Slow axoplasmic transport: a fiction?

Álvarez, Jaime; Torres, Juan Carlos

doi:10.1016/s0022-5193(85)80028-x

Cited by 40 publications

(20 citation statements)

References 33 publications

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“…Constants for synthesis and degradation of proteins, and for diffusion, uptake and leakage of amino acids were taken or derived from published values, and the equations solved by iteration (Álvarez and Torres, 1985). Virtual waves are similar to observed waves in several respects: (i) with time, the peak moves away, albeit its velocity is in the lower range of reported values, (ii) the leading slope becomes less steep, and (iii) the overall label decreases (Fig.…”

Section: Scrutiny Of the Slow Wavesmentioning

confidence: 88%

“…These notions, complemented with appropriate assumptions to fi ll gaps, were accepted by the scientifi c community, and are still standard textbook notions. Regrettably, when inconsistencies arose, some were addressed with unsupported assumptions, and others went unnoticed or ignored (cf Álvarez and Torres, 1985;Álvarez, 1992;Álvarez et al, 2000), and were never discussed at large.,…”

Section: Discussionmentioning

confidence: 99%

“…At time zero, a pulse of label is given to the cell body. Curves are the distribution of the label at the time indicated (from Álvarez and Torres, 1985; by permission of Elsevier). C', events underlying C according to MM: tracers diffuse from cell body to axon, are incorporated into axoplasmic proteins and upon their degradation, tracers are re-cycled.…”

Section: Scrutiny Of Protein Stability In Axonsmentioning

confidence: 99%

“…In the simulation, when the cell body is made to re-supply the axon with precursors, the virtual maximum stays in the fi rst segment throughout the post-pulse period, (see Fig. 10, in Álvarez and Torres, 1985). In goldfi sh, following a pulse of tracers to the eye, the radioactive maximum remains in the fi rst segment of the optic nerve throughout the survival time (Grafstein and Murray, 1969).…”

Section: Scrutiny Of the Slow Wavesmentioning

confidence: 99%

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Slow axoplasmic transport under scrutiny

Court

Álvarez

2011

Biol. Res.

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We dedicate this paper to Antonio Giuditta and Edward Koenig who laid the basis to understand the origin of axoplasmic protein. ABSTRACTThe origin of axoplasmic proteins is central for the biology of axons. For over fi fty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that confi gure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate indepth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fi elds.

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Section: Scrutiny Of the Slow Wavesmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Scrutiny Of Protein Stability In Axonsmentioning

confidence: 99%

Section: Scrutiny Of the Slow Wavesmentioning

confidence: 99%

See 2 more Smart Citations

Slow axoplasmic transport under scrutiny

Court

Álvarez

2011

Biol. Res.

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“…Modified from Iñiguez and Álvarez, 1999. added time and again. For example, transported proteins should spend years in transit, time enough for complete degradation before reaching their destination (Álvarez and Torres, 1985). The other view claims that the axoplasm synthesizes its own proteins, a view largely ignored -despite the evidence accumulated for fifty years-on the ground that ribosomes have not been observed in the axoplasm.…”

Section: Protein Synthesis In Axonsmentioning

confidence: 99%

Local regulation of the axonal phenotype, a case of merotrophism

Court

Álvarez

2005

Biol. Res.

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In this essay, we show that several anatomical features of the axon, namely, microtubular content, caliber and extension of sprouts, correlate on a local basis with the particular condition of the glial cell, i.e., the anatomy of axons is dynamic, although it is seen usually in its 'normal' state. The occurrence of ribosomes and messenger RNAs in the axon suggests that axoplasmic proteins are most likely synthesized locally, at variance with the accepted notion that they are supplied by the cell body. We propose that the supporting cell (oligodendrocyte or Schwann cell) regulates the axonal phenotype by fine-tuning the ongoing axonal protein synthesis.

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Protein synthesis in presynaptic endings from squid brain: Modulation by calcium ions

et al. 1999

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Previous biochemical, autoradiographic, and ultrastructural data have shown that, in the synaptosomal fraction of the squid optic lobe, protein synthesis is largely due to the presynaptic terminals of the retinal photoreceptor neurons (Crispino et al. [1993a] Mol. Cell. Neurosci. 4:366-374; Crispino et al. [1993b] J. Neurochem. 61:1144-1146; Crispino et al. [1997] J. Neurosci. 17:7694-7702). We now report that this process is close to its maximum at the basal concentration of cytosolic Ca++, and is markedly inhibited when the concentration of this ion is either decreased or increased. This conclusion is supported by the results of experiments with: 1) compounds known to increase the level of cytosolic Ca++, such as A23187, ionomycin, thapsigargin, and caffeine; 2) compounds sequestering cytosolic calcium ions such as BAPTA-AM; and 3) agents that block the role of Ca++ as second messenger, such as TFP and W7, which inhibit calmodulin, and calphostin, which inhibits protein kinase C. We conclude that variations in the level of cytosolic Ca++ induced in presynaptic terminals by neuronal activity may contribute to the modulation of the local synthesis of protein.

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Slow axoplasmic transport: a fiction?

Cited by 40 publications

References 33 publications

Slow axoplasmic transport under scrutiny

Slow axoplasmic transport under scrutiny

Local regulation of the axonal phenotype, a case of merotrophism

Protein synthesis in presynaptic endings from squid brain: Modulation by calcium ions

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