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Biomedical subjects

W G McLean

Publications and source records attributed to W G McLean.

At least 73 records · Page 4Linked to original sources
PubMed1982

Axonal transport of protein in motor fibres of experimentally diabetic rats--fast anterograde transport.

Fast axonal transport of radiolabelled proteins in motor fibres of rat sciatic nerves was studied after 14 days of streptozotocin-induced diabetes. The rate of fast transport as measured at two time intervals after application of [3H]leucine to the motor neurone cell bodies in the spinal cord was reduced by 21% in diabetic rats. There was no significant change in the time between injection of isotope and the start of fast transport. The amount of axonal transport of radiolabelled proteins as measured by accumulation of proteins proximal to a ligation on the sciatic nerve was also unchanged. The reduction in fast transport rate in the diabetic rats was eliminated by maintenance of normal blood glucose levels in twice daily insulin administration. The results are discussed with regard to the known effects of experimental diabetes on axonal transport in sensory fibres and to the role of fast axonal transport in peripheral neuropathies in general.

Animals↗
PubMed1982

The turnover of acetylcholine in ligated sciatic nerves of the rat.

The accumulation of acetylcholine (ACh) and choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities proximal to a crush on rat sciatic nerves was investigated after superfusion of the nerves in situ with or without inhibitors of ACh synthesis and/or AChE. 9 h after crushing of nerves, the ACh-content of the 5 mm segment of nerve immediately proximal to the crush was increased from 37 +/- 5 to 80 +/- 4 pmol (mean +/- SE), while ChAT-activity was increased to 112 +/- 10% and AChE-activity to 198 +/- 19% over that in non-ligated nerves. Superfusion of the nerves for 8 h with Krebs' bicarbonate medium had no effect on enzyme accumulations, but reduced the ACh content to 59 +/- 4 pmol. The presence of hemicholinium 3 (HC-3) (2 X 10(-5) M) in the superfusion medium reduced the ACh content markedly (to 17 +/- 2 pmol), but had no effect on enzyme accumulations at the crush. Adding eserine (10(-5) M) or soman (10(-6) M) to the superfusion medium increased ACh content to 133 +/- 8 pmol and 101 +/- 8 pmol, respectively, and markedly reduced AChE-activity; ChAT activity was not effected. Superfusion with a combination of HC-3 and eserine caused a marked reduction in ACh content compared with eserine alone; the effect was less with soman. The results are consistent with the view that the ACh which accumulates proximal to crush exists in a protective organelle, but that there is a continuous turnover of ACh due to leakage of ACh from the organelle, both during axonal transport and after accumulation.

Acetylcholine↗
PubMed1980

Blockage of axonal transport induced by acute, graded compression of the rabbit vagus nerve.

Rapid axonal transport in rabbit vagus nerve was studied during and after graded nerve compression. Proteins of the rapid axonal transport were labelled by micro-injection of 3H-leucine into the nodose ganglion and the cervical vagus nerve was subjected to graded compression by a small "mini-cuff" applied directly to the exposed nerve trunk. The results showed that even slight trauma to the nerve, in this model represented by a pressure at 50 mmHg applied for two hours, may induce accumulation of axonally transported proteins at the level of compression. This transport block was, however, reversible within one day. 200 mmHg and 400 mmHg applied for two hours similarly induced a block of axonal transport persisting up to at least one and three days respectively after the compression. Time for recovery of normal transport was correlated with the magnitude of the pressure applied to the nerve. The results indicate that axons may survive, that is not undergo Wallerian degeneration, after blockage of rapid axonal transport persisting at least one day after the compression trauma.

Animals↗
PubMed1976

Action of chloroquine on in vivo RNA and protein biosynthesis in the retina and the optic pathway of the rabbit.

The in vivo action of chloroquine on RNA and protein metabolism in the optic pathway of the albino or pigmented rabbit was examined. To study the acute effects, chloroquine in a dose of 500 mug was injected into the vitreous body of one eye. The following day the animals were injected into both eyes with [3H]uridine or [3H]leucine. At various time intervals following the isotope injections the retinal synthesis and the axonal transport of labelled RNA or protein was studied. The results showed no significant difference between the drug-treated and the control side with respect to synthesis and axonal transport of RNA or protein. Nor was any selective effect noticed on the synthesis of different RNA fractions from the retina. In long-term experiments chloroqune (100 mg/kg body weight) was administered via their drinking water 3 days a week for a period of 6 or 8 months. Following an intraocular injection of [3H]leucine no significant change in rapid axonal transport could be found in those chronically treated rabbits.

Animals↗
PubMed1975

Slow axonal transport or proteins; blockade by interruption of contact between cell body and axon.

The influence of ligation and colchicine treatment on the axonal transport of slowly migrating [3H]leucine-labelled proteins was studied in the vagus nerve of the rabbit. Two days after [3H]leucine labelling of the dorsal motor nucleus of the vagus nerve, ligation or local application of 60 mM colchicine immediately blocked the further progression of slowly migrating proteins distal to the site of treatment. Application of 50-100 mug colchicine to the nerve cell bodies 2 days after labelling blocked the transport of slowly migrating proteins within the next 24 h. It is suggested that contact between nerve cell body and the axon is necessary for the maintenance of the slow transport of proteins in these nerves.

Animals↗
PubMed1974

The effect of nerve stimulation on the axonal transport of noradrenaline and dopamine-beta-hydroxylase.

1 A method for stimulating the lumbar sympathetic outflow from the spinal cord of the rat is described which does not require artificial respiration of the animal.2 In some, but not all experiments continuous stimulation at 2 Hz or intermittently at 10 Hz accelerated the rate at which noradrenaline and dopamine-beta-hydroxylase accumulated central to a ligature on the sciatic nerve by approximately 40%.3 It is concluded that, although nervous activity is not necessary for axonal transport of transmitter granules in sympathetic neurones, intense nervous activity may accelerate the rate of granule transport.

Animals↗