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Biomedical subjects

P Slater

Publications and source records attributed to P Slater.

At least 127 records · Page 7Linked to original sources
PubMed1979

The effect of morphine and some other narcotic analgesics on brain tryptophan concentrations.

An acute dose of morphine increased brain tryptophan in mice. This effect was not prevented by naloxone nor was it produced by other narcotic analgesics. Dextrorphan, but not levorphanol, had a similar effect to morphine. A large dose of tryptophan had no effect on the antinociceptive action of morphine in mice. Morphine increased brain tryptophan in rats. This effect was prevented by naloxone. A large dose of tryptophan antagonised the antinociceptive action of morphine in the rat.

Analgesics, Opioid↗
PubMed1979

Repertory grid and biochemical characterization of depression: a comparison of case reports.

Two cases of depression are presented: One which responded to psychotherapy and the other which responded to medication. These cases were evaluated by repertory grid analysis and by biochemical analysis. These results serve as the basis for a discussion of the use of such analysis as predictors of response in depression to psychotherapy or medication.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

The effect of 6-hydroxydopamine on the antinociceptive action of morphine.

The role of brain catecholamines in the antinociceptive action of morphine was investigated. Intraventricular 6-hydroxydopamine which depleted brain noradrenaline in the rat had no effect on morphine's antinociceptive action but combined treatment with pargyline and 6-hydroxydopamine to further deplete brain dopamine potentiated morphine's action. It was also shown that when dopamine receptors were blocked, the antinociceptive action of morphine was potentiated whereas alpha- and beta-adrenoceptor antagonists had no effect. 6-Hydroxydopamine had two effects in mice tested on the hot-plate. It produced a hyperalgesia and antagonized the antinociceptive action of morphine. This antagonism of morphine appeared to be the result of the depletion of noradrenaline rather than dopamine. Intraventricular injection of both catecholamines restored the antinociceptive action of morphine in 6-hydroxydopamine-treated mice but dopamine was ineffective in the presence of a dopamine beta-hydroxylase inhibitor. It is suggested that the antinociceptive action of morphine is expressed by noradrenergic neurones in the mouse and by both noradrenergic and dopaminergic neurones in the rat.

Analgesics↗
PubMed1978

The effects of a permanent and selective depletion of brain catecholamines on the antinociceptive action of morphine.

6-Hydroxydopamine was given to newborn mice. After 60 days their brains were deficient in noradrenaline and dopamine while morphine's antinociceptive action was reduced. 6-Hydroxydopa was administered to adult mice. This depleted brain noradrenaline and reduced morphine's antinociceptive action. Newborn rats received 6-hydroxydopa. After 60 days morphine's antinociceptive action was potentiated, brain noradrenaline was reduced while dopamine had increased. Adult rats were treated with 6-hydroxydopa. This reduced brain noradrenaline but did not affect morphine's antinociceptive action. Guanethidine, which depletes noradrenaline in the peripheral nervous sytem, was given to newborn animals of both species. It had no effect on morphine's antinociceptive action. It is concluded that in the mouse the antinociceptive action of morphine relies in part on normal brain noradrenaline function and dopamine is not directly involved. In the rat morphine's action is affected by neurotoxic drugs which alter brain dopamine function.

Analgesics↗
PubMed1978

Effect of tolerance to morphine, ethanol and barbiturate on amphetamine circling in rats with a striatal dopamine lesion.

The (+)-amphetamine circling rate of rats with unilateral 6-OHDA lesions in the striatum was recorded. Morphine tablets were implanted subcutaneously for chronic treatment. In the morphine-dependent animal the circling rate to amphetamine given 4 days after morphine was first implanted was depressed but after withdrawal with naloxone a day later the rate increased, returning to normal after 21 days. Barbiturate physical dependence was induced by adding increasing amounts of barbitone to the drinking water of lesioned rats over four weeks after which the amphetamine circling response was depressed and remained so after the barbituate was withdrawn. Ethanol tolerance was induced by adding ethanol to the drinking water of lesioned rats for four weeks. Neither the induction of tolerance over this period nor ethanol withdrawal had any effect on the circling response to amphetamine. The change in the response of striatal dopamine neurons to amphetamine that occurs after chronic morphine treatment, cannot be produced by chronic treatment with either barbitone or ethanol. The neurochemical bases of barbiturate and ethanol tolerance are different from morphine tolerance.

Animals↗
PubMed1978

The Middlesex Hospital Questionnaire: a validity study.

The MHQ is a brief self-rating inventory purporting to measure aspects of six distinct categories of psychoneurosis and affective status. It has been found to be a reliable instrument and also valid as a profile measure. Two individual scales have also previously been explored in respect of validity. The present report describes a further attempt to examine the validity of individual scales in relation to pertinent single clinical diagnostic entities in a study involving 800 patients. The phobic and obsessional scales are found to be particularly accurate and differentiating in this respect. Patients variously diagnosed as suffering from anxiety states, depressive states and personality disorder tend to score very highly on several scales. The instrument serves overall to distinguish satisfactorily between such populations and others suffering from schizophrenia and anorexia nervosa. It also markedly differentiates them from 'normal' populations.

Anorexia Nervosa↗
PubMed1977

The efferent projections of the nucleus accumbens in the rat.

The efferent projections of the nucleus accumbens have been examined in the rat. This has been achieved by mapping the distribution of degenerating axons and terminals following the placement of small electrolytic lesions within the accumbens. Quantitatively, the majority of accumbens efferent fibres appear to terminate in the diencephalon, while there are also projections to cortical and brain stem structures. The evidence suggests that the nucleus accumbens sends efferent fibres to the cingulum, lateral hypothalamus, globus pallidus, thalamus (including the reuniens, gelatinosus, parataenial, medial and anteromedial nuclei) and the substantia nigra.

Animals↗
PubMed1977

The neurological basis of motor asymmetry following unilateral 6-hydroxydopamine brain lesions in the rat: the effect of motor decortication.

The role of the motor cortex in the mediation of asymmetric movement after unilateral 6-hydroxydopamine (6-OHDA) brain lesions has been examined in the rat. The effect of unilateral and bilateral sensorimotor decortication upon spontaneous and drug (apomorphine and amphetamine)-induced motor asymmetry has been studied following unilateral injection of 6-OHDA into the lateral hypothalamus. Both bilateral decortication and unilateral decortication on the side of the 6-OHDA lesion caused a transient reversal of the spontaneous motor asymmetry normally seen in 6-OHDA lesioned animals. Neither unilateral nor bilateral sensorimotor decortication abolished drug-induced turning behaviour. It is postulated that subcortical basal ganglia efferent pathways may be involved in the mediation of motor asymmetry after unilateral 6-OHDA lesions of the nigrostriatal dopaminergic projection.

Amphetamine↗