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Biomedical subjects

S L Handley

Publications and source records attributed to S L Handley.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects on the 5-hydroxytryptamine-induced head-twitch of drugs with selective actions on alpha1 and alpha2-adrenoceptors.

Effects of agents with selectivity for the alpha1- or alpha2-adrenoceptor have been investigated on the head twitches induced by 5-HT injected into the cerebral ventricles in the mouse. Alpha-adrenoceptor agonists inhibited head-twitching with a rank order of potency: guanabenz, clonidine, phenylephrine, methoxamine. The antagonists yohimbine and piperoxane, potentiated the head-twitch frequency. These results suggest that there may be an involvement of an alpha2-adrenoceptor. Small doses of phenylephrine (s.c.) potentiated the head-twitch. Methoxamine, injected intracerebroventricularly potentiated the head-twitch only when alpha2-adrenoceptors were blocked by a small dose of yohimbine. Prazosin and thymoxamine inhibited the head-twitch, suggesting that alpha1-adrenoceptors also modulate this phenomenon. Yohimbine and phenylephrine increased the incidence of spontaneous head-twitches. A tonic noradrenergic input may be necessary for the occurrence of the head-twitch induced by 5-HT.

Adrenergic alpha-Agonists↗
PubMed1980

Tryptophan, cortisol and puerperal mood.

Plasma cortisol, free and total tryptophan were determined in 71 subjects on 8 occasions between 36 weeks gestation and 6 weeks post-partum. Affect was measured by rating scales and clinical interview. Twenty-eight subjects were judged to have experienced post-partum 'blues'. Seasonal variation occurred in the incidence of 'blues' and in cortisol and free tryptophan levels. Puerperally-depressed mood was correlated with high cortisol at 38 weeks irrespective of season. Free tryptophan was reduced in 'blues' subjects but only at the time of year when free tryptophan was normally high. Total tryptophan was low antenatally; a rapid rise on days 1 and 2 post-partum was superimposed on a slower return to normal. This initial peak was clearly absent in 37 per cent of subjects. Its absence was significantly related to occurrence of post-partum 'blues' and of complaints of depression in the ensuing 6 months. This finding is discussed in relation to the possible occurrence of an occult disturbance of tryptophan handling in subjects susceptible to depression.

11-Hydroxycorticosteroids↗
PubMed1978

Influence of catecholamines on dexamphetamine-induced changes in locomotor activity.

In the mouse, central noradrenaline receptor stimulation by clonidine, or intracerebroventricular injection of noradrenaline or alpha-methylnoradrenaline, caused marked enhancement of the locomotor stimulant effects of dexamphetamine in doses that were without effect when given alone. A minimally locomotor-stimulant dose of apomorphine reduced the effect of dexamphetamine. Pimozide and phenoxybenzamine each virtually abolished locomotor stimulation after dexamphetamine, while FLA63 caused significant reduction. Phenoxybenzamine also abolished the enhancement by clonidine. The intensity of the dexamphetamine effect was dose-related, while in the case of apomorphine the duration rather than the intensity was related to the dose administered. Clonidine potentiated apomorphine locomotor stimulation; following this drug combination, the nature of the movements more closely resembled those seen after dexamphetamine. The results suggest the involvement of both noradrenaline and dopamine in the dexamphetamine response.

Animals↗
PubMed1978

On the mechanism of amphetamine-induced behavioural changes in the mouse. II. Effects of agents stimulating noradrenergic receptors.

The effects of three "noradrenergic stimulants", norepinephrine and alpha-methylnorepinephrine administered into the cerebral ventricles and of parenterally injected clonidine, have been observed on 18 separate items of dexamphetamine-induced behaviour in the mouse. Stereotyped behaviour was depressed by the "noradreneric stimulants" except for compulsive gnawing, which was markedly enhanced. Aspects of locomotor activity were enhanced except when compulsive gnawing was strong, at which time they were suppressed. Elements of heightened arousal were enhanced. It is suggested that these may be a positive noradrenergic component in the genesis of compulsive gnawing, locomotor activity and heightened arousal. The dominance of compulsive gnawing over certain other dexamphetamine-induced behaviours may lead indirectly to the suppressor effects of the noradrenergic stimulants on these behaviours.

Animals↗
PubMed1978

On the mechanism of amphetamine-induced behavioural changes in the mouse. I. An observational analysis of dexamphetamine.

The effects of dexamphetamine have been studied on 18 separate items of observed behaviour in the mouse. The intensity of dexamphetamine action was assessed by scoring differences in behaviour from control (vehicle injected) mice and by measuring ED50 values for dexamphetamine to cause detectable differences from controls for each individual item. The experiments were performed blind in that the observer had no knowledge of the dose of dexamphetamine given to the test group or even whether these had received dexamphetamine at all. The results show a clear division of behavioural items into two groups according to ED50 values; group 1 with ED50 values greater than 15 mg/kg was associated with falls in whole-brain norepinephrine. Group 1 contained elements of increased motor activity, the stereotypies (except compulsive gnawing) and certain aspects of increased alertness. Group 2 consisted of compulsive gnawing and the remaining aspects of increased alertness. Compulsive gnawing was negatively correlated in intensity with the majority of other behavioural items but no other evidence was found for a smooth replacement of one type of activity by another with increasing dose.

Animals↗
PubMed1978

On the mechanism of amphetamine-induced behavioural changes in the mouse. III. Effects of apomorphine and Fla 63.

The effects on 18 items of dexamphetamine-induced behaviour of increasing the ratio of dopaminergic to noradrenergic activity have been investigated in mice. The dopamine-beta-oxidase inhibitor bis-(4-methyl-1-homopiperazinyl-thiocarbonyl)-disulfide (Fla 63) produced varying degrees of reduction in the intensity of all items except raised body position, which was enhanced. Apomorphine alone induced compulsive gnawing and increased locomotor activity but produced long-lasting suppression of these and certain other items induced by dexamphetamine. Vocalisation, touch and startle responses and stereotyped sniffing were, however, unaffected while compulsive grooming and elevated body position were enhanced. The results are discussed in the context of the relative contribution of noradrenergic and dopaminergic mechanisms to the behavioural effects of dexamphetamine.

Animals↗
PubMed1977

Mood changes in puerperium, and plasma tryptophan and cortisol concentrations.

Eighteen women aged 18-31 years were studied daily during the second to fifth postpartum days to assess mood changes and plasma tryptophan and cortisol concentrations. Psychiatric rating scales, clinical interviews, and published biochemical methods were used. Over the period plasma free tryptophan concentrations tended to rise and plasma cortisol concentrations to decline. There was a positive correlation between plasma free tryptophan concentrations and mood state.

Adolescent↗
PubMed1977

The interaction of some kynurenine pathway metabolites with 5-hydroxytryptophan and 5-hydroxytryptamine.

The kynurenine pathway metabolites kynurenine, 3-hydroxykynurenine and xanthurenic acid have been tested against 5-hydroxytryptamine (5-HT) and 5-hydroxytryptophan (5-HTP)-induced head twitches in the mouse in a dose-range of 0.5--5.0 mg/kg. Kynurenine and 3-hydroxykynurenine were highly active. Low doses caused marked potentiation of the twitch response to both 5-HT and 5-HTP with increased toxicity of 5-HT. High doses caused antagonism of both responses. Xanthurenic acid was inactive over the same dose range. The effects of kynurenine could not be duplicated in the guinea-pig ileum. The relevance of these results to the involvement of kynurenine pathway metabolites in depressive illness is discussed.

5-Hydroxytryptophan↗