Chapter 19 Nitric oxide and the developmental remodeling of retinal connections in the brain

Wu, Hope H.; Waid, David K.; McLoon, Steven C.

doi:10.1016/s0079-6123(08)62546-7

Cited by 55 publications

(20 citation statements)

References 80 publications

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“…Previous work has indicated that NMDA receptor activation results in the generation of nitric oxide (NO), which is involved in the elimination of the ipsilaterally projecting axons (Ernst et al, 1998). In vitro NO causes growth cone collapse and retraction (Renteria and ConstantinePaton, 1996), consistent with its suggested role in vivo during refinement of the retinotectal projection (Wu et al, 1996;Ernst et al, 1998Ernst et al, , 1999. However, both appropriately and inappropriately located axons are exposed to NO in the tectum.…”

Section: Neurotrophins Interact With Nitric Oxide To Regulate Axonal mentioning

confidence: 78%

“…During development each retina forms an inappropriate ipsilateral projection to target visual centers that is eliminated in an activity-dependent manner (Wu et al, 1996;Mize et al, 1998). Previous work has indicated that NMDA receptor activation results in the generation of nitric oxide (NO), which is involved in the elimination of the ipsilaterally projecting axons (Ernst et al, 1998).…”

Section: Neurotrophins Interact With Nitric Oxide To Regulate Axonal mentioning

confidence: 99%

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Neurotrophins and the dynamic regulation of the neuronal cytoskeleton

Gallo

Letourneau

2000

J. Neurobiol.

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The morphology of neuronal axons and dendrites is dependent on the dynamics of the cytoskeleton. An understanding of neurodevelopment and adult neuroplasticity must therefore include a detailed description of the intrinsic and extrinsic mechanisms that regulate the organization and dynamics of actin filaments and microtubules. In this paper we review recent advances in the understanding of the dynamic regulation of neuronal morphology by interactions among cytoskeletal components and the regulation of the cytoskeleton by neurotrophins.

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Section: Neurotrophins Interact With Nitric Oxide To Regulate Axonal mentioning

confidence: 78%

Section: Neurotrophins Interact With Nitric Oxide To Regulate Axonal mentioning

confidence: 99%

Neurotrophins and the dynamic regulation of the neuronal cytoskeleton

Gallo

Letourneau

2000

J. Neurobiol.

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“…The most complete studies have been performed in chick. The ipsilatcral retinal projection, which is normally transient, is partially preserved by daily intraperitoneal injections of NoArg or NAME [11,12] and both of these inhibitors disrupt the topography of the contralateral retinotectal pathway [11], McLoon and co workers [11] have also shown that the ipsilatcral and con tralateral retinal afferents to the rat SC do not segregate completely after NoArg administration. A somewhat dif ferent effect has been reported in the ferret LGN, where the segregation of the 'on' and 'o ff sublaminae is dis rupted by either focal or systemic inhibition of NOS [ 13,14].…”

Section: Absence Of An Effect Of Nos Inhibitors On Chat Fiber Developmentioning

confidence: 99%

“…In the visual system, NO appears to be involved in both fiber retraction and the refinement of topographic maps. Peak NOS expression occurs in cells at the time at which axons from the retina are retracting in both the chick optic tectum [ 10] and the rat superior colliculus (SC) [11], Monocular enucleation reduces NOS expression dur ing this period [10] and interruption of NO release using inhibitors of NOS disrupts topographic refinement of both the ipsilateral and contralateral retinotectal pathways in chicks [11,12], A similar effect has been shown in the lat eral geniculate nucleus o f the ferret where NOS inhibitors block segregation of the 'on' and 'off' sublaminae of this nucleus [13,14], On the other hand, the eye-specific segre gation of ipsilateral and contralateral retinal input to the ferret LGN is not disrupted by inhibition of NOS [14] and the topography of ipsilateral and contralateral retinal afferents projecting to the SC is not altered in neuronal NOS genetic knockout mice that presumably lack NO [15]. Our understanding of the role of NO in fiber refinement is, therefore, in its formative stages.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Nitric Oxide Synthase Fails to Disrupt the Development of Cholinergic Fiber Patches in the Rat Superior Colliculus

et al. 1997

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Nitric oxide may serve as a retrograde messenger to refine or stabilize synapses in the developing nervous system. Whether this action is dependent upon glutamate and the N-methyl-D-aspartate receptor is not yet established. We have used the patch-cluster system in the intermediate gray layer (IGL) of the rat superior colliculus (SC), a system receiving both glutamatergic and cholinergic input, to study this question. The normal distribution and development of nitric oxide synthase (NOS) in SC was examined using nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry in Sprague-Dawley rats aged P4 to adulthood. Fibers containing acetylcholine (ACh) were identified using choline acetyltransferase (ChAT) immunocytochemistry. In addition, Nω-nitro-L-arginine, an inhibitor of NOS, was injected intraperito-neally from birth until P10, P14, PI 8, or P21–22 to determine if NOS inhibition would disrupt the formation of the ACh patches. Control animals were studied from the same age groups. Our results show NADPH-d-labeled cells within the periaqueductal gray and the deep gray layer of SC by P4, the earliest age examined. By P8–P9, cells in the IGL were well labeled by NADPH-d, while few in the superficial layers (SL) were labeled. SL cells were visible by P10 and were intensely labeled by P14. IGL cells transiently expressed NADPH-d in that the number of labeled cells increased from P8 to P35, then decreased in the adult. ChAT-labeled fibers first appeared in the IGL at P10, formed a characteristic two-tier pattern by PI4, and established obvious patches by P21. Inhibition of NOS from birth produced no qualitative differences in the distribution or density of either ChAT-labeled fibers or NADPH-d-labeled cells and fibers at any of the ages examined. We therefore conclude that NO does not contribute to the refinement of cholinergic fiber patches in the rat SC, probably because the fiber system is not glutamatergic.

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“…NO is a free radical gas that may mediate synaptic plasticity, because it is able to diffuse in a retrograde direction to signal to presynaptic axons the activity that has occurred in postsynaptic neurons (Bredt et al, 1990;Gally et al, 1990;Garthwaite, 1991;Montague et al, 1991;Dawson et al, 1992;Wood and Garthwaite, 1994). In chick, the retinotectal pathway, which is normally eliminated during development, is partially spared by systemic application of a nitric oxide synthase (NOS) inhibitor, an effect which is also NMDA dependent (Wu et al, 1994(Wu et al, , 1996Ernst et al, 1998Ernst et al, , 1999. NOS inhibition also blocks segregation of the "on" and "off" sublamine of the ferret lateral geniculate nucleus, an effect that is also mediated by the NMDA receptor and impulse activity (Hahm et al, 1991;Cramer et al, 1996Cramer et al, , 1998Cramer and Sur, 1997).…”

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confidence: 99%

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.

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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.

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Chapter 19 Nitric oxide and the developmental remodeling of retinal connections in the brain

Cited by 55 publications

References 80 publications

Neurotrophins and the dynamic regulation of the neuronal cytoskeleton

Neurotrophins and the dynamic regulation of the neuronal cytoskeleton

Inhibition of Nitric Oxide Synthase Fails to Disrupt the Development of Cholinergic Fiber Patches in 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

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