Fast axonal transport in motor nerve regeneration

Griffin, John W.; Drachman, Daniel B.; Price, Donald L.

doi:10.1002/neu.480070407

Cited by 95 publications

(47 citation statements)

References 45 publications

(50 reference statements)

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“…A similar result for glycoproteins labeled with [3H]fucose has been found in crushed rabbit hypoglossal nerve (Frizeil and Sjostrand, 1974). Total amounts of rapidly transported protein labeled with [3H]leucine have also been observed to increase in regenerating mammalian peripheral nerve (Griffin et al, 1976). Since transport of [3H] serotonin remains stably reduced during this period of time, this result may indicate that some of the [3H] fucosyl glycoprotein has been incorporated into organelles other than the transmitter vesicle as a consequence of axotomy.…”

Section: Methodsmentioning

confidence: 96%

Routing of transmitter and other changes in fast axonal transport after transection of one branch of the bifurcate axon of an identified neuron

Aletta¹,

Goldberg²

1984

J. Neurosci.

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The regulation of the quantities and types of organelles that leave the neuronal cell body destined for use in the axon and its terminals is not well understood. We had previously found that transport of transmitter undergoes a precise down regulation when most of one branch of the bifurcate axon of an identified serotonergic neuron was removed. We have now investigated further the nature of the regulatory event and the reason for its initiation by eliminating portions of the axonal tree of this neuron. We find that the down regulation is more likely to be due to the loss of synapses than of axon because transport of [3H]serotonin decreases as much when an axonal branch is transected distally as after a proximal transection. Transport of [3H]fucosyl glycoprotein, which normally is associated with the serotonergic vesicle in this axon, decreases to the same extent as transport of [3H]serotonin following proximal transection. The glycoprotein down regulation occurs much more rapidly, possibly due to an inhibition of vesicle synthesis. A secondary rise in transport of [3H] fucosyl glycoprotein 3 days to 2 weeks after axotomy suggests that the radiolabeled glycoprotein has undergone a redistribution into organelles not normally labeled and transported in intact neurons in large amounts, since [3H]serotonin transport remains stably diminished during this period. We also describe here a case of routing of rapidly transported material. When one axonal branch is cut far from the point of bifurcation (-10 mm), ["Hlserotonin is directed away from the branch lacking its synaptic terminals and into the remaining intact branch even though the transected branch is physically capable of transporting its normal amount of [3H]serotonin. We suggest that the presence of synaptic endings influences both the export of transmitter vesicles from the cell body and the partitioning of vesicles among axon collaterals.Fast axonal transport supplies axon collaterals and terminals with newly synthesized organelles and macromolecules from the cell body of the neuron (Ochs, 1982). The collaterals and terminals are themselves incapable of synthesizing these materials. In a healthy mature

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Section: Methodsmentioning

confidence: 96%

Routing of transmitter and other changes in fast axonal transport after transection of one branch of the bifurcate axon of an identified neuron

Aletta¹,

Goldberg²

1984

J. Neurosci.

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“…One hundred gCi of E L- [4,5 3H]leucine (specific activity 50 Ci/mmol; Radiochemical Cen-E tre, Amersham, UK) were injected into the area of the motor neurone ~. cell bodies through a glass micropipette with a tip diameter of 15 um, according to the method of Lasek [10] as modified by Griffin et al [11] r and the exact spinal coordinates of Forman and Berenberg [12]. Four to eight injections (total 3 t.t 0 were made each time (Fig.…”

Section: Axonal Transportmentioning

confidence: 99%

Effects of nerve compression on fast axonal transport in streptozotocin-induced diabetes mellitus

