Requirement of a colchicine‐sensitive component of the cytoskeleton for acetylcholine receptor recovery

Hardwick, Jean C.; Parsons, Rodney L.

doi:10.1111/j.1476-5381.1995.tb13246.x

Cited by 9 publications

(3 citation statements)

References 28 publications

(67 reference statements)

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“…We found that m.e.p.c. amplitude recovery is also decreased in muscle preparations treated with colchicine (Hardwick & Parsons, 1995). In the absence of carbachol exposure, m.e.p.c.…”

Section: Discussionmentioning

confidence: 88%

Necessity of protein kinase C activity for maintenance of acetylcholine receptor function at snake twitch fibre endplates

Hardwick

Parsons

1995

British J Pharmacology

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1The extent of recovery of endplate sensitivity following a 5 or 10 min exposure to carbachol was determined from measurements of miniature endplate current (m.e.p.c.) 6 Only large amplitude ACh-activated channels (-50 pS) were recorded from fibres either in the presence of 50 liM sphingosine or from fibres chronically exposed to PMA. However, following recovery from a 10 min exposure to 540 tiM carbachol, both small conductance (-25 pS) and large conductance ACh-activated channels were recorded in both sphingosine-and phorbol-treated preparations. The conductance of these two populations of channels was virtually identical to those seen in staurosporinetreated fibres following carbachol exposure. 7 We conclude that protein kinase C is required for full recovery of AChR sensitivity following carbachol-induced receptor inactivation. Exposure to high concentrations of agonist for prolonged periods appears to result in the inactivation of a subpopulation of receptors. These receptors must be replaced or reactivated by a process involving protein kinase C. When this phosphorylation step is inhibited, the AChRs remain in an activatable form, but with a reduced conductance.

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“…We found that m.e.p.c. amplitude recovery is also decreased in muscle preparations treated with colchicine (Hardwick & Parsons, 1995). In the absence of carbachol exposure, m.e.p.c.…”

Section: Discussionmentioning

confidence: 88%

Necessity of protein kinase C activity for maintenance of acetylcholine receptor function at snake twitch fibre endplates

Hardwick

Parsons

1995

British J Pharmacology

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“…We have shown that this cell response to T3 required intact microtubules. Colchicine (lop5 to lop4 M ) was shown to interfere with elements of the cytoskeleton and to alter phosphorylation, which led to poor recovery of acetylcholine receptors in the membrane of snake costocutaneous muscle fibers (19). might interfere with the BAR intracellular trafficking was not confirmed by our study of BAR cell repartition.…”

Section: Discussionmentioning

confidence: 60%

Nongenomic Effect of Triiodothyronine on Cell Surface -Adrenoceptors in Cultured Embryonic Cardiac Myocytes

Vassy

Nicolas²,

Yin³

et al. 1997

Experimental Biology and Medicine

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We studied the time course of cell surface beta-adrenoceptors (BAR) in cardiomyocytes in response to a single triiodothyronine (T3) (10(-8) M) stimulation. An early first increase of BAR density was observed within 2 hr (+ 10% versus control cells, P < 0.05), and a plateau was maintained for 17-20 hr. This effect was followed by a much greater, late increase of BAR density, starting around 22 hr and lasting until 48 hr post T3 addition (+40% versus control cells; p < 0.05). Since reverse T3 studied in the same conditions had no effect in this system, we concluded that this T3 effect was specific. We hypothesized that the early response might be nongenomic because the early effect of T3 was still observed in the presence of cycloheximide (2 x 10(-5) M) whereas the late increase was totally suppressed by the drug. The early response to T3 required intact microtubules, since colchicine (2 x 10(-5) M) was able to block the increase in the cell surface BAR number, but it did not involve a change in BAR distribution between external and internal sites, as the external to total BAR ratio remained stable. The measurement of the rate of BAR disappearance from the cell surface allowed us to hypothesize that T3 induced a modification of the turnover in cell surface BAR.

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“…Disruption of microtubules by colchicin has been reported to increase conductance of Clchannels in skeletal muscle (21), and decreased conductance of snake twich fibre end plates (20). The mechanism of this functional change and the role of cytoskeletal structures in the transmembrane ion transport is not known.…”

Section: Applications Of Microtubule Inhibitors In Future Researchmentioning

confidence: 99%

The Most Important Microtubule Natural Inhibitors

Patočka

1999

Acta Med. (Hradec Kralove, Czech Repub.)

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Requirement of a colchicine‐sensitive component of the cytoskeleton for acetylcholine receptor recovery

Cited by 9 publications

References 28 publications

Necessity of protein kinase C activity for maintenance of acetylcholine receptor function at snake twitch fibre endplates

Necessity of protein kinase C activity for maintenance of acetylcholine receptor function at snake twitch fibre endplates

Nongenomic Effect of Triiodothyronine on Cell Surface -Adrenoceptors in Cultured Embryonic Cardiac Myocytes

The Most Important Microtubule Natural Inhibitors

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