Taxol-induced neuropathy: chronic effects of local injection
Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were cau...
Ausführliche Beschreibung
Gespeichert in:
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E-Artikel |
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Englisch |
| Erschienen: |
1986 |
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| Umfang: |
14 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Journal of neurocytology - 1972, 15(1986) vom: Apr., Seite 483-496 |
| Übergeordnetes Werk: |
volume:15 ; year:1986 ; month:04 ; pages:483-496 ; extent:14 |
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| 520 | |a Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. | ||
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(DE-627)NLEJ189905166 DE-627 ger DE-627 rakwb eng Taxol-induced neuropathy: chronic effects of local injection 1986 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. Springer Online Journal Archives 1860-2002 Röyttä, M. oth Raine, C. S. oth in Journal of neurocytology 1972 15(1986) vom: Apr., Seite 483-496 (DE-627)NLEJ188984046 (DE-600)2007301-X 1573-7381 nnns volume:15 year:1986 month:04 pages:483-496 extent:14 http://dx.doi.org/10.1007/BF01611731 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 15 1986 4 483-496 14 |
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(DE-627)NLEJ189905166 DE-627 ger DE-627 rakwb eng Taxol-induced neuropathy: chronic effects of local injection 1986 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. Springer Online Journal Archives 1860-2002 Röyttä, M. oth Raine, C. S. oth in Journal of neurocytology 1972 15(1986) vom: Apr., Seite 483-496 (DE-627)NLEJ188984046 (DE-600)2007301-X 1573-7381 nnns volume:15 year:1986 month:04 pages:483-496 extent:14 http://dx.doi.org/10.1007/BF01611731 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 15 1986 4 483-496 14 |
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(DE-627)NLEJ189905166 DE-627 ger DE-627 rakwb eng Taxol-induced neuropathy: chronic effects of local injection 1986 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. Springer Online Journal Archives 1860-2002 Röyttä, M. oth Raine, C. S. oth in Journal of neurocytology 1972 15(1986) vom: Apr., Seite 483-496 (DE-627)NLEJ188984046 (DE-600)2007301-X 1573-7381 nnns volume:15 year:1986 month:04 pages:483-496 extent:14 http://dx.doi.org/10.1007/BF01611731 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 15 1986 4 483-496 14 |
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(DE-627)NLEJ189905166 DE-627 ger DE-627 rakwb eng Taxol-induced neuropathy: chronic effects of local injection 1986 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. Springer Online Journal Archives 1860-2002 Röyttä, M. oth Raine, C. S. oth in Journal of neurocytology 1972 15(1986) vom: Apr., Seite 483-496 (DE-627)NLEJ188984046 (DE-600)2007301-X 1573-7381 nnns volume:15 year:1986 month:04 pages:483-496 extent:14 http://dx.doi.org/10.1007/BF01611731 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 15 1986 4 483-496 14 |
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(DE-627)NLEJ189905166 DE-627 ger DE-627 rakwb eng Taxol-induced neuropathy: chronic effects of local injection 1986 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. Springer Online Journal Archives 1860-2002 Röyttä, M. oth Raine, C. S. oth in Journal of neurocytology 1972 15(1986) vom: Apr., Seite 483-496 (DE-627)NLEJ188984046 (DE-600)2007301-X 1573-7381 nnns volume:15 year:1986 month:04 pages:483-496 extent:14 http://dx.doi.org/10.1007/BF01611731 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 15 1986 4 483-496 14 |
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Taxol-induced neuropathy: chronic effects of local injection |
| abstract |
Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. |
| abstractGer |
Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. |
| abstract_unstemmed |
Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ189905166</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707133548.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070525s1986 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ189905166</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Taxol-induced neuropathy: chronic effects of local injection</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1986</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">14</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally related to the slow progressive accumulation of microtubules and other axoplasmic constituents. This culminated in the appearance of giant axonal spheroids and profiles similar to the retraction bulbs of Wallerian degeneration. From these axonal bulbs, many of which arose at nodes of Ranvier, groups of regenerating sprouts emanated. During the acute phase of taxol neurotoxicity, some swollen axons were divested of their myelin sheaths and remained demyelinated for many weeks. After 4 weeks, remyelination was apparent along some fibres. In addition to the accumulation of profiles usually associated with retraction bulbs, there was a vast increase in microtubules, some of which were aligned in concentric rings and formed channels for mitochondria. Microtubule anomalies were also visualized in distal portions of affected fibres and in regenerating sprouts. In contrast, Schwann cells displayed microtubule abnormalities only at the site of the lesion where excessive microtubule polymerization caused the displacement of ribosomes from rough endoplasmic reticulum. Distally, Schwann cells were essentially normal. Axonal depletion and regenerating sprouts were noted further downstream in the tibial nerve, and the gastrocnemius muscle showed changes similar to denervation atrophy. These results extend previous observations by demonstrating chronic, reparatory and reversible phenomena, the implications of which are discussedvis á vis axoplasmic transport and nerve regeneration.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Röyttä, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Raine, C. S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Journal of neurocytology</subfield><subfield code="d">1972</subfield><subfield code="g">15(1986) vom: Apr., Seite 483-496</subfield><subfield code="w">(DE-627)NLEJ188984046</subfield><subfield code="w">(DE-600)2007301-X</subfield><subfield code="x">1573-7381</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:15</subfield><subfield code="g">year:1986</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:483-496</subfield><subfield code="g">extent:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01611731</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">15</subfield><subfield code="j">1986</subfield><subfield code="c">4</subfield><subfield code="h">483-496</subfield><subfield code="g">14</subfield></datafield></record></collection>
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