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Biomedical subjects

B Csillik

Publications and source records attributed to B Csillik.

At least 55 records · Page 3Linked to original sources
PubMed1988

Transganglionic regulation and fine structural localization of lectin-reactive carbohydrate epitopes in primary sensory neurons of the rat.

Light- and electron microscopic lectin histochemical studies showed that small dorsal root ganglion cells of the rat projecting to substantia gelatinosa Rolandi (Lamina II) contain terminal alpha-D-galactose carbohydrate epitopes; while those projecting to Waldeyer's marginal zone (Lamina I) and the outer part of Lamina II contain terminal beta-D-galactose residues. These glycoconjugates are manufactured in the Golgi apparatus and transported to preterminal and terminal axoplasmic surface membranes. Both of the axolemmal carbohydrate moieties were shown to be subjected to transganglionic regulation, even though the effects of transganglionic degenerative atrophy become evident considerably later than the depletion of axoplasmic marker substances like fluoride resistant acid phosphatase and thiamine monophosphatase.

Animals↗
PubMed1988

Transganglionic regulation of primary sensory neurons.

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.

Acid Phosphatase↗
PubMed1988

Competitive mechanisms of basic peptides inducing transganglionic degenerative atrophy.

In addition to the classical microtubule inhibitors (antimitotic agents), transganglionic degenerative atrophy of central terminals of primary sensory neurons can be induced also by means of applying to a peripheral nerve basic polypeptides (Polymyxin B and Colimycin) and two basic derivatives of glutamic acid that do not exert any microtubule inhibition. This effect is independent of other pharmacological effects (histamine liberation, Ca2+ -binding, etc.) of the applied compounds, and probably it is based on a competitive reaction with nerve growth factor.

Animals↗
PubMed1987

Transganglionic degenerative atrophy in the substantia gelatinosa of the spinal cord after peripheral nerve transection in rhesus monkeys.

The effect of sciatic nerve transection on its centrally located terminals in the spinal cord was analyzed by electron microscopy in adult rhesus monkeys one and three months following lesion. Although the peripheral and intermediate portions of the dorsal roots, where the axons are enveloped by Schwann cells were normal, their central portion and their terminals in the substantia gelatinosa were remarkably altered. Transganglionic degenerative atrophy (TDA) is characterized by three distinct types of electron-microscopic alterations. The first type exhibits a conspicuous electron density of the terminal and pre-terminal axoplasm. Importantly, shrinkage replaces fragmentation and glial engulfement of the terminal seen in the course of Wallerian degeneration. The second type is characterized by the disappearance of synaptic vesicles from the terminals. The third type of TDA consists of intricate labyrinthine structures, composed of flattened profiles of axonal, dendritic and glial elements. The complex and diverse cellular changes that occur in the upper dorsal horn following peripheral nerve injury may provide the structural basis of plasticity of the primary nociceptive system.

Animals↗
PubMed1987

Transganglionic regulation of the primary sensory neuron.

Central terminals of the primary sensory neurons depend on the integrity of the retrograde transport mechanism within the peripheral axon. Whenever retrograde transport is impaired (either by injury or by blockade induced by perineural application of microtubule inhibitors) central terminals undergo transganglionic degenerative atrophy (TDA), characterized by depletion of substance P, somatostatin, FRAP (fluoride resistant acid phosphatase), TMPase (thiamine monophosphatase) and lectin-binding fucose-terminated glyco-conjugates. The TDA is essentially a failure of the central terminals to bind the above genuine marker substances. TDA-inflicted central terminals undergo a slowly proceeding ultrastructural deterioration, accompanied by derangement of the dorsal root potential, reflecting decreased functional activity of synaptic transmission between first and second-order cells. One of the important trophic substances carried by retrograde axoplasmic transport to dorsal root ganglion cells is nerve growth factor (NGF); blockade of NGF transport results in TDA; conversely, locally applied NGF delays or prevents TDA.

Animals↗
PubMed1986

Comparative electron histochemistry of thiamine monophosphatase and substance P in the upper dorsal horn.

The genuine marker enzyme of primary nociceptive neurons, thiamine monophosphatase (TMPase) has been localized in the substantia gelatinosa of the rat spinal cord by means of light-and electron microscopic histochemistry; localization of substance P has been studied by light-and and electron microscopic immunohistochemical methods. It has been shown that TMPase and substance P are located in two, regionally and structurally different populations of axon terminals. Substance P is contained both in A delta and in drC axons. In the postero-lateral funiculus of the white matter, substance P-positive axons establish axo-somatic synaptic contacts with large multipolar neurons of Cajal's interstitial nucleus.

Animals↗
PubMed1986

Thiamine monophosphatase: a genuine marker for transganglionic regulation of primary sensory neurons.

