acid-phosphatase and Nerve-Degeneration

The periodontal ligament receives a rich sensory nerve supply and contains many nociceptors and mechanoreceptors. Although its various kinds of mechanoreceptors have been reported in the past, only recently have studies revealed that the Ruffini endings--categorized as low-threshold, slowly adapting, type II mechanoreceptors--are the primary mechanoreceptors in the periodontal ligament. The periodontal Ruffini endings display dendritic ramifications with expanded terminal buttons and, furthermore, are ultrastructurally characterized by expanded axon terminals filled with many mitochondria and by an association with terminal or lamellar Schwann cells. The axon terminals of the periodontal Ruffini endings have finger-like projections called axonal spines or microspikes, which extend into the surrounding tissue to detect the deformation of collagen fibers. The functional basis of the periodontal Ruffini endings has been analyzed by histochemical techniques. Histochemically, the axon terminals are reactive for cytochrome oxidase activity, and the terminal Schwann cells have both non-specific cholinesterase and acid phosphatase activity. On the other hand, many investigations have suggested that the Ruffini endings have a high potential for neuroplasticity. For example, immunoreactivity for p75-NGFR (low-affinity nerve growth factor receptor) and GAP-43 (growth-associated protein-43), both of which play important roles in nerve regeneration/development processes, have been reported in the periodontal Ruffini endings, even in adult animals (though these proteins are usually repressed or down-regulated in mature neurons). Furthermore, in experimental studies on nerve injury to the inferior alveolar nerve, the degeneration of Ruffini endings takes place immediately after nerve injury, with regeneration beginning from 3 to 5 days later, and the distribution and terminal morphology returning to almost normal at around 14 days. During regeneration, some regenerating Ruffini endings expressed neuropeptide Y, which is rarely observed in normal animals. On the other hand, the periodontal Ruffini endings show stage-specific configurations which are closely related to tooth eruption and the addition of occlusal forces to the tooth during postnatal development, suggesting that mechanical stimuli due to tooth eruption and occlusion are a prerequisite for the differentiation and maturation of the periodontal Ruffini endings. Further investigations are needed to clarify the

Topics: Acid Phosphatase; Animals; Axons; Cholinesterases; Collagen; Dendrites; Electron Transport Complex IV; Mechanoreceptors; Mitochondria; Nerve Degeneration; Nerve Regeneration; Neuronal Plasticity; Neurons, Afferent; Nociceptors; Periodontal Ligament; Receptors, Nerve Growth Factor; Schwann Cells; Tooth Eruption

Topics: Acid Phosphatase; Animals; Axonal Transport; Axons; Cyclic AMP; Hydrolysis; Lysosomes; Mitochondria; Myelin Sheath; Nerve Degeneration; Nerve Regeneration

Topics: Acid Phosphatase; Amino Acids; Animals; Axons; Basophils; Botulinum Toxins; Cell Nucleolus; Cell Nucleus; Cholinesterases; Cytoplasm; Endoplasmic Reticulum; Golgi Apparatus; Lysosomes; Microscopy, Electron; Mitochondria; Motor Neurons; Nerve Degeneration; Nerve Regeneration; Nerve Tissue Proteins; Peripheral Nerve Injuries; Ribosomes; RNA; Sex Chromatin

In order to clarify the role of lysosomal enzymes in the developmental mechanisms of cerebral lesions under chronic hypertensive conditions, we histochemically and biochemically investigated acid phosphatase, N-acetyl-beta-glucosaminidase, and cathepsin B in the cerebral cortex and subcortical white matter in stroke-prone spontaneously hypertensive rats (SHRSP). Histochemical investigation showed that SHRSP had an increased number of cells with positive reaction to these enzymes in the edematous cortex and degenerated subcortical white matter. The cells with positive reaction were made up of reactive astrocytes and microglias. The activities of all enzymes in the aged SHRSP were higher than those in normotensive rats, the differences being significant at 24 weeks of age. The present study suggests that chronic hypertension or chronic edema causes increased activities of lysosomal enzymes in the cerebral cortex and subcortical white matter, and that the activated lysosomal enzymes take part in the developmental mechanisms of cystic formation as well as the diffuse degeneration of the white matter.

Topics: Acetylglucosaminidase; Acid Phosphatase; Animals; Astrocytes; Brain; Brain Edema; Cathepsin B; Cerebral Cortex; Cerebrovascular Disorders; Enzyme Activation; Hypertension; Male; Nerve Degeneration; Neurons; Rats; Rats, Inbred SHR; Rats, Inbred WKY

Structural and functional properties of central terminals of primary sensory neurons are regulated by nerve growth factor supplied by retrograde axoplasmic transport to dorsal root ganglion cells. Two important aspects of this regulatory system: transganglionic degenerative atrophy and regenerative synaptoneogenesis are reviewed in view of electron histochemical, electrophysiological and clinical studies performed during the last decade in the authors' laboratory and abroad.

