Specificity in signaling

Dahlstrom, Kurt M.

doi:10.1349/ddlp.1952

Cited by 15 publications

(25 citation statements)

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“…As seen in Fig. 1 the levels remained around normal up to day 13 after the DISCUSSION There seems to be little doubt that the recovered noradrenaline, observed in the adrenergic axons of the sciatic nerve, is stored within amine storage granules, since tetrabenazine, a shortlasting blocker of the noradrenaline storage mechanism in the granules (Pletscher, Brossi & Gey, 1962;Haggendal, 1968), or a second injection of reserpine, can disperse the reappeared noradrenaline (Dahlstrom, 1967).…”

Section: Ligated Nervesmentioning

confidence: 88%

“…With the use of the histochemical fluorescence method of Hillarp, Falck and coworkers (for ref. and description see Corrodi & Jonsson, 1967) it has been demonstrated that the very first reappearance of noradrenaline after reserpine depletion occurs in the nerve cell body in a zone around the nucleus (Carlsson, Falck & Hillarp, 1962;Dahlstrom, Fuxe & Hillarp, 1965;Dahlstrom, 1967). At about 24 h after the reserpine treatment most nerve cell bodies have about normal levels of catecholamine-fluorescence, several, however, having supranormal amounts of catecholamine.…”

mentioning

confidence: 99%

“…The accumulation of noradrenaline above a constriction of peripheral adrenergic nerves has been studied both histochemically (Dahlstrom & Fuxe, 1964;Dahlstrom, 1965 ;Kapeller & Mayor, 1966) and quantitatively (Dahlstrom & Haggendal, 1966a, 1967. The rapidly occurring accumulation has been interpreted to arise from a piling up above the lesion of amine storage granules, synthesized in the nerve cell body and transported proximo-distally in the axon (Dahlstroni & Haggendal, 1966a, 1967Dahlstrom, 1966). The minimal effective rate of this transport and the average life-span of the granules in the terminals have for the rat been calculated to be about 5 mm/h, and several weeks, respectively (Dahlstrom & Haggendal, 1966a).…”

mentioning

confidence: 99%

“…The catecholamine-depleting effect of reserpine has been demonstrated to be due to a blockage of the catecholamine-storage mechanism in the amine storage granules of central and peripheral catecholamine-containing neurons (Carlsson, Hillarp & Waldeck, 1963 ;Carlsson, 1965). This blockage is long-lasting, and after high doses of reserpine it even seems to be irreversible, since recovery to normal levels takes several weeks in peripheral tissues and in the central nervous system (Dahlstrom & Haggendal, 1966b). With the use of the histochemical fluorescence method of Hillarp, Falck and coworkers (for ref.…”

mentioning

confidence: 99%

“…In the non-terminal axons noradrenaline-fluorescence has been demonstrated about 3 4 cm away from the perikarya as early as 15-18 h after the injection of the drug. At 30-36 h the recovery has proceeded further, permitting about "normal" amounts of noradrenaline to accumulate above a ligation made 1 h before death (Dahlstrom, 1967).…”

mentioning

confidence: 99%

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Recovery of noradrenaline in adrenergic axons of rat sciatic nerves after reserpine treatment

Dahlström

Häggendal

1969

Journal of Pharmacy and Pharmacology

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The recovery of noradrenaline in adrenergic axons of the rat sciatic nerve after a single dose of reserpine (10 mg/kg i.p.) has been studied in unligated nerves and nerves ligated for 6 h. In unligated nerves the recovery at 24 h after reserpine was about 14% of normal. The noradrenaline content then slowly rose to reach about normal concentrations 6–7 days after reserpine injection. In nerves ligated 6 h before death, about 8·0 ng of noradrenaline accumulated proximal to the ligation in normal animals. At 6 and 12 h after reserpine about 4% of normal amounts of noradrenaline were found. Thereafter the amount of accumulated noradrenaline rapidly increased to about normal levels on day 2 after reserpine. At this time the content in unligated nerves was only about 45% of normal unligated nerve. On days 3–5 after reserpine, supranormal accumulations of noradrenaline were found (statistically highly significant), having a maximum at day 4 of about 145% of normal. At this time the noradrenaline content in unligated nerve was only about 80% of normal. The results may indicate an increased synthesis and increased rate of downtransport of amine storage granules during the early recovery phase after reserpine. This phenomenon may be part of a feed‐back mechanism operating after depletion of the transmitter in the nerve terminals.

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Section: Ligated Nervesmentioning

confidence: 88%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Recovery of noradrenaline in adrenergic axons of rat sciatic nerves after reserpine treatment

Dahlström

Häggendal

1969

Journal of Pharmacy and Pharmacology

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Slow accumulation of choline acetyltransferase in crushed sciatic nerves of the rat

et al. 1973

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SUMMARYCholine Acetyltransferase (ChAc) activity has been estimated using a microradiochemical method in short segments of rat sciatic nerve at different times after crushing the nerve once or with a second crush 2 cm distal to the first. Above a single or proximal crush, the ChAc levels rose slowly in the 5 mm immediately above the crush to reach about 14 times control at 24 hr. Distal to a single crush and between two crushes no change was detected in ChAc-activity up to 18-24 hr. The results are discussed in relation to the rapid accumulation of acetylcholine (ACh) above a crush, and redistribution between two crushes which have previously been demonstrated in the same preparation. It is concluded that the rate of transport of ChAc is probably much slower than that of ACh, and that their mechanisms of transport are not the same.

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The effect of different types of axonal trauma on the synthesis and transport of amine storage granules in rat sciatic nerves

Karlström

Dahlström

1973

J. Neurobiol.

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SUMMARYIn crushed sciatic nerves of rat the accumulation of noradrenaline (NA), proximal to a ligation, proceeds approximately linearly up to 48 hr after operation, as was earlier reported. After 48 hr the NA in the proximal portion ceases to increase. The reasons for this arrest in NA-accumulation have been studied in the present investigation. Rat sciatic nerves were cut, ligated, or crushed at a low level 1-23 days prior to sacrifice. Two hours before death, the nerves were crushed at a level of about 2 cm proximal to the initial operations.Using a histochemical fluorescence method, the relative accumulation of NA above the second high crush was studied. In previously cut or ligated nerves, the NA accumulation observed was very low or zero by 7-9 days, and remained low during the observation period. In previously crushed nerves the NA accumulation was also decreased to rather low levels by 7-9 days. At 15 days, however, the NA accumulation was larger again, and histochemically normal accumulation was observed 17-23 days after the initial crush operation.The results may indicate that axonal trauma causes a depression in the synthesis and transport of amine storage granules in the adrenergic neurons. Furthermore, the degree and duration of depression seemed to vary with the type of trauma performed. Crushing the nerves, which leaves the connective tissues sheaths uninterrupted, facilitating thus regeneration, appeared to cause a less marked and shorter-lasting depression than cutting or ligating the nerves.

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Specificity in signaling

Cited by 15 publications

References 0 publications

Recovery of noradrenaline in adrenergic axons of rat sciatic nerves after reserpine treatment

Recovery of noradrenaline in adrenergic axons of rat sciatic nerves after reserpine treatment

Slow accumulation of choline acetyltransferase in crushed sciatic nerves of the rat

The effect of different types of axonal trauma on the synthesis and transport of amine storage granules in rat sciatic nerves

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