The dependence of motoneurons on their target muscle during postnatal development of the mouse

Crews, L. Lee; Wigston, Donald J.

doi:10.1523/jneurosci.10-05-01643.1990

Cited by 99 publications

(79 citation statements)

References 44 publications

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“…Progressive fading of FG (up to a 90-95%) in motoneurones has been previously described by using 2% FG (Crews and Wigston, 1990;Novikova et al, 1997). Our FG-DY group showed that about 27% of the motoneurones contained only DY labelling (second tracer).…”

Section: Labelling With the First Tracer: Neuronal Death Versus Tracesupporting

confidence: 72%

“…Thus, authors have reported a non-significant motoneuronal loss of about 10% after median and ulnar nerve transection in adult mice (Pollin et al, 1991), about 15% after forelimb amputation in mice (Crews and Wigston, 1990), and about 20% after nerve section in the rat axillary region (Gu et al, 1997). A loss of about 20 to 30% hypoglossal motoneurones (Snider and Thanedar, 1989;Törnqvist and Aldskogius, 1994) and facial motoneurones (Yu, 1988;Mattson et al, 1998) was described after cranial nerve section in adult rats.…”

Section: Labelling With the First Tracer: Neuronal Death Versus Tracementioning

confidence: 99%

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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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Section: Labelling With the First Tracer: Neuronal Death Versus Tracesupporting

confidence: 72%

Section: Labelling With the First Tracer: Neuronal Death Versus Tracementioning

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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“…Moreover, although LBR is performed before the onset of naturally occurring PCD, death that occurs as a result of this manipulation does not ensue until the normal period of PCD, suggesting there is a period of time before the onset of PCD during which MNs survive in the absence of target-derived trophic support . MNs die in animals subjected to embryological or neonatal axotomy or nerve crush; however, these cells are relatively spared later postnatally, implying that MN target dependence declines with age (Crews and Wigston, 1990;Kuno, 1990;Oppenheim et al, 1990;Lowrie and Vrbova, 1992;Houenou et al, 1994). ; n ϭ 8).…”

Section: Trophic Sources For Mnsmentioning

confidence: 99%

“…Although the target has been extensively investigated as a principle source of trophic support for developing MNs, its requirement for the maintenance of MNs diminishes with age (Crews and Wigston, 1990;Kuno, 1990;Lowrie and Vrbova, 1992;Houenou et al, 1994). The number of MNs that die as a result of axotomy, limb amputation, and nerve crush is diminished as the organism ages, although it is unclear whether MNs become trophic-independent or, if with age, they come to depend on alternative sources of trophic support (Snider and Thanedar, 1989;Crews and Wigston, 1990).…”

Section: Introductionmentioning

confidence: 99%

“…The number of MNs that die as a result of axotomy, limb amputation, and nerve crush is diminished as the organism ages, although it is unclear whether MNs become trophic-independent or, if with age, they come to depend on alternative sources of trophic support (Snider and Thanedar, 1989;Crews and Wigston, 1990). Numerous other putative trophic sources exist, including glia (e.g., Schwann cells and astrocytes), afferents, and components of the extracellular matrix (Okado and Oppenheim, 1984;Eagleson et al, 1985;Furber et al, 1987;Yin et al, 1994;Riethmacher et al, 1997;Arce et al, 1998;Wong et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Astrocyte and Muscle-Derived Secreted Factors Differentially Regulate Motoneuron Survival

Taylor¹,

Gifondorwa²,

Newbern³

et al. 2007

J. Neurosci.

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During development, motoneurons (MNs) undergo a highly stereotyped, temporally and spatially defined period of programmed cell death (PCD), the result of which is the loss of 40 -50% of the original neuronal population. Those MNs that survive are thought to reflect the successful acquisition of limiting amounts of trophic factors from the target. In contrast, maturation of MNs limits the need for target-derived trophic factors, because axotomy of these neurons in adulthood results in minimal neuronal loss. It is unclear whether MNs lose their need for trophic factors altogether or whether, instead, they come to rely on other cell types for nourishment. Astrocytes are known to supply trophic factors to a variety of neuronal populations and thus may nourish MNs in the absence of target-derived factors. We investigated the survival-promoting activities of muscle-and astrocyte-derived secreted factors and found that astrocyteconditioned media (ACM) was able to save substantially more motoneurons in vitro than muscle-conditioned media (MCM). Our results indicate that both ACM and MCM are significant sources of MN trophic support in vitro and in ovo, but only ACM can rescue MNs after unilateral limb bud removal. Furthermore, we provide evidence suggesting that MCM facilitates the death of a subpopulation of MNs in a p75 NTR -and caspase-dependent manner; however, maturation in ACM results in MN trophic independence and reduced vulnerability to this negative, pro-apoptotic influence from the target.

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Inhibition of lipid peroxidation attenuates axotomy-induced apoptotic degeneration of facial motor neurons in neonatal rats

1996

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The purpose of this study was to investigate the role of oxygen radical‐induced lipid peroxidative mechanisms in trophic deprivation‐induced apoptotic motor neuronal degeneration by testing the ability of the 21‐aminosteroid lipid peroxidation inhibitor tirilazad mesylate (U‐74006F) to attenuate the retrograde degeneration of facial motor neurons following axotomy in 14‐day‐old rat pups. On day 0, the right facial nerve of each rat was transected at its point of exit from the stylomastoid foramen. Pups were treated orally with either 10 or 30 mg/kg U‐74006F or cyclodextrin vehicle 10 min before axotomy, and post‐treated once a day from days 1 to 6, and then once every other day from days 8 to 21. The rats were sacrificed 3 weeks post‐transection and the surviving motor neurons, identified through choline acetyl‐transferase immunocytochemistry, were counted in three regions (planes) in the facial nucleus. In vehicle‐treated rats, 56.2% (region A), 50.6% (region B), and 57.4% (region C) of the motor neurons in the ipsilateral facial nucleus survived 21 days following facial nerve axotomy in comparison to the non‐axotomized contralateral nucleus (P < 0.0001). Treatment with 10 mg/kg U‐74006F significantly enhanced motor neuron survival in regions B and C to 72.8% (P < 0.01) and 66.7% (P < 0.02%), respectively. The 30 mg/kg dose level also increased survival rates to 64.2% (P < 0.02) and 67.9% (P < 0.01), respectively. A second experiment demonstrated that oral dosing with U‐74006F (30 mg/kg), when limited to the first 5 days after axotomy, also significantly blunted retrograde degeneration measured at 21 days post‐axotomy. The efficacy of the lipid peroxidation inhibitor U‐74006F in protecting a portion of the facial motor neuron pool from post‐axotomy degeneration suggests that lipid peroxidation may play a mechanistic role in trophic deprivation‐induced apoptotic neuronal death. © 1996 Wiley‐Liss, Inc.

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The dependence of motoneurons on their target muscle during postnatal development of the mouse

Cited by 99 publications

References 44 publications

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

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

Astrocyte and Muscle-Derived Secreted Factors Differentially Regulate Motoneuron Survival

Inhibition of lipid peroxidation attenuates axotomy-induced apoptotic degeneration of facial motor neurons in neonatal rats

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