Topics: Acid Phosphatase; Animals; Axonal Transport; Axons; Female; Ganglia, Spinal; Macaca mulatta; Male; Nerve Degeneration; Nerve Regeneration; Neurons, Afferent; Phosphoric Monoester Hydrolases; Rats; Rats, Inbred Strains

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

Topics: Acid Phosphatase; Animals; Cerebellum; Hot Temperature; Microscopy, Electron; Nerve Degeneration; Neuroglia; Organ Culture Techniques; Rats; Rats, Inbred Strains

Topics: Acid Phosphatase; Animals; Atrophy; Female; Ganglia; Male; Nerve Crush; Nerve Degeneration; Rats; Rats, Inbred Strains; Sciatic Nerve

Blockade of axonal transport or transection of the rat sciatic nerve results in transganglionic degenerative atrophy (TDA) of nerve terminals containing fluoride-resistant acid phosphatase (FRAP) in the Rolando substance of the spinal cord. Application of vinblastine (9 micrograms) in a cuff around the sciatic nerve of adult rats blocked the retrograde transport of [125I]NGF in sensory fibers; this amount of vinblastine is identical to the threshold amount that induces TDA. Conversely, application of NGF to the proximal stump of the transected sciatic nerve prevented or delayed the occurrence of TDA as reflected by the maintenance of FRAP in the upper dorsal horn, that otherwise would inevitably disappear following the peripheral nerve lesion. These results suggest that endogenous NGF transported retrogradely in peripheral sensory fibers of the adult rat under normal conditions may be responsible for the regulation of the structural and functional integrity of the central terminals of these FRAP-containing primary sensory neurons and that TDA may be the consequence of the failure of NGF to reach the perikarya of these neurons.

Topics: Acid Phosphatase; Animals; Axonal Transport; Ganglia, Spinal; Male; Nerve Degeneration; Nerve Growth Factors; Neurons, Afferent; Rats; Rats, Inbred Strains; Substantia Gelatinosa; Vinblastine

Alterations in the dorsal root potential (DRP) which was evoked by stimulation of the common peroneal nerve of the rat, have been studied in the course of transganglionic degenerative atrophy (TDA) of primary sensory terminals in the upper dorsal horn. TDA was induced by perineural application of Vinca alkaloids around the sciatic nerve. In 9 to 30 days after this treatment, latency of DRP increased, whereas its amplitude and duration decreased. In this period, no C fibre response could be elicited. As a possible mechanism underlying the alterations of DRP, the functional consequences of atrophic changes of primary central afferent terminals are being discussed in terms of the close correlation between structure and function and the possible inferences of the electrophysiological reaction to the therapeutic application of Vinca alkaloids in the iontophoretic treatment of chronic intractable pain.

Topics: Acid Phosphatase; Animals; Atrophy; Electrophysiology; Histocytochemistry; Male; Nerve Degeneration; Rats; Rats, Inbred Strains; Spinal Cord; Spinal Cord Diseases; Spinal Nerve Roots

In the small-optic-lobes (sol) and sine oculis (so) mutants of Drosophila melanogaster extensive cell death occurs in the optic lobes during the first half of pupal development. Gynandromorph flies show that the sol mutation acts primarily on cells of the medulla cortex. Degeneration of medullar ganglion cells occurs at an early stage of cellular differentiation, when their axons have not yet participated in the formation of the second optic chiasma. The so gene, on the other hand, acts on the eye anlagen. The analysis of chimeric flies demonstrates that degeneration in the optic lobes of so flies is a consequence of eye reduction. At the level of the second optic chiasma extensive axonal degeneration can be observed in the mutant. Neurons seem to die after their failure to establish a sufficient number of functional contacts. In sol;so double mutants, the mutational effects are cumulative causing complete degeneration of columnar cell types in pupae without any eye anlage. The tiny rudiments of the optic lobes in eyeless double mutants still contain tangential neurons of the medulla and of the lobula complex. The central brain is reduced in size due to the missing visual fibers, however, its overall appearance is surprisingly normal.

Topics: Acid Phosphatase; Animals; Axons; Drosophila melanogaster; Female; Microscopy, Electron; Mosaicism; Mutation; Nerve Degeneration; Nervous System; Nuclear Transfer Techniques; Optic Chiasm; Optic Lobe, Nonmammalian; Ovum; Species Specificity

Intravascularly injected horseradish peroxidase selectively labels certain classes of cells in the brains of chick embryos: phagocytes, which have characteristic distributions and resemble either gitter cells or microglia; and some, but not all, dying neurons. Healthy neurons are not labelled. If the isthmo-optic nucleus is caused to degenerate by an intraocular injection of colchicine on the opposite side, most of its neurons take up peroxidase. However, destroying the afferents to the isthmo-optic nucleus increases its loss of neurons without affecting the number labelled. In sections double-reacted for horseradish peroxidase and endogenous acid phosphatase, all, and indeed only, the peroxidase-labelled cells exhibit intense, clumped acid phosphatase activity which resists glutaraldehyde fixation. This is true of all cell types in both normal and operated embryos. Even healthy neurons exhibit acid phosphatase activity, but this can be distinguished, because it is largely inhibited by fixation with glutaraldehyde.