Thiamine monophosphatase (TMPase) has been selectively localized in small dorsal root ganglion cells and in their central and peripheral terminals. Light microscopic localization of TMPase, and its alterations due to transganglionic effects, are identical with those of fluoride-resistant acid phosphatase (FRAP), but are not contaminated by the ubiquitous lysosomal reaction inevitable in trivial acid phosphatase-stained sections. TMPase is inhibited by 0.1 mM NaF, which is slightly less than the concentration needed to inhibit FRAP (0.2-0.4 mM). It is assumed that TMPase and FRAP are identical enzymes. In the perikaryon of small dorsal root ganglion cells, TMPase is located in the cisterns of the endoplasmic reticulum and in the Golgi apparatus. The central terminals of these cells are scalloped (sinusoid) axon terminals, surrounded by membrane-bound TMPase activity. Central terminals outline substantia gelatinosa Rolandi throughout the spinal cord, as well as the analogous nucleus spinalis trigemini in the medulla. TMPase-active central terminals outline "faisceau de la corne postérieure" in the sacral cord, as well as Lissauer's tract in the thoracic, upper lumbar, and sacral segments, and the paratrigeminal nucleus and the terminal (sensory) nucleus of the ala cinerea in the brainstem. Peripheral terminals displaying TMPase activity are fine nerve plexuses of C fibers. The TMPase activity of the central terminals disappears after dorsal rhizotomy in the course of Wallerian degeneration, and is depleted in the course of transganglionic degenerative atrophy (after transection of the related peripheral sensory nerve). TMPase is an outstanding genuine marker for the study of transganglionic regulation in Muridae.

Acid Phosphatase↗
PubMed1985

Transganglionic regulation of central terminals of dorsal root ganglion cells by nerve growth factor (NGF).

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.

Acid Phosphatase↗
PubMed1985

Fine structure of growth cones in the upper dorsal horn of the adult primate spinal cord in the course of reactive synapto-neogenesis.

Following transganglionic degenerative atrophy of primary afferent terminals induced by a crush-injury of the sciatic nerve, a regenerative process takes places in the upper dorsal horn of the lumbar spinal cord in the primate Macacus rhesus. Axonal growth cones are characterized by cisterns of axoplasmic reticulum; filopodia emanating from growth cones are electron-optically translucent sheet-like expansions, often containing growth-cone vesicles. Axoplasmic reticulum appears also in preterminal portions of regenerating axons. Dendritic growth cones contain a fine, filamentous matrix; electron-dense membrane specializations can be seen in well-defined areas of their surfaces. Immature synapses are formed between filopodia of axonal growth cones and dendritic growth cones. Electron-microscopic structures of this unique CNS regeneration are similar to those seen in the course of embryonic development of the spinal cord.

Animals↗
PubMed1984

Depletion of substance P and somatostatin in the upper dorsal horn after blockade of axoplasmic transport.

In the upper dorsal horn of the rat lumbosacral spinal cord, substance P and somatostatin are present in two distinct and different populations of primary central afferent terminals. Substance-P-positive terminals are mainly concentrated in lamina I, while somatostatin-positive terminals are confined to lamina II. Although these two populations of primary afferent terminals differ at light- and electron-microscopic level, they are equally affected by transganglionic degenerative atrophy (TDA) which is induced by the blockade of axoplasmic transport in the segmentally related, ipsilateral sensory nerve by the local application of Vinblastin, a microtubule inhibitor. In consequence, substance P and somatostatin are depleted in the medial and intermediate portions of the upper dorsal horn, while the lateralmost area, which represents the postaxial portion of the dermatome, remains virtually intact. Substance P and somatostatin in propriospinal elements and the axonal meshwork within the dorsolateral funicle are not affected by TDA. Neurotensine, a propriospinal neuropeptide, does not show any alterations in the affected spinal segments.

Animals↗
PubMed1984

Nerve growth factor regulates central terminals of primary sensory neurons.

Transection of peripheral sensory axons results in transganglionic degenerative atrophy of central terminals of the affected primary sensory neurons. Nerve growth factor applied at the central stump of the transected nerve prevents or delays transganglionic degenerative atrophy. It is concluded that, under normal conditions, nerve growth factor taken up by receptors at peripheral sensory nerve endings and transported retrogradely to perikarya in dorsal root ganglia, regulates synthesis of neuroproteins destined for maintenance of central terminals of these neurons. Accordingly, transganglionic degenerative atrophy is the consequence of failure of nerve growth factor to reach perikarya of primary sensory neurons.

Animals↗
PubMed1983

Calcium binding of presynaptic protrusions as revealed by X-ray spectrum averaging in the rat neuromuscular junction.

Presynaptic calcium binding sites were demonstrated by means of X-ray microprobe analysis in rat neuromuscular junctions subjected to perfusion with a calcium containing (5 mM) aldehyde fixative. Type A calcium binding sites are triangular structures facing the junctional folds, identical with presynaptic protrusions of the active zone. Since, because of low concentration and disturbing effects, calcium peaks cannot be detected if using the conventional single shot analysis, the spectrum averaging technique was used. While gradual rising of the calcium peak from the background can be established in the course of averaging 9 spectra obtained from several Type A sites, spectra obtained from indifferent areas of the presynaptic membrane exhibited a less intensive phenomenon. The results are in agreement with previous data obtained by means of electron cytochemical methods, suggesting that Type A sites may play an important role in the regulation of calcium influx to the intraaxonal area. Junctional folds on the postsynaptic membrane may funnel calcium ions exactly to these restricted places of the nerve membrane and, at the arrival of nerve action potential, calcium ions may enter directly to the active zone. This way, a relatively small amount of calcium is sufficient to release neurotransmitter from the terminal.

Animals↗
PubMed1983

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

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.

Acid Phosphatase↗
PubMed1983

Functional impairment of the primary nociceptive analyser in the course of transganglionic degenerative atrophy.

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.

Acid Phosphatase↗