The effects of drugs which destroy the sympathetic nervous system on the retrograde transport of nerve growth factor

Johnson, Eugene M.; Macia, Richard A.; Andres, Roger Y.; Bradshaw, Ralph A.

doi:10.1016/0006-8993(79)91050-3

Cited by 24 publications

(11 citation statements)

References 14 publications

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“…Pilot ex periments had shown that the dose of colchicine injected was sufficient to block both retrograde (and antero grade) transport of horseradish peroxidase, which indi cates that the retrograde transport of all substances will have been blocked since they are all believed to be translocated by the same microtubule-associated mecha nism [13]. That the retrograde effects of colchicine appli cation arc due to the perikaryon being deprived of neuro trophic support owing to the blockade of axoplasmic transport is virtually certain in the case of sympathetic neurons, since to survive they require NGF, which they can normally obtain only via colchicine-sensitive retro grade transport [14,15], and since systemically adminis tered NGF counteracts the toxic effects of colchicine (or other tubulin-binding substances) on sympathetic neu rons [16,17]. In the ION, the same is likely to be true, although our only evidence is that the neuronal death provoked in the ION by an intraocular injection of col chicine is of a particular morphologic type that occurs reliably when the ION is prevented (by any of several means: early retinal ablation, late destruction of the reti nal target cells, or blockade of axoplasmic transport) from receiving retrograde maintenance, but not when the ION neurons die from other causes such as deafferentation [7][8][9].…”

Section: Discussionmentioning

confidence: 99%

Timing of Neuronal Death following Successive Blockade of Protein Synthesis and Axoplasmic Transport in the Axonal Target Territory

Blaser¹,

Clarke²

1992

Dev Neurosci

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Neurons in the isthmo-optic nucleus (ION) of chick embryos can withstand a substantial cycloheximide-induced reduction in protein synthesis in their target territory, the retina, at the very time when their survival is known to depend on a retrograde signal from the latter. We here test the hypothesis that this resistance to the cycloheximide injection might be due to the accumulation in the ION of a reserve of retina-derived trophic molecules (or of resulting second messengers). Following an intraocular injection of cycloheximide at E15 to deplete the hypothetical reserve in one ION, both eyes received injections of colchicine (which blocks axoplasmic transport) at E16. The resulting time course of cell death was very similar in the two IONs, which refutes the hypothesis. The most plausible alternative is that there is a reserve of trophic substance in the retina capable of maintaining the ION for about 1 day.

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Section: Discussionmentioning

confidence: 99%

Timing of Neuronal Death following Successive Blockade of Protein Synthesis and Axoplasmic Transport in the Axonal Target Territory

Blaser¹,

Clarke²

1992

Dev Neurosci

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“…Previous studies of 125 I-NGF transport from the anterior chamber of the eye to the superior cervical ganglion have also shown a greater degree of 6-OHDA inhibition of the later phases of 125 I-NGF transport compared with earlier phases. 18 Neonatal guanethidine treatment results in nearly complete sympathectomy in adult animals, which has been verified by histologic, physiologic, and biochemical methods. 13~15 125 I-NGF transport to the superior cervical ganglion was decreased 98% after guanethidine in the current experiments, which parallels histologic evidence of devastation of the neuronal population in the ganglion.…”

Section: Discussionmentioning

confidence: 85%

Retrograde Axonal Transport in Rat Ileal Mesenteric Nerves: Characterization Using Intravenously Administered 125I-Nerve Growth Factor and Effect of Chemical Sympathectomy