Topics: Acid Phosphatase; Animals; Brain; Chick Embryo; Glutaral; Horseradish Peroxidase; Nerve Degeneration; Neurons; Peroxidases; Phagocytes; Time Factors

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 varicosities measure 1...2 micrometer in diameter. Electron microscopically, FRAP-positive amyelinate axons containing lysosomes are partly embedded in Schwann cells. Removal of the cervical superior ganglion does not induce any alteration of FRAP-positive axons, while destruction of the Gasserian ganglion results in Wallerian degeneration. No FRAP-positive nerve fibers were found in rat incisors. Since, in the rat, only molar teeth are equipped with nociceptive terminals while continuously growing incisors lack pain fibers, it is concluded that FRAP-positive varicose axons in the dental pulp represent nerve endings of trigeminal primary nociceptive neurons.

Topics: Acid Phosphatase; Animals; Axons; Dental Pulp; Fluorides; Molar; Nerve Degeneration; Nociceptors; Rats; Staining and Labeling; Trigeminal Ganglion

Latency to the hind-paw lick in the hot-plate test (54 degrees C) is significantly increased (P less than 0.001) in the course of transganglionic degenerative atrophy of central terminals of primary sensory neurons. This was induced by a 30 min perineural application of 10(-8) mol Formyl-Leurosin, which results in the blockade of retrograde axoplasmic transport without Wallerian degeneration of the peripheral nerve. Values of latency return to normal in the course of synaptoneogenetic restoration of neuronal connectivity in the upper dorsal horn. The results are compatible with the working hypothesis that the beneficial effect of chronic pain therapy with Vinca alkaloid iontophoresis might be due to the fact that transganglionic degenerative atrophy is followed by the establishment of a sound, normal wiring in the upper dorsal horn in the course of restorative synaptoneogenesis.

Topics: Acid Phosphatase; Animals; Atrophy; Axonal Transport; Female; Ganglia, Spinal; Nerve Degeneration; Neurons, Afferent; Pain; Rats; Reaction Time; Sciatic Nerve; Spinal Cord; Substantia Gelatinosa; Vinblastine; Vinca Alkaloids; Vincristine

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. Restoration of fluoride-resistant acid phosphatase activity (the marker enzyme of primary nociceptive neurons) in the Rolando substance is due to regenerative sprouting of the formerly atrophied central terminals. Since peripherally-applied Vinca alkaloids induce transganglionic degenerative atrophy of the central terminals without inducing Wallerian degeneration of the peripheral nerve, and since this effect (virtually a synaptic uncoupling) is only temporary, this approach may be used in the treatment of otherwise intractable neuralgias without inducing irreparable alterations.

Topics: Acid Phosphatase; Animals; Atrophy; Axonal Transport; Axons; Female; Fluorides; Ganglia, Spinal; Interneurons; Male; Microtubules; Nerve Degeneration; Nerve Regeneration; Neurons; Nociceptors; Rats; Sciatic Nerve; Vinblastine; Vinca Alkaloids; Vincristine

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

1. Degeneration of nerve terminals of the submaxillary gland of the rat proceeds at a faster rate after crushing adrenergic nerves close to the gland than after ganglionectomy. 2. Bretylium, pargyline, nialamide and clorgyline delayed degeneration to the same extent after either type of denervation. 3. Chlorpromazine and pentobarbitone also delayed adrenergic degeneration, effect related to the hypothermia induced by these drugs. 4. Colchicine applied on the nerve trunk innervating the right gland delayed not only degeneration of the ipsilateral nerve terminals but the contralateral gland as well. 5. From the data obtained it seems probable that the drugs tested delay adrenergic nerve degeneration at the levels of nerve terminals. This effect is not related to lysosomal stabilization.

