Motor Nerve Sprouting

Brown, Michael C.; Holland, R. L.; Hopkins, William G.

doi:10.1146/annurev.ne.04.030181.000313

Cited by 500 publications

(203 citation statements)

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“…It is also well known that denervated target cells provide signals that promote neuronal sprouting, even by uninjured neighboring axons (7,13,37). Such signaling can occur via several means.…”

Section: Discussionmentioning

confidence: 99%

A monoclonal antibody that blocks the activity of a neurite regeneration-promoting factor: studies on the binding site and its localization in vivo.

Chiu¹,

Matthew²,

Patterson³

1986

The Journal of Cell Biology

111

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Abstract. Work from several laboratories has identified a proteoglyean complex secreted by a variety of non-neuronal cells that can promote neurite regeneration when applied to the surface of culture dishes. Using a novel immunization protocol, a monoclonal antibody (INO) was produced that blocks the activity of this outgrowth-promoting factor (Matthew, W. D., and P. H. Patterson, 1983, Cold Spring Harbor Symp. Quant. Biol. 48:625-631). We have used the antibody to analyze the components of the active site and to localize the complex in vivo. INO binding is lost when the complex is dissociated; if its components are selectively reassociated, INO binds only to a complex containing two different molecular weight species. These are likely to be laminin and heparan sulfate proteoglycan, respectively. On frozen sections of adult rat tissues, INO binding is present on the surfaces of glial cells of the peripheral, but not the central, nervous system. INO also binds to the basement membrane surrounding cardiac and skeletal muscle cells, and binding to the latter greatly increases after denervation. In the adrenal gland and kidney, INO selectively reacts with areas rich in basement membranes, staining a subset of structures that are immunoreactive for both laminin and heparan sulfate proteoglycan. In general, the outgrowth-blocking antibody binds to areas known to promote axonal regeneration and is absent from areas known to lack this ability. This suggests that this complex, which is active in culture, may be the physiological substrate supporting nerve regeneration in vivo.oNs damaged in the peripheral nervous system (PNS) 1 of adult mammals have the capacity to regenerate over long distances. The prerequisites for successful neurite outgrowth include the presence of trophic factors, such as nerve growth factor (3), and/or an appropriate surface on which to grow (30). The molecular nature of the surfaces that allow or stimulate regeneration in vivo is not known. Experiments in culture, however, have delineated a number of candidate molecules that can promote neurite outgrowth under specific conditions. For instance, surfaces coated with laminin or fibronectin stimulate a much more rapid and extensive regeneration of neuronal processes than can serum-or collagen-coated plastic (2,4,9,24,29,31,39,44). The finding that laminin, in particular, provides an especially good substrate for outgrowth is of interest because a variety of non-neuronal cells secrete neurite regeneration-promoting factors (1,12,14,26), some of which are extracellular matrix complexes containing primarily laminin and heparan sulfate proteoglycan (HeSPG) (8,16,28).Since laminin is a component of a naturally occurring,1. Abbreviations used in this paper: CM, conditioned medium; CNS, central nervous system; DRG, dorsal root ganglion; HeSPG, heparan sulfate proteoglycan; PNS, peripheral nervous system. neurite-promoting complex, and purified laminin can stimulate outgrowth in culture, the question arises as to whether there is a role for the HeSPG compo...

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Section: Discussionmentioning

confidence: 99%

A monoclonal antibody that blocks the activity of a neurite regeneration-promoting factor: studies on the binding site and its localization in vivo.

Chiu¹,

Matthew²,

Patterson³

1986

The Journal of Cell Biology

111

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“…potentials, strong unit forces). 22,23 Axons that remain intact can sprout locally to innervate four to six times more muscle fibers, 40 which is key to retention of innervation and functional use of these muscles. However, muscles innervated by few motoneurons will likely have coarser force control because each unit will make a relatively greater contribution to whole muscle force.…”

Section: Figmentioning

confidence: 99%

Motoneuron Death after Human Spinal Cord Injury

Grumbles

Thomas

2017

Journal of Neurotrauma

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The severe muscle weakness and atrophy measured after human spinal cord injury (SCI) may relate to chronic muscle denervation due to motoneuron death and/or altered muscle use. The aim of this study was to estimate motoneuron death after traumatic human SCI. The diameter and number of myelinated axons were measured in ventral roots post-mortem because ventral roots contain large diameter (> 7 lm) myelinated axons that typically arise from motoneurons and innervate skeletal muscle. In four cases (SCI levels C7, C8, T4, and L1) involving contusion (n = 3) or laceration (n = 1), there was a significant reduction in the number of large diameter myelinated axons at the lesion epicenter (mean -standard error [SE]: 45 -11% Uninjured), one level above (51 -14%), and one (27 -12%), two (45 -40%), and three (54 -23%) levels below the epicenter. Reductions in motoneuron numbers varied by side and case. These deficits result from motoneuron death because the gray matter was destroyed at and near the lesion epicenter. Muscle denervation must ensue. In seven cases, ventral roots at or below the epicenter had large diameter myelinated axons with unusually thin myelin, a sign of incomplete remyelination. The mean -SE g ratio (axon diameter/fiber diameter) was 0.60 -0.01 for axons of all diameters in five above-lesion ventral roots, but increased significantly for large diameter fibers ( ‡ 12 lm) in three roots at the lesion epicenter. Motoneuron death after human SCI will coarsen muscle force gradation and control, while extensive muscle denervation will stifle activity-based treatments.

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“…However, the number of regenerating motor axons can not be directly correlated with the muscle potentials recorded due to two well known phenomena; the terminal sprouting of regenerative motor axons that may increase to 2-3 times the size of their complementary motor units (Brown et al, 1981), and the changes in type of motor units after denervation and reinnervation (Gordon et al, 1999).…”

Section: Neuronal Labelling and Electrophysiological Recordingsmentioning

confidence: 99%

On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

Puigdellı́vol-Sánchez

Valero‐Cabré

Prats-Galino

et al. 2002

Journal of Neuroscience Methods

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The usefulness of three retrograde fluorescent dyes for tracing injured peripheral axons was investigated. The rat sciatic was transected bilaterally and the proximal end briefly exposed to either Fast Blue (FB), Fluoro-Gold (FG) or to Diamidino Yellow (DY) on the right side, and to saline on the left side, respectively. The nerves were then resutured and allowed to regenerate.Electrophysiological tests three months later showed similar latencies and amplitudes of evoked muscle and nerve action potentials between tracer groups. The nerves were then cut distal to the original injury and exposed to a second (different) dye. Five days later, retrogradely labelled neurones were counted in the dorsal root ganglia (DRGs) and spinal cord ventral horn. The number of neurones labelled by the first tracer was similar for all three dyes in the DRG and ventral horn except for FG, which labelled fewer motoneurones. When used as second tracer, DY labelled fewer neurones than FG and FB in some experimental situations. The total number of neurones labelled by the first and/or second tracer was reduced by about 30% compared to controls. The contributions of cell death as well as different optional tracer combinations for studies of nerve regeneration are discussed.

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Motor Nerve Sprouting

Cited by 500 publications

References 0 publications

A monoclonal antibody that blocks the activity of a neurite regeneration-promoting factor: studies on the binding site and its localization in vivo.

A monoclonal antibody that blocks the activity of a neurite regeneration-promoting factor: studies on the binding site and its localization in vivo.

Motoneuron Death after Human Spinal Cord Injury

On the use of fast blue, fluoro-gold and diamidino yellow for retrograde tracing after peripheral nerve injury: uptake, fading, dye interactions, and toxicity

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