the retinocollicular pathway.

show abstract

Normal development of the ipsilateral retinocollicular pathway and its disruption in double endothelial and neuronal nitric oxide synthase gene knockout mice

Cork

Mize

2000

J. Comp. Neurol.

Self Cite

View full text Add to dashboard Cite

The development of the ipsilateral retinocollicular pathway involves activity-dependent refinement in which misdirected axons retract to form a precise retinotopic map in adults. This refinement is altered by disruption of genes for the endothelial and neuronal isoforms of nitric oxide synthase (e,nNOS), but the extent of disruption during early development is not known. Therefore, we studied the refinement of this pathway in normal C57/BL6 and e,nNOS double knockouts from P4 to P21 and in adults. Anterograde tracers were injected into one eye to localize the ipsilateral retinal projection (IRP) within the superior colliculus (SC). At P4, the IRP in normal mice was distributed throughout the dorsoventral extent of the superficial gray layer (SGL) across most of the rostrocaudal axis of SC. Between P4 and P9, the pathway retracted to the rostromedial SC, and retracted further between P15 and P21, such that multiple patches of label were seen only in the rostral 200-300 microm. Refinement also began to occur between P4 and P9 in e,nNOS double knockout mice, but labeling was more extensive in P9, P15, and P21 knockout animals. This delay in refinement was confirmed quantitatively at P15 where differences in the area occupied by the pathway were statistically significant. The refinement process is therefore in progress in both normal and e,nNOS knockout mice before eye opening but is significantly delayed in the double knockouts. The IRP in normal mice is also more exuberant at early ages, and the process of refinement more protracted than has been previously reported, suggesting that there is a prolonged critical period of synaptic plasticity.

show abstract

Chapter 10 The role of nitric oxide in development of the patch—cluster system and retinocollicular pathways in the rodent superior colliculus

Cited by 39 publications

References 85 publications

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Nitric Oxide Synthase Regulates Morphogenesis of Zebrafish Spinal Cord Motoneurons

Expression of neuronal nitric oxide synthase in the developing superficial layers of the rat superior colliculus

Normal development of the ipsilateral retinocollicular pathway and its disruption in double endothelial and neuronal nitric oxide synthase gene knockout mice

Contact Info

Product

Resources

About