Topics: Acid Phosphatase; Animals; Body Temperature; Bretylium Compounds; Chlorpromazine; Colchicine; Denervation; Female; Lysosomes; Nerve Degeneration; Nerve Endings; Norepinephrine; Rats; Rats, Inbred Strains; Receptors, Adrenergic; Submandibular Gland; Sympathectomy

Topics: Acid Phosphatase; Animals; Animals, Newborn; Capsaicin; Fatty Acids, Unsaturated; Fluorides; Male; Nerve Degeneration; Nerve Fibers; Neurons, Afferent; Peptides; Rats; Rats, Inbred Strains; Somatostatin; Spinal Cord; Substance P

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

Earlier observations indicated that cutting the photoreceptor (R) cell perikarya in the retina of the flies Musca domestica and Calliphora erythrocephala resulted in an extremely rapid degeneration of the R-cell axons. The process manifested itself within minutes and secondary lysosomes appeared early on in the degenerating axons. In this study, biochemical assays of the classical lysosomal marker enzyme acid phosphatase (AcPase) showed a rapid increase in activity upon cutting the retina, reaching a peak around 5 min, followed by a drop and a subsequent slow steady rise in activity between about 4 and 24 h after the cut. Inhibitor studies indicated that at least 2 different acid phosphatases were involved, which showed identical activity changes. EM cytochemical studies with either beta-glycerophosphate or cytidine monophosphate as substrates indicated that the degeneration-dependent AcPase activity originated exclusively in one specific glial cell type in the distal lamina, the satellite glia. These cells are contiguous with R-cell axons in the pseudocartridges, directly proximal to the basement membrane of the retina. In normal uncut flies, reaction product indicative of AcPase activity was found in satellite glial cells in both rough ER (and perinuclear cisternae) and in smooth ER, the 2 types of cisternae being clearly in continuity. The electron-dense reaction product resulting from AcPase activity often showed continuity between the smooth ER of satellite glial cells and extracellular sites between the satellite glia and R-axons. This may result from the low levels of AcPase being synthesized in rough ER, and then exported to extra-cellular sites. Within minutes of cutting the retina the freqeuncy of satellite glia smooth ER staining for AcPase increases significantly. Increases in AcPase activity were subsequently found sequentially in extracellular sites, in axons in the distal lamina, and finally in the axon terminals. The time course for these increases in AcPase activity correlated well with the time course of the fine-structural pathological changes in the axons. A significant feature of the satellite glia cells is the massive packing of unidirectional microtubules (MTs), running perpendicular to the projections of the R-axons--in the same direction as AcPase transport. The MTs terminate at the glial membrane directly adjacent to the axon. The smooth ER cisternae interdigitate among the MTs and may be structurally connected to them by thin fi

Topics: Acid Phosphatase; Animals; Axons; Diptera; Endoplasmic Reticulum; Microscopy, Electron; Microtubules; Nerve Degeneration; Neuroglia; Photoreceptor Cells; Thiamine Pyrophosphatase; Time Factors

The studies were performed on 24 young, adult dogs. In 16 of the animals sections were made of the descending ramus of the hypoglossal nerve and of the stem of the hypoglossal nerve at various levels: at the base of the skull (superior hypoglossectomy), proximally from the descending ramus (middle hypoglosectomy), and at the entrance to the tongue (inferior hypoglossectomy). Phantom operations were performed in 4 animals and material from 4 others (not operated on) was used for control purposes. The post-operative survival rate ranged from 10 to 29 days. In all 4 cases rostral spinal cervical ganglia were collected. In half of the cases the materials were stained with cresyl violet and further quantitative and qualitative studies of retrograde neuronal changes were performed. The remaining half of the material, prepared with Gomori method on acid phosphatase, was subject to statistical analysis of the degree of acid phosphatase activity. The increase or decrease in number of neurons of definite degree of activity was taken as an index of the increase or decrease of enzymatic activity. As a result of transection of the hypoglossal nerve and its descending ramus, in cresyl violet material, qualitative and quantitative degenerative changes were found in dorsal root ganglia C1 to C3 on the operated side. It was also found that corresponding to the tigrolytic changes in the neurons of the above mentioned ganglia there was an increase of activity for acid phosphatase. The same kinds of changes were found in the spinal ganglia C2 and C3 after transection of the hypoglossal nerve at the entrance to the muscles of the tongue. These results lead the authors to suggest that the tongue motor apparatus receives afferent innervation from neurons locates homolaterally in spinal ganglia C2 and C3.

Topics: Acid Phosphatase; Afferent Pathways; Animals; Cell Count; Dogs; Ganglia, Sympathetic; Hypoglossal Nerve; Nerve Degeneration; Neurons; Spinal Cord; Tongue

The autonomic nerve plexus of the ciliary muscle was examined with the electron microscope in normal rhesus monkeys of different ages. In the anterior region of the muscle, at the boundary with the poorly innervated scleral spur and trabecular meshwork, 3.8-7.1% of the axons exhibit either degenerative or regenerative features. The cytoplasm of degenerating axons contains lamellated, dense and multivesicular bodies, vesicles, whorls of filaments, and membranous debris. The plasma membrane is often discontinuous and, on occasion, axonal debris and degenerative organelles are freely dispersed in the connective tissue spaces of the muscle. Degenerating axons contain a granular reaction product when stained for acid phosphatase activity. Regenerating axons are characterized by tightly packed mitochondria, glycogen particles, and aggregates of synaptic vesicles; they synapse with muscle cells and are negative to the acid phosphatase reaction. A quantitative analysis showed that in the anterior region of the ciliary muscle degenerating and regenerating axons increase in number with age, although the total number of axonal profiles remains constant. In the age groups examined, degenerating axons occurred with the same frequency as regenerating axons, thus, the age-dependent increase in axonal degeneration is accompanied by a parallel increase in axonal regeneration. We conclude that autonomic nerve endings in the anterior part of the ciliary muscle undergo a continuous process of renewal that is more prominent in old age.

