Retrograde axonal transport of endogenous protein: differences between motor and sensory axons

Bisby, Mark A.

doi:10.1111/j.1471-4159.1977.tb07737.x

Cited by 43 publications

(15 citation statements)

References 10 publications

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“…In the present study n o redistribution to a higher level could he seen and the proximal slope, although slightly changing with time, could not be used to calculate a slow rate o f transport. Bisby (1977) observed that the migrating material behaved differently in crushed sensory and motor axons and this could possibly explain some of the difffrences between the present results and those of Ochs (1975). Another obvious difference was that the frog nerves were ligated at their distal ends whereas the cat nerves were intact.…”

Section: Hansoncontrasting

confidence: 46%

Axonal transport in transplanted frog sciatic nerve

Hanson

1981

Acta Physiologica Scandinavica

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Axonal transport was studied in transplanted frog sciatic nerves-dorsal ganglia for periods up to three months. The ganglia were either labeled prior to, or after varying periods of transplantation and the distribution of labeled proteins compared. The survival of the preparations was assessed by studying their ability to transmit compound action potentials, to maintain axonal transport and by their ultrastructural appearance. The sensory neurons retained their fast axonal transport and excitability during the transplantation periods. Morphologically about 30% of the axons appeared normal after one month of transplantation. The amount and distribution of protein incorporated radioactivity in the ganglia and the nerve changed with time but the decrease in the ganglia was not accompanied by a corresponding increase in the nerve. There was no evidence for a distinct slow phase of transport in spite of a functional fast transport system. The results indicate that either slow transport stops when the normal balance between release, degradation and recirculation is distributed by the presence of a ligature or that there is a continuous change in the composition of transported material with the time after labeling which is not reflected in altered transport characteristics.

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Section: Hansoncontrasting

confidence: 46%

Axonal transport in transplanted frog sciatic nerve

Hanson

1981

Acta Physiologica Scandinavica

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“…tal to a double ligature during a 9-24 h collection interval in sciatic nerve following injection of [35S]methionine and [3H]fucose into the fifth lumbar dorsal root ganglion of rats intoxicated with 100 mg/kg or more. Distal accumulation of label is held to represent retrograde fast component of axonal transport (Bisby, 1977). The early collection period (9-15 h) primarily reflects the transport velocity and the time in turnaround from the anterograde to the retrograde transport, whereas the amount in transport and the velocity predominates the accumulation during the long interval (9-24 h).…”

Section: Discussionmentioning

confidence: 99%

Early and Dose‐Dependent Decrease of Retrograde Axonal Transport in Acrylamide‐Intoxicated Rats

Jakobsen

Sidenius

1983

Journal of Neurochemistry

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The effect of retrograde axonal transport of doses of acrylamide ranging from 50 to 500 mg/kg was studied in sensory nerve of rats. Accumulation of trichloroacetic acid-phosphotungstic acid-insoluble label was measured in a collection segment distal to a double ligature placed on the sciatic nerve at intervals 9-15 h and 9-24 h following injection into the dorsal root ganglion of the fifth lumbar root of [35S]methionine and [3H]fucose. After a dose of 100 mg/kg of acrylamide no neurological signs of neuropathy had yet appeared, but retrograde buildup of protein label was significantly reduced for the long interval (2.20 +/- 0.49 arbitrary units (AU) (mean +/- SD) versus 2.81 +/- 0.57 AU in controls, 2p = 0.034). No abnormality of the short interval appeared before a dose of 500 mg/kg was reached. The retrograde transport abnormality was dose-related (r = -0.85, n = 28, and 2p = 1.2 x 10(-8)), as was the degree of neuropathy evaluated by "blind" neurological scoring (r = 0.88, n = 14, and 2p = 2.8 x 10(-5)). After a dose of 500 mg/kg, when the rats were severely disabled with almost total incoordination of the hindlegs, the retrograde accumulation of the long interval was profoundly depressed (1.08 +/- 0.28 AU versus 2.81 +/- 0.57 AU in controls, 2p = 1.2 x 10(-7)). Similar changes were seen in accumulation of glycoprotein label. After the rats had recovered for 4-10 weeks neurological signs of neuropathy had disappeared and the transport abnormality had improved. To test the specificity of acrylamide on the retrograde transport defect N-hydroxymethylacrylamide and methylene-bisacrylamide, which do not induce neuropathy, were studied. None of these related compounds influenced the transport. These observations imply that in acrylamide intoxication a defect in the amount of material carried by retrograde axonal transport rather than in "turnaround" time or in transport velocity is present, that the transport abnormality precedes the development of neuropathy, and that it is related to the degree of the neurological disability. We suggest that the retention of protein in the distal axons in the functional counterpart of the well-known accumulation of vesicular organelles in the preterminals.

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“…In all experiments precursor was injected at time zero into the vicinity of sciatic nerve motoneurons or the L5 dorsal root ganglion (DRG) as previously described (BISBY, 1976b(BISBY, , 1977.…”

Section: Methodsmentioning

confidence: 99%

REVERSAL OF AXONAL TRANSPORT AT A NERVE CRUSH¹

Bisby

Bulger

1977

Journal of Neurochemistry

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142

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Abstract— —We have compared retrograde axonal transport of 3H‐labeled protein in normal rat motor and sensory axons, and axons which were injured by a distal ligation of the sciatic nerve. After injection of L‐[3H]leucine into the vicinity of the neuron cell bodies, labeled protein was transported into the axons. A premature return of protein towards the cell bodies occurred in the injured axons, which we interpret as a reversal of axonal transport occurring at the site of injury. We estimate that reversal of transport occurred within 1.9–2.4 h of the arrival of labeled protein at the injury, and that the minimum velocity of the subsequent retrograde transport was 112–133 mm day−1. The ability of the injured axons to reverse transport developed about 0.8 h after making the injury. A large fraction of the orthograde transported protein was returned towards the cell body: it is estimated that by 28 h after labeled protein in sensory axons reached the injury, 46% of the3H‐labeled protein originally transported to the injury site had been returned. In intact sensory nerves at this time only 15% of the transported protein had returned. It is suggested that axonal injury produces a sudden increase in the return of newly synthesized protein to the cell body, and that this might serve as a signal for chromatolysis.

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Retrograde axonal transport of endogenous protein: differences between motor and sensory axons

Cited by 43 publications

References 10 publications

Axonal transport in transplanted frog sciatic nerve

Axonal transport in transplanted frog sciatic nerve

Early and Dose‐Dependent Decrease of Retrograde Axonal Transport in Acrylamide‐Intoxicated Rats

REVERSAL OF AXONAL TRANSPORT AT A NERVE CRUSH¹

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Retrograde axonal transport of endogenous protein: differences between motor and sensory axons

Cited by 43 publications

References 10 publications

Axonal transport in transplanted frog sciatic nerve

Axonal transport in transplanted frog sciatic nerve

Early and Dose‐Dependent Decrease of Retrograde Axonal Transport in Acrylamide‐Intoxicated Rats

REVERSAL OF AXONAL TRANSPORT AT A NERVE CRUSH1

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REVERSAL OF AXONAL TRANSPORT AT A NERVE CRUSH¹