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B Grafstein

Publications and source records attributed to B Grafstein.

At least 55 records · Page 3Linked to original sources
PubMed1981

The relationship between extracellular amino acids and protein synthesis is altered during axonal regeneration.

The incorporation of [3H]proline into proteins of goldfish retinal ganglion cells was measured by light microscopic autoradiography of isolated retinas that had been incubated in labeled medium under pulse-chase conditions. It was found that the composition of the immediate precursor pool for protein synthesis is more directly influenced by extracellular amino acids in regenerating cells 14 d after axotomy than in sham-operated controls.

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PubMed1981

Effect of a conditioning lesion on optic nerve regeneration in goldfish.

Following a 'test lesion' (crush) of the optic nerve in goldfish, histological study of axons in silver-stained sections showed that outgrowth of the leading axons began after an initial delay of 4.3 days and proceeded at 0.34 +/- 0.03 mm/day. When a 'conditioning lesion' (crush at the same site) preceded the testing lesion by 2 weeks, the initial delay was 2.5 days and the outgrowth rate was 0.74 +/- 0.13 mm/day (P less than 0.01). Two additional methods, utilizing intraocular injections of tritiated proline or fucose to label axonally transported proteins, were used to examine the outgrowth of leading optic axons. (a) Measurement of the distances reached by labeled axons in the nerve at 6 and 10 days after a testing lesion alone yielded an initial delay of 4.6 days and an outgrowth rate of 0.41 +/- 0.04 mm/day. However, when a conditioning lesion preceded the testing lesion, labeled optic axons were already found to have reached the optic tectum by 10 days after the testing lesion, indicating an outgrowth rate in excess of 0.64 mm/day. (b) Determination of the times at which labeled axons arrived at the optic tectum showed that the outgrowth rate after a testing lesion along was 0.40 mm/day whereas when the testing lesion was preceded by a conditioning lesion it was 0.74 mm/day. Thus, as a result of a conditioning lesion the initial delay was reduced by nearly half and the outgrowth rate was nearly doubled.

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PubMed1980

Early stages of axonal regeneration in the goldfish optic tract: an electron microscopic study.

Two hours after the goldfish optic tract was cut, the severed axons in the retinal stump of the tract showed ballooning of the axoplasm and myelin sheath in the region of the cut, with accumulation in the swollen axon of various organelles, including dense cored vesicles. By day 1 the myelin sheath had degenerated back to a node of Ranvier and the tip of the severed axon had formed a myelin-free terminal bulb with a well-organized core of 9-10 nm filaments. By 2 days, such terminal bulbs were often seen to be extended on a neck of cytoplasm a few micrometers in length, presumably indicating axonal outgrowth. In addition, occasional small bundles of axon sprouts were first seen at this time. The sprouts had a diameter of about 2 micrometers and contained a central core of 9-10 nm filaments surrounded by a mantle of cell organelles (smooth endoplasmic reticulum, mitochondria and diverse vesicles), with few if any microtubules. Sprouts within a bundle were separated by fairly uniform 10-15 nm spaces. Beginning at 3 days, significant numbers of microtubules appeared in the sprouts, and there was an increasing proportion of small diameter (greater than or equal to 0.3 micrometer) sprouts. Thus it was not until 3 days that the sprouts took on the appearance usually considered to be typical of regenerating axons. By 6 days a dense layer of glial cells or macrophages formed a cap over the cut surface of the tract. Penetrating this layer were bundles containing up to 20-30 axon sprouts and also single axons which may have been serving as 'pioneering' fibres to which later-emerging axons would attach. There was no evidence that the regenerating axons were guided by the glial cells. At 6 days astroglia began to separate individual axons within the bundles but oligodendrocytes were still inactive at this time.

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PubMed1978

Axonal transport of lipid in goldfish optic axons.

After injection of labeled glycerol, choline, or serine into the eye of goldfish, labeled lipids were axonally transported along the optic nerve to the optic tectum. Although the different precursors were presumably incorporated into somewhat different lipid populations, all three were approximately equally effective in labeling the lipids transported to the tectum, but the amount of transported material remaining in the nerve was different, being highest with choline and lowest with serine. The labeled lipids appeared in the tectum within 6 hr of the injection, indicating a fast rate of transport, but continued to accumulate over a period of 1--2 weeks, which presumably reflects the time course of their release from the cell body. Since there was a gradual increase in the proportion of labeled lipid in the tectum during this period, some other process in addition to fast axonal transport may have affected the distribution of the lipids along the optic axons. When [3H]choline was used as precursor, the transported material included a small amount of TCA-soluble material, which was probably mainly phosphorylcholine, with labeled acetylcholine appearing in only insignificant amounts. With serine, which gave rise to a large amount of axonally transported protein in addition to lipid, a late increase in the amount of labeled lipid in the tectum was seen, accompanied by a decrease in labeling of the protein fraction.

Acetylcholine↗
PubMed1977

Axonal regeneration in the rat sciatic nerve: effect of a conditioning lesion and of dbcAMP.

After the sciatic nerve had been crushed at the level of the mid-thigh, the rate of outgrowth of the regenerating axons was measured by using the pinch test to locate the leading sensory axons. This standard crush lesion ("testing" lesion) elicited axonal outgrowth at a rate of 4.3 +/- 0.1 mm/day, with an initial delay (before the axons entered the degenerating distal stump) of 1.6 days. A "conditioning" lesion (transection of the tibial nerve at the ankle), made two weeks before the testing lesion, caused an increase of 23% in the outgrowth rat (P less than 0.02), with no appreciable change in the initial delay. Dibutyryl cyclic AMP (dbcAMP) was found to have no effect on the rate of axonal outgrowth measured by the pinch test. Histological examination of the pinch-tested nerves showed that the drug also had no effect on the numbers of regenerating silver-stained axons or fluorescent noradrenergic axons seen at various levels distal to the testing lesion.

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