Topics: Acid Phosphatase; Aging; Animals; Autonomic Nervous System; Axons; Cell Membrane; Cytoplasm; Haplorhini; Macaca mulatta; Muscles; Nerve Degeneration; Nerve Endings; Nerve Regeneration

A histochemical study concerning the activity of phosphatases and esterases of the brain has been undertaken in rats experimentally intoxicated by the fungicide ethyl-mercury-p-toluenesulfanilide (EMTS). The results have shown that compared with other mercury compounds, both organic and inorganic ones, such as corrosive sublimate and calomel, EMTS proved to be a less induced of alterations in the activity of cerebral hydrolases. The brains of animals intoxicated by EMTS revealed a notable decrease of ATP-ase and acid phosphatase activity as well as a moderate drop of AChE activity. Instead, the neuronal TPPase activity was distinctly elevated. Degenerative changes of neurons were observed in various regions of the experimental brains, the pyramidal cells of the Ammon's horn being affected most severely.

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Brain; Cholinesterases; Esterases; Ethylmercury Compounds; Female; Histocytochemistry; Male; Nerve Degeneration; Phosphoric Monoester Hydrolases; Rats; Thiamine Pyrophosphatase

Topics: Acid Phosphatase; Animals; Carbamoyl-Phosphate Synthase (Ammonia); Female; Lysosomes; Nerve Degeneration; Nodose Ganglion; Phosphotransferases; Rats; Vagotomy; Vagus Nerve

Removing the right hind limb of Rana pipiens larvae at different stages during development initiates diverse responses within lateral motor column (LMC) neurons whose axons have entered the limb and are forming neuromuscular junctions; Severing the hind limb at stage V inhibits the future differentiation of LMC neurons and, ultimately, 95% of the presumably injured cells degenerate; Ultrastructural observations indicate that the affected neurons become pyknotic, but display little evidence of lysosomal involvement. However, a quite different reaction is encountered when limb ablation is delayed to stage X. At this stage, LMC neurons rapidly disclose an intense retrograde response, which includes the genesis of numerous secondary lysosomes in degenerating cells; If, however, limb removal is postponed until stage XV or XX then a clasic chromatolysis can be recognized in axotomized neurons. The intensity of the chromatolysis appears to be inversely related to the age of the neurons. This investigation tends to support the premise that differentiating LMC neurons pass through three crucial stages in their development which can be identified following axotomy.

Topics: Acid Phosphatase; Age Factors; Animals; Anura; Cell Count; Cell Differentiation; Cytoplasmic Granules; Hindlimb; Lysosomes; Motor Neurons; Nerve Degeneration; Rana pipiens; Retrograde Degeneration; Spinal Cord

Ultrastructural studies of spinal cord in rats subjected to hyperbaric oxygen exposure and experimental spinal cord trauma have resulted in frequent degeneration of axons. In both experimental situations central nervous system myelinated fibers containing complex cytoplasmic interdigitations of electron lucent, normal appearing cytoplasm, and dense cytoplasm, interpreted as degenerative, were observed. In some of the complex profiles the electron lucent cytoplasm could be traced back to the inner mesaxon, where its relation to the latter indicated a glial origin. Cytochemical evaluation of acid phosphatase activity in the complex cytoplasmic interdigitations revealed that both components contain significant lysosomal activity. The complex structures are interpreted as being sequestrations of degenerating axoplasm by distal adaxonal oligodendroglial processes, possibly representing an unusual form of heterophagocytosis.

Topics: Acid Phosphatase; Animals; Axons; Female; Hyperbaric Oxygenation; Nerve Degeneration; Nerve Fibers, Myelinated; Neuroglia; Oligodendroglia; Rats; Spinal Cord Injuries

Disappearance of fluorid-resistant acid phosphatase activity from the ipsilateral Rolando substance after transection of the peripheral nerve, is shown to be due to the cessation of enzyme supply from dorsal root ganglion cells to their central terminals. This is accompanied by (or ensues in consequence of) a fine structural derangement of these terminals ("degenerative atrophy"). Fine structural alterations of axon terminals undergoing degenerative atrophy, though similar to some extent to those seen during early phases of a Wallerian degeneration, are markedly different. Also myelinated nerve fibers, both in the dorsal horn and in dorsal columns, are affected by degenerative atrophy. This important, new trophical feature of sensory ganglion cells suggests a delicate metabolic balance between peripheral and central axonal branches of bipolar (pseudounipolar) cells. Degenerative atrophy raises serious implications in evaluating hodological experiments based upon Wallerian degeneration and offers new perspectives for theoretical and clinical neurology.