McLean

et al. 1986

Diabetologia

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Summary. The hypothesis that nerves in diabetes mellitus exhibit an increased susceptibility to compression was experimentally tested. Inhibition of fast axonal transport was induced by local compression in sciatic nerves of rats with streptozotocin-induced diabetes mellitus. Fast anterograde axonal transport was measured after application of 3H-leucine to the motor neurone cell bodies in the spinal cord. The sciatic nerve was subjected to local, graded compression in vivo by a small compression chamber. The amount of accumulation of proteins was quantified by calculation of a transport block ratio. Compression at 30 mm Hg for 3 h induced a significantly greater (p<0.05) accumulation of axonally transported proteins at the site of compression in nerves of diabetic animals (transport block ratio: 1.01_+0.35; n=7) than in nerves of controls (0.67 + 0.16; n = 7). Accumulation was significantly higher in ligature experiments of both control (1.34_+ 0.44; n = 8; p < 0.01) and diabetic animals (1.45 _+ 0.30; n = 8; p < 0.05), indicating that the block of transport in compressed nerves was incomplete. Neither sham compressed diabetic (0.50+0.09; n=6) nor control (0.49_+0.11; n=6) nerves showed any block of axonal transport. The possible causes of the increased inhibition of fast axonal transport in diabetic rats are discussed. The results indicate that diabetes may lead to an increased susceptibility of peripheral nerves to compression.Key words: Compression, diabetes mellitus, streptozotocin, axonal transport, compression syndromes, mononeuropathy, neuropathy.The clinical symptoms of neuropathy in diabetes mellitus are well known, and include primarily sensory complaints, occasionally accompanied by muscular weakness and autonomic symptoms. Sensory and muscular dysfunction in extremities may, however, also be caused by entrapment of peripheral nerves such as ulnar nerve compression at the elbow and median nerve compression at the wrist, i. e. the carpal tunnel syndrome. A high frequency of such mononeuropathies has been reported among diabetic patients, which suggests enhanced vulnerability of peripheral nerves to trauma [1]. It has also been suggested that peripheral nerves in experimental diabetes have a greater susceptibility to injury [2][3][4].Axonopathy, which can be characterised by abnormalities in axonal transport, may be an important factor in the neuropathies which accompany diabetes [5][6][7]. Based upon previous experience on the effects of peripheral nerve compression [for review see 8] and the hypothesis that diseased neurones, such as those in diabetes mellitus, are more susceptible to compression * Present address: Department of Anatomy and Neurobiology, Washington University, School of Medicine, St. Louis, Missouri, USA trauma than are healthy neurones [9], we decided to investigate the effects of experimental nerve compression on fast axonal transport in streptozotocin-induced diabetes mellitus Materials and methods Animals and induction of diabetesRandom-bred and weight-matched female Sprague-Dawle...

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“…Microiqjection Procedures. Spinal cord injections were performed according to the method of Lasek (21) as modified by Griffin et al (22). The L4 and L5 segments of anesthetized adult rats were exposed by laminectomy of the T13 and L1 vertebrae.…”

mentioning

confidence: 99%

Developing dorsal root ganglion neurons require trophic support from their central processes: evidence for a role of retrogradely transported nerve growth factor from the central nervous system to the periphery.

Yip¹,

Johnson²

1984

Proc. Natl. Acad. Sci. U.S.A.

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Injury to the peripheral processes produces a profound cell loss (40-50%) in the dorsal root ganglion of newborn rats. Although division of central processes produces littie or no cellular change in sensory ganglion of adult animals, no Information has been available on the effect of dorsal root section in developing dorsal root ganglion. We show that 6 days after dorsal rhizotomy on newborn rats, there is a 50% decrease in neuronal number in L5 dorsal root ganglion. A combined central and peripheral lesion of the sensory process results in a greater decrease in neuronal number (70%). Both of these effects can be prevented by the concomitant treatment with nerve growth factor. We also demonstrate that 12'I-labeled nerve growth factor is retrogradely transported with high selectivity from the spinal cord to the dorsal root ganglion via the dorsal roots. The results indicate that trophic support for developing sensory neurons is provided through the central processes. This is presumably due to the uptake and retrograde transport of a trophic factor by the terminals of the central processes. The data suggest that nerve growth factor may be the trophic factor. (7) and the flow of axoplasm is slower than in the large peripherally directed axons (8, 9).Populations of developing neurons come under the influence of their peripheral fields and are able to make compensatory adjustments according to the sizes of the afferent input they receive (10-12) and the efferent output they project (13-16). The adjustments are made by way of corresponding alterations in cell number and size within the developing neuronal population. The sensory ganglion is unique in the sense that its target areas include both central neurons in the spinal cord and the innervated organs in the periphery. Despite the lack of morphological alteration reported after sectioning of the central process in adult animals, it is possible that developing DRG neurons receive trophic support from both central and peripheral target zones.Nerve growth factor (NGF) has long been thought to act as a trophic factor transferring information from the peripheral target organs to the innervating sympathetic and sensory neurons. Our recent findings (17) have demonstrated that eliminating the peripheral target influence by crushing the sciatic nerve in the newborn rat resulted in a substantial loss (40-50%) of neurons in L5 DRG. Treatment with NGF prevented the decrease in neuronal number of the axotomized DRG. In the present study, we examine the effects of central process axotomy on the survival of the neonatal neurons to evaluate the relative roles of central and peripheral contacts on the development of the DRG neurons and to determine if exogenous NGF can prevent the observed deleterious effects of central axonal injury.

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Fast axonal transport in motor nerve regeneration

Cited by 95 publications

References 45 publications

Routing of transmitter and other changes in fast axonal transport after transection of one branch of the bifurcate axon of an identified neuron

Routing of transmitter and other changes in fast axonal transport after transection of one branch of the bifurcate axon of an identified neuron

Effects of nerve compression on fast axonal transport in streptozotocin-induced diabetes mellitus

Developing dorsal root ganglion neurons require trophic support from their central processes: evidence for a role of retrogradely transported nerve growth factor from the central nervous system to the periphery.

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