acid-phosphatase and Wallerian-Degeneration

Topics: 5'-Nucleotidase; Acid Phosphatase; Adenosine Triphosphatases; Animals; Astrocytes; Cats; Encephalomyelitis, Autoimmune, Experimental; Guinea Pigs; Immunohistochemistry; Microscopy, Electron; Nerve Degeneration; Nucleotidases; Optic Nerve Diseases; Rats; Thiamine Pyrophosphatase; Wallerian Degeneration

Transcutaneous iontophoresis of microtubule inhibitors (Vinblastin, Vincristin, Formyl-Leurosin) in rats induces depletion of fluoride-resistant acid phosphatase (FRAP) and transganglionic degenerative atrophy (trggl. deg. atr.) of the central terminals of primary nociceptive neurons, probably via blockade of axoplasmic transport in the peripheral sensory nerves. Radiochemical experiments prove that about 0.2% of the microtubule inhibitors applied iontophoretically at the skin reach the level of nociceptive axon terminals. 40 out of 48 patients suffering from chronic intractable pain of diverse etiology (postherpetic, paresthetic, ischaemic and trigeminal neuralgia, alcoholic and diabetic polyneuropathy, meralgia, brachialgia, discopathia, arthropathia and terminal pain) were successfully treated with Vinblastin or Vincristin iontophoresis. Iontophoretically applied microtubule inhibitors do not affect the blood cell count, have no side-effects and do not impair the skin at the site of application.

Topics: Acid Phosphatase; Animals; Atrophy; Axonal Transport; Humans; Iontophoresis; Microtubules; Muridae; Nerve Degeneration; Nociceptors; Substantia Gelatinosa; Vinblastine; Vinca Alkaloids; Vincristine; Wallerian Degeneration

Topics: Acid Phosphatase; Animals; Antineoplastic Agents; Axonal Transport; Brain; Capsaicin; Fluorides; Ganglia, Spinal; Histocytochemistry; Humans; Isoenzymes; Microscopy, Electron; Nerve Endings; Nerve Regeneration; Neural Pathways; Neurons; Nociceptors; Spinal Cord; Subcellular Fractions; Substantia Gelatinosa; Synaptosomes; Wallerian Degeneration

In adult rabbits, unilateral enucleation was performed and morphological changes resulting from disconnection of the axons from their perikaryons of the optic nerve evaluated by means of light and electron microscopy. The morphological changes were compared with histochemically determined activities of several hydrolytic and oxidoreductive enzymes. The results obtained lead to the following conclusions: 1. Astroglial cells displaying increased enzymic activity of many hydrolases and oxidoreductases constitute the main cellular component of the mature optic nerve undergoing Wallerian degeneration. 2. Oligodendroglial cells of the degenerating optic nerve were found as well inside as in their usual position i.e. outside the axons. These cells displayed only slightly expressed morphological or histochemical signs of an increased biological activity. 3. In the mature optic nerve undergoing Wallerian degeneration some signs of remyelination i.e. formation of an aberrant myelin without proper connection to axons, were observed. 4. An intact functional connection between the perikaryons, the axons and myelin sheaths is in the mature optic nerve not indispensable for initiation of myelinogenesis during Wallerian degeneration.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Astrocytes; Hydrolases; Lipid Metabolism; Myelin Sheath; Nerve Degeneration; Nerve Regeneration; Neuroglia; Oligodendroglia; Optic Nerve; Oxidoreductases; Rabbits; Vacuoles; Wallerian Degeneration

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 examined in rabbits, 5, 23, 63 and 173 days afterwards. The following results were obtained: 1. The reactive cells appearing in the immature optic nerve undergoing Wallerian degeneration exhibit distinctly increased activities of many hydrolytic and oxidoreductive enzymes. 2. The histoenzymic pattern of changes displayed by the reactive cells occurring in the immature, degenerating optic nerve is distinct from and bears no relation to that seen in the normally developing optic nerve. 3. The genetic formation contained in the oligodendroglial cells is not the sole factor safeguarding the transformation of immature and mature oligodendroglia into myelinating cells.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Cholinesterases; Esterases; Hypertrophy; Nerve Degeneration; Neuroglia; Optic Nerve; Oxidoreductases; Rabbits; Thiamine Pyrophosphatase; Wallerian Degeneration

Topics: Acid Phosphatase; Animals; Demyelinating Diseases; Disease Models, Animal; DNA; Encephalomyelitis, Autoimmune, Experimental; Glucosephosphate Dehydrogenase; Haplorhini; Humans; Hydrolases; L-Lactate Dehydrogenase; Mice; Multiple Sclerosis; Wallerian Degeneration

Topics: 5'-Nucleotidase; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Guinea Pigs; Phosphoric Monoester Hydrolases; Protein Tyrosine Phosphatases; Spinal Cord; Wallerian Degeneration