Calcitonin gene-related peptide is released from cholinergic synapses.
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Animals↗
Biomedical subjects
B Csillik
Publications and source records attributed to B Csillik.
Light and electron microscopic localization of B-50 (GAP43) in the rat spinal cord during transganglionic degenerative atrophy and regeneration.
Crush or transection of a peripheral nerve is known to induce transganglionic degenerative atrophy (TDA) in the segmentally related, ipsilateral Rolando substance of the spinal cord. When the lost peripheral connectivity is reestablished, the consecutive regenerative synaptoneogenesis results in restoration of the circuitry in the formerly deteriorated upper dorsal horn. Enhanced expression of the growth-associated protein (GAP43) B-50 occurs during neuronal differentiation, axon outgrowth, and peripheral nerve regeneration. This study documents changes in immunocytochemical distribution of B-50 in the regions of the lumbar spinal cord which are segmentally related to the axotomized sciatic nerve. At the light microscopic level, a weak B-50 immunoreactivity (BIR) is present in the neuropil of the upper dorsal horn of control animals. After unilateral transection and ligation of the sciatic nerve, BIR increased in the ipsilateral upper dorsal horn at 17 days postinjury, but decreased again after 24 days with respect to the contralateral side. Differences between effects of crush and transection were prominent in combined crush-cut experiments as well (i.e., after unilateral crush and contralateral transection and ligation of the sciatic nerve). Electron microscopic studies show that in the uninjured and injured spinal cord, BIR is detected in axons and axon terminals, but not all are stained. After transection of the sciatic nerve, BIR is found in afflicted primary sensory axon terminals, including those contacting substantia gelatinosa neurons and in axon terminals undergoing glial phagocytosis. The localization of BIR seen after crushing the sciatic nerve is similar. However, at 24 days after crush, BIR is detected also in axonal growth cones. In the ventral horn of control animals, synaptic boutons impinging upon motor neurons exhibited weak BIR. At 17 days after unilateral transection of the sciatic nerve, the pericellular BIR surrounding motor neurons is decreased at the ipsilateral with respect to the contralateral side, whereas 24 days after crush injury it increased considerably. Our results show that peripheral nerve injury inducing TDA also affects BIR distribution in the spinal gray matter. Successful regeneration of the peripheral nerve after crush lesion is associated with enhanced expression of B-50 in growth cones of sprouting central axons. The neuroplastic response of B-50 is in line with a function of B-50 in axonal sprouting and reactive synaptogenesis.
Animals↗
Structural and molecular plasticity in the dorsal horn: a genuine model for neuronal and synaptic group selection.
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Animals↗
Transganglionic effects of Nocodazole, a new synthetic microtubule inhibitor, upon the histochemical structure of the spinal upper dorsal horn.
Perineural application of Nocodazole (R 17934 of Janssen Pharmaceutica), a new synthetic microtubule inhibitor, induces transganglionic degenerative atrophy of central terminals in the spinal cord of the inflicted primary sensory neurons. This drug offers new possibilities for clinical trials aiming to relieve chronic pain by subcutaneous injection of a microtubule inhibitor.
Animals↗
[Anatomy in Hungary and the Society of Anatomy].
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Anatomy↗
Vasoactive intestinal polypeptide in dorsal root terminals of the rat spinal cord is regulated by the axoplasmic transport in the peripheral nerve.
Vasoactive intestinal polypeptide (VIP) immunoreactivity in the upper spinal dorsal horn is markedly increased after transection, crush or vinblastine treatment of the ipsilateral, segmentally related peripheral nerve. After regeneration of the peripheral nerve, VIP disappears from the upper dorsal horn. Transection-induced VIP increase is abolished by rhizotomy. It is concluded that the expression of VIP is restricted by factor(s) carried by retrograde axoplasmic transport to dorsal root ganglion cells.
Animals↗
A case for transmitter plasticity at the molecular level: axotomy-induced VIP increase in the upper spinal dorsal horn is related to blockade of retrograde axoplasmic transport of nerve growth factor in the peripheral nerve.
Blockade of retrograde axoplasmic transport in peripheral nerves, by means of perineurally applied microtubule inhibitors, results in an increased vasoactive intestinal polypeptide (VIP) reaction of the segmentally related, ipsilateral upper dorsal horn. Similar effect is elicited by the perineural application of an anti-Nerve Growth Factor (anti-NGF) serum. At the same time, both treatments result in depletion of Substance P from the same region of the spinal cord. It is assumed that this striking example of transmitter plasticity, obviously taking place at the molecular level, is due to a stimulating effect of NGF upon the perikaryal Substance P-synthesizing mechanism in dorsal root ganglion cells, and the inhibitory effect of NGF upon the VIP synthesizing machinery in these same nerve cells.
