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Biomedical subjects

T W Stone

Publications and source records attributed to T W Stone.

At least 289 records · Page 16Linked to original sources
PubMed1975

The mechanism of action of amantadine in Parkinsonism: a review.

Studies of the mechanism of action of amantadine are reviewed. Data from pharmacological, behavioural and neurochemical experiments seem to indicate that the most likely effects of amantadine to be important in the alleviation of Parkinsonian symptoms are an indirect dopamine-releasing action and a direct stimulation of dopamine receptors. These effects may have a relative importance of approximately 4 : 1. Evidence favouring inhibition of dopamine uptake does exist, but the balance of opinion seems to be that this action is far too weak to contribute substantially to amantadine's action in vivo.

Amantadine↗
PubMed1974

On the mechanism of action of clonidine: effects on single central neurones.

1 Noradrenaline and clonidine were applied by microiontophoresis to single neurones in the cerebral cortex and medullary reticular formation of anaesthetized rats.2 Of a total of 247 neurones studied, 79% of medullary units and 60% of cortical units responded in the same manner to both noradrenaline and clonidine. The usual response was a depression of neuronal firing rate.3 It proved possible to antagonize some responses to both substances by the microiontophoresis of bulbocapnine, whilst leaving unaffected similar responses to 5-hydroxytryptamine.4 On 13% of the cells, clonidine produced an increase of firing rate. This effect could not be attributed to a post-synaptic antagonism of tonically released endogenous noradrenaline, but may indicate a presynaptic action of clonidine, reducing noradrenaline release.5 These observations are thought to support the idea that clonidine may have an agonist action on noradrenaline receptors in the brain.

Animals↗
PubMed1973

Cortical pyramidal tract interneurones and their sensitivity to L-glutamic acid.

1. Pyramidal tract interneurones, defined as neurones which are activated synaptically as a result of pyramidal tract stimulation, have been identified in the rat cerebral cortex. The number of evoked spikes depended upon stimulus strength, and stimulation in a specific thalamic nucleus produced a burst of activity lasting for up to 1 sec.2. These cells are readily excited by a brief (50 msec) pulse of glutamate applied by micro-iontophoresis. Other, unidentified cells are not so responsive.3. Synaptically evoked spikes resulting from pyramidal tract stimulation can be blocked by the iontophoretic and I.P. administration of substances shown to antagonize glutamate excitation of cells.4. The results support suggestions that glutamic acid is a neurotransmitter in the cerebral cortex. The evidence presented further indicates that glutamic acid could be the transmitter released by the pyramidal tract.

Acetylcholine↗