Motoneurons of the rat sciatic nerve

Swett, John E.; Wikholm, Richard P.; Blanks, Robert H. I.; Swett, Anne L.; Conley, Lynn C.

doi:10.1016/0014-4886(86)90161-5

Cited by 204 publications

(124 citation statements)

References 64 publications

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“…They were localized in the ventral horn of the lumbar spinal cord in the region corresponding to L3 and L4. The distribution of labeled cells was found to be similar to that previously reported (Nicolopoulos-Stournaras and Iles, 1983;Swett et al, 1986). Fig.…”

Section: True Blue (Tb)supporting

confidence: 87%

A sequential double labeling technique for studying changes in motoneuronal projections to muscle following nerve injury and reinnervation

Katada¹,

Vos²,

Swelstad³

et al. 2006

Journal of Neuroscience Methods

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Abstract:The purpose of this study was to develop an anatomical technique that could directly demonstrate the motoneuron projections to the muscle both before injury and again following reinnervation. Investigation focused on the identification of a long-term retrograde fluorescent tracer that would label original motoneurons and persist long enough for reinnervating motoneurons to become labeled by a second fluorescent tracer. True Blue (TB) was evaluated as a potential long-term tracer, Fluoro-ruby (FR) and Fluoro-emerald (FE) were tested as potential short-term tracers in 45 adult Sprague-Dawley rats. In the initial phase of the study, TB was injected into the tibialis anterior (TA) muscle in 16 rats and sacrificed 1 week to 6 months later, to study its persistence. During the second stage, a short-term tracer was injected into the TA muscles bilaterally in 15 rats with survival time ranging from 4-28 days. Sequential double labeling was subsequently performed using the combination of TB and FR in 14 rats. The number and brightness of TB cells did not change over 6 months time, a period sufficient for complete reinnervation.FR and FE showed maximum labeling of motoneurons at 1 week after tracer application.In the double labeling study, we could easily distinguish double-labeled cells from those labeled only by TB or FR. These results suggest that sequential double labeling of TB and FR is a valuable method for long-term muscle reinnervation studies.

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Section: True Blue (Tb)supporting

confidence: 87%

A sequential double labeling technique for studying changes in motoneuronal projections to muscle following nerve injury and reinnervation

Katada¹,

Vos²,

Swelstad³

et al. 2006

Journal of Neuroscience Methods

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“…These ages were selected because demyelination begins around P90 in cx32 Ϫ/Y mice and becomes prominent by P158 (Anzini et al, 1997;Scherer et al, 1998). Because myelinated motor fibers are much more affected than are myelinated sensory fibers in cx32 Ϫ/Y mice, we focused on the femoral motor nerve because it contains a higher proportion of motor axons than does the sciatic nerve (60 vs 20% of myelinated axons) (Boyd and Davey, 1968;Swett et al, 1986).…”

Section: A Cx32 Transgene Prevents Demyelination In Cx32mentioning

confidence: 99%

Transgenic Expression of HumanConnexin32in Myelinating Schwann Cells Prevents Demyelination inConnexin32-Null Mice

Scherer¹,

Xu²,

Messing³

et al. 2005

J. Neurosci.

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Mutations in Gap Junction ␤1 (GJB1), the gene encoding the gap junction protein connexin32 (Cx32), cause the X-linked form of Charcot-Marie-Tooth disease (CMT1X), an inherited demyelinating neuropathy. We investigated the possibility that the expression of mutant Cx32 in other cells besides myelinating Schwann cells contributes to the development of demyelination. Human Cx32 was expressed in transgenic mice using a rat myelin protein zero (Mpz) promoter, which is exclusively expressed by myelinating Schwann cells. Male mice expressing the human transgene were crossed with female Gjb1/cx32-null mice; the resulting male offspring were all cx32-null (on the X chromosome), and one-half were transgene positive. In these transgenic mice, all of the Cx32 was derived from the expression of the transgene and was found in the sciatic nerve but not in the spinal cord or the liver. Furthermore, the Cx32 protein was properly localized (within incisures and paranodes) in myelinating Schwann cells. Finally, the expression of human Cx32 protein "rescued" the phenotype of cx32-null mice, because the transgenic mice have significantly fewer demyelinated or remyelinated axons than their nontransgenic littermates. These results indicate that the loss of Schwann-cell-autonomous expression of Cx32 is sufficient to account for demyelination in CMT1X.

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“…We killed the mice at P158 because demyelination becomes prominent by this age (Anzini et al, 1997;Scherer et al, 1998;Scherer et al, 2005). Because myelinated motor fibers are much more affected than are myelinated sensory fibers in Gjb1 Ϫ/Y mice, we focused on the femoral motor nerve because it is smaller and contains a higher proportion of motor axons than does the sciatic nerve (Boyd and Davey, 1968;Swett et al, 1986). These results are summarized in Table 2, and examples are shown in Figure 7 and supplemental Figure 2 (available at www.jneurosci.org as supplemental material).…”

Section: Gjb1-null Nervesmentioning

confidence: 99%

Prenylation-Defective Human Connexin32 Mutants Are Normally Localized and Function Equivalently to Wild-Type Connexin32 in Myelinating Schwann Cells

Huang

Sirkowski²,

Stickney³

et al. 2005

J. Neurosci.

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Mutations in GJB1, the gene encoding the gap junction protein connexin32 (Cx32), cause the X-linked form of Charcot-MarieTooth disease, an inherited demyelinating neuropathy. The C terminus of human Cx32 contains a putative prenylation motif that is conserved in Cx32 orthologs. Using [ 3 H]mevalonolactone ([ 3 H]MVA) incorporation, we demonstrated that wild-type human connexin32 can be prenylated in COS7 cells, in contrast to disease-associated mutations that are predicted to disrupt the prenylation motif. We generated transgenic mice that express these mutants in myelinating Schwann cells. Male mice expressing a transgene were crossed with female Gjb1-null mice; the male offspring were all Gjb1-null, and one-half were transgene positive; in these mice, all Cx32 was derived from expression of the transgene. The mutant human protein was properly localized in myelinating Schwann cells in multiple transgenic lines and did not alter the localization of other components of paranodes and incisures. Finally, both the C280G and the S281x mutants appeared to "rescue" the phenotype of Gjb1-null mice, because transgene-positive male mice had significantly fewer abnormally myelinated axons than did their transgene-negative male littermates. These results indicate that Cx32 is prenylated, but that prenylation is not required for proper trafficking of Cx32 and perhaps not even for certain aspects of its function, in myelinating Schwann cells.

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Motoneurons of the rat sciatic nerve

Cited by 204 publications

References 64 publications

A sequential double labeling technique for studying changes in motoneuronal projections to muscle following nerve injury and reinnervation

A sequential double labeling technique for studying changes in motoneuronal projections to muscle following nerve injury and reinnervation

Transgenic Expression of HumanConnexin32in Myelinating Schwann Cells Prevents Demyelination inConnexin32-Null Mice

Prenylation-Defective Human Connexin32 Mutants Are Normally Localized and Function Equivalently to Wild-Type Connexin32 in Myelinating Schwann Cells

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