Animals↗
Effect of lanthanum-induced blockade of calcium channels on nerve regeneration.
Systemic lanthanum chloride administration results in impeded myelin formation of regenerating peripheral axons and in marked decrease of regenerative elongation of dorsal root axons within the upper dorsal horn of the spinal cord. It is assumed that the inhibitory action of lanthanum ions is based on a competitive antagonism with calcium ions, insofar as lanthanum ions induce blockade of calcium channels in axonal growth cones. Consequently, motility: of axonal filopodia emanating from axonal growth cones, instrumental in longitudinal growth of regenerating central axons, is inhibited by lanthanum ions. Supposedly, a similar inhibitory action upon rotational movement of Schwann cells results in the retarded myelinization of peripheral axons.
Animals↗
Alterations in glial fibrillary acidic protein immunoreactivity in the upper dorsal horn of the rat spinal cord in the course of transganglionic degenerative atrophy and regenerative proliferation.
Transection of a peripheral nerve induces marked increase in the glial fibrillary acidic protein (GFAP) immunoreactivity in the ipsilateral, segmentally related upper dorsal horn. Increase of GFAP immunoreaction is similar to, but not identical with, that observed after dorsal rhizotomy. If the peripheral nerve succeeds in regenerating, GFAP immunoreactivity in the upper dorsal horn returns to normal. It is concluded that the amount and distribution of GFAP is determined by transganglionic degenerative atrophy. Wallerian degeneration and regenerative proliferation of dorsal root axon terminals, respectively.
Animals↗
Primary afferent origin of substance P-containing axons in the superficial dorsal horn of the rat spinal cord: depletion, regeneration and replenishment of presumed nociceptive central terminals.
Substance P-like immunoreactivity (SPLI) was localized in the superficial spinal dorsal horn of the rat by means of light and electron microscopic immunocytochemical techniques. Serial immunocytochemical sections were subjected to densitometric measurements with an electronic Image Analyser, and with aid of a computer program, a two-dimensional reconstruction of the fine neuroanatomical structure of the SPLI-active regions of the lumbosacral upper superficial spinal dorsal horn was obtained. SPLI activity in the superficial dorsal horn outlines four well-marked and distinctly differing regions, called, in the mediolateral sequence, areas A, B, C, and D, plus Cajal's noyeau interstitiel ("lateral spinal nucleus" = "nucleus of the dorsolateral fascicle," L). Lumbosacral dorsal rhizotomy results in an almost complete depletion of SPLI from ipsilateral areas A, B, C, and D; it induces decreased SPLI in the area of the lateral spinal nucleus (L), ipsi- or contralaterally in an alternating fashion. Transection of the segmentally related, ipsilateral peripheral nerve induces a marked depletion of SPLI from areas A, B, and C but only a slight decrease in area D and virtually none in the area of L. Whereas a simple crush of the peripheral nerve (axocompression) induces only a slight depletion of SPLI, if any, semiautomatic densitometric analysis of serial immunocytochemical sections proves that a controlled crush injury (axocontusion) results in depletion of SPLI from the upper dorsal horn, similar to transection of the peripheral nerve. Following regeneration of the ipsilateral, segmentally related peripheral nerve, the original immunocytochemical structure of the superficial dorsal horn is re-established by SPLI-positive axonal sprouts originating from previously damaged dorsal root axons.
Afferent Pathways↗
Enzyme translocation in the course of regeneration of central primary afferent terminals in the substantia gelatinosa of the adult rodent spinal cord.