Topics: Acid Phosphatase; Animals; Cauda Equina; Female; Histocytochemistry; Male; Nerve Degeneration; Neurons; Rats; Retrograde Degeneration; Sciatic Nerve; Spinal Cord; Spinal Nerve Roots; Substantia Gelatinosa

Lysosomes were studied by both cytochemical and quantitative methods in normal and degenerating neuroblasts of the chick embryo spinal ganglia. In normal neuroblasts (primitive and intermediate neuroblasts) both primary lysosomes and autophagic vacuoles were found; these organelles were usually located in the region containing the Golgi complex. In degenerating neuroblasts lysosomes appeared sharply decreased in number with respect to normal neuroblasts. Moreover, lysosomes were always evident as intact organelles surrounded by a membrane and the acid phosphatase activity appeared localized exclusively within these bodies. A diffuse distribution of acid phosphatase activity was only found in a limited number of cases during the terminal stage of the process. Possibly in these cases the enzymatic activity depended on the cells which enveloped the degenerated neuroblast remnants. The present results indicate that lysosomes do not play a primary role in the degenerative process studied.

Topics: Acid Phosphatase; Animals; Autolysis; Cell Differentiation; Cell Survival; Chick Embryo; Ganglia, Spinal; Lysosomes; Microscopy, Electron; Nerve Degeneration; Neurons

A magnesium deficient diet caused transient but marked degenerative changes in the rat hypothalamo-hypophysial neurosecretory system which strongly resembled in many ultrastructural respects those induced by a prolonged administration of aldosterone as previously reported by us. The possible mechanism for this selective alteration in the neurosecretory neurons has been briefly discussed with regard to aldosterone secretion.

Topics: Acid Phosphatase; Aldosterone; Animals; Axons; Cell Nucleus; Cytoplasmic Granules; Endoplasmic Reticulum; Golgi Apparatus; Hypothalamo-Hypophyseal System; Magnesium Deficiency; Male; Nerve Degeneration; Neurons; Pituitary Gland, Posterior; Pituitary-Adrenal System; Rats; Supraoptic Nucleus; Time Factors

Topics: Acid Phosphatase; Animals; Atrophy; Axons; Nerve Degeneration; Nerve Endings; Nerve Regeneration; Rats; Sciatic Nerve; Spinal Cord

Changes in immature rats in motor neurones after axotomy were studied by enzyme-histochemical methods. Increased activity of dehydrogenases in these neurones demonstrates enhanced metabolism and there was also increase of acid phosphatases. Decreased activity of acetylcholinesterase and indoxylacetate esterase in the neurones and their processes seems to indicate impaired neuronal function to transmit impulses. "Retrograde" reaction in the immature and the grown up animal is in general of the same kind but takes place quicker in the immature rat. However, in new-born and very young animals, it is difficult to recognize alterations in the anterior horn of the spinal cord. Therefore, nervous tissue of new-born animals seems not to respond as it does some days later in ontogenesis.

Topics: Acetylcholinesterase; Acid Phosphatase; Age Factors; Animals; Animals, Newborn; Anterior Horn Cells; Denervation; Glutamate Dehydrogenase; Histocytochemistry; Motor Neurons; NADH Tetrazolium Reductase; Nerve Degeneration; Quinone Reductases; Retrograde Degeneration; Succinates

The role of the Golgi apparatus and the Golgi-endoplasmic reticulum-lysosome complex (GERL) in the genesis of lysosomes was examined in differentiating and degenerating motor neurons of anuran larvae. Acid phosphatase, aryl sulfatase, and thiolacetic acid esterase were utilized as marker enzymes for the lysosomal system, while nucleoside diphosphatase and thiamine pyrophosphatase labeled the inner saccule(s) of the Golgi apparatus. Reduced osmium tetroxide was routinely deposited in the outer Golgi saccule regardless of the state of neuronal maturation. In all young neurons, the disposition of acid hydrolase reaction product paralleled the formation of GERL, with no lytic activity in the Golgi apparatus per se. Hypertrophy of the Golgi apparatus and GERL was observed in the early phases of degeneration, and both organelles apparently exhibit extensive hydrolytic activity. Dense bodies, autophagic vacuoles, and primary lysosomes were found arising from GERL, while the Golgi apparatus may produce primary lysosomal granules during regression. On the other hand, in differentiating neurons, hydrolytic activity was restricted to GERL and an occasional dense body and autophagic vacuole. These studies illustrate a parallelism between the development of GERL and genesis of primary and secondary lysosomes during neuronal cytodifferentiation, and implicate GERL and possibly the Golgi apparatus in lysosomal packaging in degenerating neurons.