Schmidt¹,

Yip

1985

Diabetes

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We have previously demonstrated the reproducible occurrence of dystrophic axonopathy and a defect in the retrograde axonal transport of 125I-nerve growth factor (125I-NGF) involving postganglionic sympathetic axons in the alimentary tract of rats with chronic streptozocin (STZ)-induced diabetes. To avoid complexities inherent in monitoring the accumulation of 125I-NGF in the superior mesenteric ganglion as a measure of retrograde transport in the peripheral axons of the extensive alimentary territory, we have examined retrograde axonal transport of 125I-NGF directly in ileal mesenteric nerves. 125I-NGF was injected systemically, and 2-2.5 h later ileal mesenteric nerve pedicles were ligated in vivo for various intervals. Retrogradely transported 125I-NGF in rat mesenteric nerves was measured distal to a ligature placed on the ileal mesenteric pedicle. Transport-unrelated processes, such as mechanical compression or bleeding at the site of ligation, did not contribute significantly to accumulation measured in this fashion. Accumulation of retrogradely transported 125I-NGF at the ligature began 4 h after ligation and remained linear for approximately 12 h. The amount of retrogradely transported 125I-NGF accumulating distal to the ligature reflected the length of the ileal segment served by the pedicle, which allowed the standardization of accumulation based on length of ileum innervated. The results of several experiments showed that 125I-NGF transport originated largely from nerve terminals within the ileal wall with a smaller component from extramural sites, probably terminals within the walls of blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…talcini et al, 1975). Destruction of nerve terminals by the drug is associated with a significant decrease in the dependent on the loss of specific binding sites in nerve retrograde transport of NGF to the superior cervical endings that are necessary for their uptake and transport ganglion (Johnson et al, 1979). This may occur with (Dumas et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Injections of the drug (100 mg/kg) were either intraperitoneal or intravenous. The two routes of administration are equally effective in reducing retrograde transport of NGF (Johnson et al, 1979).…”

Section: -Hydroxydopaminementioning

confidence: 98%

“…Since surgical axotomy produces a fall in muscarinic ligand binding that correlates temporally with increases in 6phosphogluconate dehydrogenase (EC 1.1.1.44) (Sinicropi et al, 1979) and glucose-6-phosphate dehydrogenase activity (Harkonen and Kauffman, 1974), we examined the influence of axonal injury and NGF on the activities of the oxidative enzymes of the pentose phosphate pathway and muscarinic receptor content in the superior cervical ganglion. 6-Hydroxydopamine treatment of adult rats was used to destroy nerve terminals of postganglionic fibers and to reduce retrograde transport of NGF to the ganglion in vivo (Johnson et al, 1979). Biochemical alterations produced by chemical axotomy with 6-hydroxydopamine in vivo were compared in the presence and absence of NGF administered systemically.…”

mentioning

confidence: 99%

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Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor

Dombrowski¹,

Jerkins²,

Kauffman³

1983

J. Neurosci.

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Administration of 6-hydroxydopamine to adult rats results in changes in the superior cervical ganglion similar to those noted after axotomy; namely, a decrease in muscarinic receptor binding and increases in activities of the oxidative enzymes of the pentose phosphate pathway. These changes were either prevented or attenuated markedly by the systemic administration of nerve growth factor. Administration of nerve growth factor alone did not significantly increase N-methylscopolamine binding in the ganglion or reduce the activities of the oxidative enzymes. Explants of the ganglion maintained in serum-free medium over a period of 3 days demonstrated increases in oxidative enzyme activity and a decrease in N-methylscopolamine binding. Addition of 20 nM nerve growth factor to the culture medium prevented the decline in N-methylscopolamine binding in ganglion explants. The increases in oxidative enzyme activities were unaltered. Addition of high amounts of nerve growth factor, 200 nM, resulted in a significant increase in tyrosine hydroxylase activity but no further increase in N-methylscopolamine binding in ganglion explants. Glucocorticoids added to the culture medium did not affect the muscarinic binding or enzyme activities. Thus, decreases in muscarinic binding activity which occur in the superior cervical ganglion after axotomy or 6-hydroxydopamine treatment may be explained by a loss of nerve growth factor supplied to the ganglion. Increases in the oxidative enzymes of the pentose phosphate pathway that occur in the ganglion after axonal injury appear to involve additional factors.

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The effects of drugs which destroy the sympathetic nervous system on the retrograde transport of nerve growth factor

Cited by 24 publications

References 14 publications

Timing of Neuronal Death following Successive Blockade of Protein Synthesis and Axoplasmic Transport in the Axonal Target Territory

Timing of Neuronal Death following Successive Blockade of Protein Synthesis and Axoplasmic Transport in the Axonal Target Territory

Retrograde Axonal Transport in Rat Ileal Mesenteric Nerves: Characterization Using Intravenously Administered 125I-Nerve Growth Factor and Effect of Chemical Sympathectomy

Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor

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