Synaptic circuitry in the upper dorsal horn, disorganized due to transganglionic degenerative atrophy (evoked by blockade of retrograde axoplasmic transport in the related peripheral nerve), begins to be reestablished by a process of regenerative synaptoneogenesis as soon as retrograde transport is resumed. Central axons of type C primary sensory neurons, terminating in substantia gelatinosa Rolandi, as well as their cells of origin in dorsal root ganglia are specifically and selectively labeled by the enzyme thiamine monophosphatase (TMPase). Under normal conditions, TMPase is localized in axolemmal membranes at the electron histochemical level. In axonal growth cones of regenerating central terminals, only negligible TMPase reaction was found. In axonal filopodia and young nerve sprouts, there appears an increasing number of intraaxonal grains of the reaction product. Varicous swellings (beads) of regenerating axonal sprouts are transformed into scalloped (sinusoid) en passant terminals. TMPase reaction end product, present initially in the axoplasm of beads and scalloped terminals, is successively translocated to the axolemmal membrane in the course of cytochemical maturation. Structural regeneration and cytochemical maturation of central terminals of primary sensory neurons are completed 60 days after crush injury to the related peripheral axons, i.e., about 7 weeks after the peripheral nerve has regenerated.
Animals↗
Transneuronal degeneration in the Rolando substance of the primate spinal cord evoked by axotomy-induced transganglionic degenerative atrophy of central primary sensory terminals.
Transection of the sciatic nerve in Rhesus monkeys and the consequent transganglionic degenerative atrophy (TDA) of central terminals of primary afferents result in transneuronal degeneration of substantia gelatinosa (SG) cells. Severe degeneration is characterized by an increased electron density of the nucleus and by conspicuous shrinkage of the cytoplasm, mitochondrial swelling, dilation of cisterns of the rough-surfaced endoplasmic reticulum, accumulation of free ribosomes and an electron-dense material in the cytoplasm. In the mild form, dilation of cisternal elements of the endoplasmic reticulum, swollen mitochondria and accumulation of free ribosomes takes place. About 10% of SG cells in segment L5 undergo the severe form whereas the rest shows signs of the mild form. Cytoplasmic alterations that occur during transneuronal degeneration seem to start at the level of subsurface cisterns. Dendrites and axons of transneuronally degenerating SG cells also show a conspicuous electron density. By analyzing the synaptic relationships of such "darkened" dendrites, connections in the upper dorsal horn can be deciphered. Modular units of the primary nociceptive analyzer that evaluate noxious and innocuous inputs on the basis of thin versus thick (A delta C/A beta) afferent activity and subjecting them to descending control appear to be recruited from structurally dispersed elements of synaptic glomeruli. These are arranged alongside dendritic processes of large antenna cells which relay impulses to projection cells of the spinothalamic tract.
Animals↗
Cobalt-complex ATP enhanced regeneration in the dorsal horn of the rat spinal cord.
ATP, the energy source for axoplasmic transport, is indispensable for the transport of nerve growth factor (NGF). NGF regulates the regeneration of central processes of the primary sensory neurons, by means of transganglionic regulatory mechanisms. This central regeneration was investigated with the help of the histochemical detection of fluoride-resistant acid phosphatase (FRAP), one of the marker enzymes of the primary nociceptive neurons. Transganglionic degenerative atrophy (TDA) of the central terminals of primary sensory neurons was induced with sciatic nerve crush. Dynamics of central regeneration was studied in rats treated with a cobalt-ATP complex, and with commercially available Na-ATP, respectively, by means of histochemical detection of the restitution of FRAP activity in the Rolando substance. Disappearance of FRAP activity was complete on the 6th postoperative day in the medial two-thirds of the upper dorsal horn in segments L2-L6. The regeneration (i.e. replenishment of FRAP activity) began on the 14th day and was complete by the 31st day in animals treated with cobalt-ATP, while in the animals treated with Na-ATP the replenishment of FRAP activity began on the 20th day and was complete only by the 60th day. It is concluded that the cobalt-ATP-complex significantly enhances central regeneration.
Acid Phosphatase↗
Mapping the distribution of thiamine monophosphatase, fluoride-resistant acid phosphatase, and substance P in the spinal cord with a personal computer compatible program.
Distribution of the marker enzymes fluoride-resistant acid phosphatase (FRAP) and thiamine monophosphatase (TMPase) as well as that of the marker neuropeptide substance P (SP) has been mapped by means of the semi-automatic computer program MUDH, in various experimental conditions, including degeneration, regeneration, and anti-Nerve Growth Hormone treatment of the sciatic nerve. The program is written in standard Pascal language; it is applicable to Commodore 64 and IBM compatible personal computers. Graphical illustration of values obtained in serial sections is a powerful and highly valuable contribution in the analysis of various biodynamic reactions related to transganglionic regulation of primary sensory neurons.
Acid Phosphatase↗
Prof. Ambrus Abrahám (1893-1989).
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Bibliographies as Topic↗
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↗
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↗
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↗