Topics: Acid Phosphatase; Animals; Anura; Cell Differentiation; Endoplasmic Reticulum; Golgi Apparatus; Larva; Lysosomes; Microscopy, Electron; Motor Neurons; Nerve Degeneration; Phosphoric Monoester Hydrolases; Pyrophosphatases; Rana pipiens; Sulfatases

Topics: Acid Phosphatase; Biopsy; Collagen; Demyelinating Diseases; Histocytochemistry; Humans; Hypertrophy; L-Lactate Dehydrogenase; Leprosy; Macrophages; Microscopy, Electron; Mycobacterium leprae; Myelin Sheath; Nerve Degeneration; Peripheral Nerves; Peripheral Nervous System Diseases; Schwann Cells; Sural Nerve

Topics: Acid Phosphatase; Animals; Brain; Microscopy, Electron; Nerve Degeneration; Spinal Cord; Spinal Nerve Roots; Synaptic Membranes; Synaptic Transmission; Synaptic Vesicles

Topics: Acid Phosphatase; Animals; Denervation; Female; Fluorides; Histocytochemistry; Kinetics; Male; Microscopy, Electron; Nerve Degeneration; Neuroglia; Rats; Spinal Cord; Spinal Nerve Roots; Synapses; Time Factors

Topics: Acid Phosphatase; Animals; Animals, Newborn; Histocytochemistry; Methods; Microscopy, Electron; Myelin Sheath; Nerve Degeneration; Nerve Fibers, Myelinated; Osmium; Ranvier's Nodes; Rats; Schwann Cells; Spinal Nerve Roots; Staining and Labeling

Topics: Acid Phosphatase; Adult; Brain; Cerebellum; Corpus Callosum; Esterases; Female; Humans; Lysosomes; Male; Microscopy, Electron; Middle Aged; Multiple Sclerosis; Myelin Sheath; Nerve Degeneration; Neuroglia; Peptide Hydrolases; Phagocytosis; Pons

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Basal Ganglia; Brain; Caudate Nucleus; Cerebral Cortex; Hindlimb; Histocytochemistry; Male; Manganese Poisoning; Nerve Degeneration; Neuroglia; Neurons; Nucleotidases; Paralysis; Rabbits; Substantia Nigra; Time Factors

Topics: Acid Phosphatase; Age Factors; Animals; Axons; Inclusion Bodies; Mice; Mice, Inbred Strains; Microscopy, Electron; Mitochondria; Nerve Degeneration; Nerve Fibers, Myelinated; Peripheral Nerves; Rats; Schwann Cells; Sciatic Nerve

Topics: Acid Phosphatase; Animals; Axons; Cytoplasmic Granules; Dendrites; Endoplasmic Reticulum; Female; Hybridization, Genetic; Lysosomes; Male; Microscopy, Electron; Nerve Degeneration; Nerve Endings; Nerve Regeneration; Rats; Synaptic Vesicles; Vestibular Nuclei

Topics: Acid Phosphatase; Aged; Aging; Histocytochemistry; Humans; Melanins; Middle Aged; Nerve Degeneration; Nucleic Acids; Trigeminal Nerve

Topics: Acid Phosphatase; Animals; Cell Count; Demyelinating Diseases; Histocytochemistry; Inclusion Bodies; Lipids; Male; Microscopy, Electron; Nerve Degeneration; Neuroglia; Optic Nerve; Phagocytosis; Rats

Topics: Acid Phosphatase; Animals; Axons; Cell Membrane; Demyelinating Diseases; Female; Ganglia, Spinal; Goats; Histocytochemistry; Male; Myelin Sheath; Nerve Degeneration; Peripheral Nervous System Diseases; Plant Poisoning; Schwann Cells; Sciatic Nerve; Spinal Cord; Time Factors

Topics: Acid Phosphatase; Animals; Cell Nucleus; Glossopharyngeal Nerve; Male; Nerve Degeneration; Neurochemistry; Neurons; Neurotransmitter Agents; Rats; Taste Buds; Vagus Nerve

Topics: Acid Phosphatase; Aging; Amyloidosis; Animals; Axons; Brain; Brain Diseases; Cerebral Cortex; Dementia; Dog Diseases; Dogs; Histocytochemistry; Humans; Macrophages; Microscopy; Nerve Degeneration; Neuroglia

Topics: Acid Phosphatase; Animals; Axons; Ganglia, Autonomic; Histocytochemistry; Lysosomes; Mitochondria; Nerve Degeneration; Neurons; Rabbits; Ribosomes

