wallerian degeneration/phosphatase

The Pam/Highwire/RPM-1 (PHR) proteins are key regulators of neuronal development that function in axon extension and guidance, termination of axon outgrowth, and synapse formation. Outside of development, the PHR proteins also regulate axon regeneration and Wallerian degeneration. The PHR proteins

Enzyme histochemistry of Wallerian degeneration in the immature optic nerve of rabbits.

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A histochemical study was performed on the activity of several phosphatases, esterases and oxidoreductases in the immature optic nerve of rabbits undergoing Wallerian degeneration. Unilateral enucleations of the eye bulb were performed on 7 days old animals and the degenerated optic nerves were

Neuroglia of the developing optic nerve in the course of Wallerian degeneration.

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Unilateral enucleation was performed in 8 days rabbits and morphological changes occurring in the degenerating immature optic nerve were evaluated by means of light and electron microscopy and correlated with histoenzymatic changes in the activity of various phosphatases, esterases and

Accelerated axonal loss following acute CNS demyelination in mice lacking protein tyrosine phosphatase receptor type Z.

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Protein tyrosine phosphatase receptor type Z (Ptprz) is widely expressed in the mammalian central nervous system and has been suggested to regulate oligodendrocyte survival and differentiation. We investigated the role of Ptprz in oligodendrocyte remyelination after acute, toxin-induced

Fluoride-resistant acid phosphatase (FRAP) activity of nociceptive nerve terminals in the dental pulp.

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Nerve fibers in the dental pulp of the lower molar teeth of the rat exert fluoride resistant acid phosphatase (FRAP) activity. FRAP-positive axons establish a three-dimensional nerve plexus within the pulp; the individual axons are very fine (calibre less than 1 micrometer) and only their

Protective role of the lipid phosphatase Fig4 in the adult nervous system.

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The signaling lipid phosphatidylinositol 3,5-bisphosphate, PI(3,5)P2, functions in vesicular trafficking through the endo-lysosomal compartment. Cellular levels of PI(3,5)P2 are regulated by an enzyme complex comprised of the kinase PIKFYVE, the phosphatase FIG4, and the scaffold protein VAC14.

Reversibility of microtubule inhibitor-induced transganglionic degenerative atrophy of central terminals of primary nociceptive neurons.

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Microtubule inhibitor Vinca alkaloids applied around a peripheral nerve induce transganglionic degenerative atrophy of the central terminals of primary nociceptive neurons. This effect is reversible: 40-50 days later the original histochemical structure of the central terminals is restored.

Biochemical alterations in the peripheral nerves of rats intoxicated with carbon disulphide.

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Some biochemical correlates of Wallerian degeneration of the peripheral nerve were compared in carbon disulphide (CS2) and acrylamide-induced neuropathies. Rats were exposed to CS2 at two concentrations (1.5 mg/l and 0.8 mg/l air). An increase in the activities of beta-glucuronidase and acid

Molecular plasticity of primary nociceptive neurons: relations of the NGF-c-jun system to neurotomy and chronic pain.

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Neurotomy is widely used as a model of chronic, intractable pain, the proverbial "crux medicorum". Immunohistochemical aspects of this chronic pain model are discussed in this paper, with the aim of shedding new light on the pathomechanism and possible therapeutical consequences. Central terminals

Regenerative synaptoneogenesis in the Mammalian spinal cord: dynamics of synaptochemical restoration in the Rolando Substance after transganglionic degenerative atrophy.

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Crush injury of the sciatic nerve, that results in Wallerian degeneration of axons in the peripheral stump, induces, within 10-14 days, transganglionic degenerative atrophy of central terminals of primary nociceptive neurons in the ipsilateral substantia gelatinosa Rolandi of the segmentally related

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