Temperature effects on fast axonal transport of proteinsin vitro in frog sciatic nerves

Hanson, Mats

doi:10.1016/0006-8993(73)90006-1

Cited by 96 publications

(40 citation statements)

References 24 publications

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“…Since low temperature appears to be an effective inhibitor of fast axonal transport (25), we performed similar experiments with a-LTX at 1-30C. Previous studies had shown that the toxin was effective also at this temperature.…”

Section: Resultsmentioning

confidence: 99%

Differential effect of alpha-latrotoxin on exocytosis from small synaptic vesicles and from large dense-core vesicles containing calcitonin gene-related peptide at the frog neuromuscular junction.

Matteoli

Haimann

Torri-Tarelli

et al. 1988

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

193

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The regulatory peptide called calcitonin gene-related peptide (CGRP) was detected by immunofluorescence in frog motor neurons and motor nerve terminals. In motor nerve terminals, CGRP-like immunoreactivity was found to be segregated within large dense-core vesicles. To determine whether exocytosis from acetylcholine-containing small synaptic vesicles and from CGRP-containing large dense-core vesicles can be independently stimulated, nerve-muscle preparations were exposed to alpha-latrotoxin. This toxin induced complete depletion of acetylcholine-containing small synaptic vesicles but did not induce a parallel depletion of CGRP-like immunoreactivity and of large dense-core vesicles. These effects were independent of the presence of extracellular Ca2+ and occurred both at room temperature and at low temperature (1-3 degrees C). These findings suggest that exocytosis from the two vesicle populations is mediated by distinct biochemical mechanisms, which might be differentially regulated by physiological stimuli.

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Section: Resultsmentioning

confidence: 99%

Differential effect of alpha-latrotoxin on exocytosis from small synaptic vesicles and from large dense-core vesicles containing calcitonin gene-related peptide at the frog neuromuscular junction.

Matteoli

Haimann

Torri-Tarelli

et al. 1988

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

193

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“…It is well known that rapid axonal transport, which is characterized by a velocity of approximately 400 mm/day at 37 'C (Ochs, 1972), becomes slower and slower as temperature is reduced (Edstrom & Hanson, 1973;Grafstein, Forman & McEwen, 1972;Gross, 1973;Ochs & Smith, 1975;Cosens et al 1976). Considerable slowing takes place between 37 and 22 0, a region over which microtubules are stable.…”

Section: Discussionmentioning

confidence: 99%

“…To provide fresh evidence, we decided to investigate nerves that had been exposed to low temperatures instead of drugs. Microtubules are known to depolymerize in the cold (Tilney & Porter, 1967;Rodriguez-Echandia & Piezzi, 1968), and previous work in several laboratories has indicated that there may be a critical temperature below which the velocity of rapid transport falls abruptly (Edstr6m & Hanson, 1973;Ochs & Smith, 1975;Cosens, Thacker & Brimijoin, 1976). The present experiments were designed to test the possibility that this critical temperature represents the point at which microtubules begin to depolymerize.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the temperature‐dependence of rapid axonal transport and microtubules in nerves of the rabbit and bullfrog.

Brimijoin¹,

Olsen²,

Rosenson³

1979

The Journal of Physiology

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SUMMARY1. The average velocity of transport of dopamine-fl-hydroxylase, an enzyme confined to unmyelinated adrenergic nerves, was measured in rabbit and bullfrog sciatic nerves or branches incubated in vitro at various temperatures. In parallel experiments, the number and density of microtubules were measured in crosssections of randomly selected unmyelinated axons from another set of nerves incubated under the same conditions. 2. Average transport velocity was exponentially related to temperature over a wide range, but it fell abruptly towards zero at temperatures below 13 0C in the case of rabbit nerves and 10 0C in the case of frog nerves.3. The number of microtubules per unmyelinated axon had declined considerably before the transport of dopamine-fl-hydroxylase was impaired. At 13 0C, axons in rabbit nerves lost 30 % of their microtubules. Axons in bullfrog nerves were, if anything, more sensitive to cold, losing 35 % of their microtubules at 15 0C and 65 % of them at 100 C. 4. Since the temperature-dependence of the axonal transport of dopamine-flhydroxylase is probably typical of rapid axonal transport in general, it was concluded that transport in unmyelinated axons can continue unaffected when a substantial fraction of the microtubular population has been lost. 5. Although these results could imply that microtubules are not essential for transport, they are equally compatible with the view that these organelles determine the capacity of the transport system and are normally present in excess.

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“…No evidence supports the hypothesis that axonal proteins are synthesized or glycosylated locally in the axon. There are, however, axonal transport systems which transport the newly synthesized axonal proteins from the cell body to the entire length of the axon with a maximum speed ranging from 25 to 150 mm/day in frog, dependent upon temperature (approximately 70 mm/day at 11 0C, Edstrom & Hanson, 1973). These transport systems remain active after nerve transaction (Lubinska, 1964).…”

Section: Discussionmentioning

confidence: 99%

The long‐term excitability of myelinated nerve fibres in the transected frog sciatic nerve.

Wang¹

1985

The Journal of Physiology

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SUMMARY1. The long-term excitability and the ionic currents in the nodes of Ranvier were studied in the severed frog sciatic nerve and the unoperated contralateral control nerve.2. After unilateral nerve section, compound action potentials of the nerve bundles and action potentials of single myelinated nerve fibres remained normal in amplitude and duration in either sciatic nerve for more than 38 days when frogs were kept at 11 'C. During this period the resting potentials averaged about -75 mV.3. Under voltage-clamp conditions Na currents and K currents in transacted single myelinated nerve fibres also appeared normal in their kinetics, and in their peak amplitudes. These results indicate that the Na-and K-channel densities are quantitatively unchanged after the nerve transaction, up to several weeks.4. The excitability of the severed sciatic nerve, expectedly, depends strongly on the time course ofWallerian degeneration. When frogs were kept at room temperature, the nerve excitability remained normal for only about 8-10 days, due to the faster Wallerian degeneration; whereas at 4 'C it was maintained for more than 84 days, as long as the myelinated nerve fibres did not degenerate.5. Together, these findings demonstrate that Na channels, K channels, and Na-K pumps are continuously present for several weeks in the transacted nerve before nerve degeneration. It is surmised that either, (a) these proteins are extremely stable in the transacted myelinated nerve fibres, or (b) they are supplied locally by Schwann cells, an open question recently posed by Chiu, Schrager & Ritchie (1984). In either event, the myelinated nerve fibres do not require cell bodies to provide a significant amount of new channels and pumps in order to retain their long-term excitability.

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Temperature effects on fast axonal transport of proteinsin vitro in frog sciatic nerves

Cited by 96 publications

References 24 publications

Differential effect of alpha-latrotoxin on exocytosis from small synaptic vesicles and from large dense-core vesicles containing calcitonin gene-related peptide at the frog neuromuscular junction.

Differential effect of alpha-latrotoxin on exocytosis from small synaptic vesicles and from large dense-core vesicles containing calcitonin gene-related peptide at the frog neuromuscular junction.

Comparison of the temperature‐dependence of rapid axonal transport and microtubules in nerves of the rabbit and bullfrog.

The long‐term excitability of myelinated nerve fibres in the transected frog sciatic nerve.

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