Topics: Acid Phosphatase; Animals; Gelatin; Genetics; Histocytochemistry; Leucyl Aminopeptidase; Lysosomes; Myelin Sheath; Nerve Degeneration; Peptide Hydrolases; Rats; Sciatic Nerve; Silver; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Histocytochemistry; Nerve Degeneration; Nerve Regeneration; Rats; Taste Buds; Tongue

Topics: Acid Phosphatase; Animals; Axons; Cats; Myelin Sheath; Nerve Degeneration; Rats; Schwann Cells; Sciatic Nerve

Topics: Acid Phosphatase; Aged; Amyloid; Arteries; Brain; Capillaries; Dementia; Dihydrolipoamide Dehydrogenase; Female; Histocytochemistry; Humans; Microscopy, Electron; Middle Aged; Nerve Degeneration; Neuroglia; Paranoid Disorders

Topics: Acid Phosphatase; Animals; Cholinesterases; Histocytochemistry; Nerve Degeneration; Neurons; Optic Nerve; Rabbits; Retina

Topics: Acid Phosphatase; Animals; Glucuronidase; Histocytochemistry; Macrophages; Mice; Myelin Sheath; Nerve Degeneration; Peripheral Nerves; Schwann Cells

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Cholinesterases; Electron Transport Complex IV; Glucosephosphate Dehydrogenase; Guinea Pigs; Histocytochemistry; L-Lactate Dehydrogenase; Motor Neurons; Nerve Degeneration; Nerve Regeneration; Pyrophosphatases; Spinal Cord; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Chronic Disease; Histocytochemistry; Lead Poisoning; Nerve Degeneration; Peripheral Nerves; Rats

Topics: Acid Phosphatase; Brain; Cerebrosides; Child; Diffuse Cerebral Sclerosis of Schilder; Humans; Kidney; Lipids; Nerve Degeneration; Sulfatases; Transferases

Topics: Acid Phosphatase; Axons; Cytoplasmic Granules; Dementia; Dendrites; Endoplasmic Reticulum; Frontal Lobe; Histocytochemistry; Humans; Lysosomes; Microscopy, Electron; Nerve Degeneration

Topics: Acid Phosphatase; Axons; Child; Child, Preschool; Dihydrolipoamide Dehydrogenase; Female; Globus Pallidus; Glucosephosphate Dehydrogenase; Histocytochemistry; Humans; Infant; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Muscles; Nerve Degeneration; Nervous System Diseases; Pigmentation; Reflex, Abnormal; Sensation; Skin Manifestations; Speech Disorders; Spinal Cord; Vitamin E Deficiency

Topics: Acid Phosphatase; Aphasia; Brain; Central Nervous System Diseases; Cerebral Cortex; Dementia; Deoxyribonucleases; Dihydrolipoamide Dehydrogenase; Frontal Lobe; Histocytochemistry; Humans; Lysosomes; Male; Microscopy, Electron; Middle Aged; Motor Neurons; NAD; Nerve Degeneration; Neuroglia; Oxidoreductases; Pigments, Biological; RNA; Spinal Cord

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Animals; Cats; Esterases; Geniculate Bodies; Golgi Apparatus; Histocytochemistry; Hydrolases; In Vitro Techniques; Nerve Degeneration; Neurons; Nucleotidases; Phosphoric Monoester Hydrolases

Topics: Acid Phosphatase; Animals; Demyelinating Diseases; Diphtheria; Histocytochemistry; Lysosomes; Macrophages; Nerve Degeneration; Peripheral Nervous System Diseases; Poultry; Sciatic Nerve

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Denervation; Dogs; Esterases; Ganglia, Autonomic; Histocytochemistry; Lung; Lung Transplantation; Methods; Nerve Degeneration; Nerve Regeneration; Neural Conduction; Neurons; Pneumonectomy; Succinate Dehydrogenase; Time Factors; Transplantation, Autologous

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Cats; Denervation; Electron Transport Complex II; Electrons; Epithelium; Histocytochemistry; Histology; Microscopy; Microscopy, Electron; Muscles; Nerve Degeneration; Peripheral Nerves; Phosphoric Monoester Hydrolases; Phosphotransferases; Rats; Regeneration; Research; Sciatic Nerve; Succinate Dehydrogenase

Topics: Acid Phosphatase; Autonomic Nervous System; Cats; Celiac Plexus; Histocytochemistry; Myenteric Plexus; Nerve Degeneration; Neurons; Research; Submucous Plexus; Sympathectomy

Topics: Acid Phosphatase; Axons; Cell Body; Motor Neurons; Nerve Degeneration; Nervous System Physiological Phenomena; Regeneration

Topics: Acid Phosphatase; Animals; Axons; Haplorhini; Nerve Degeneration; Pyramidal Tracts; Regeneration