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Biomedical subjects

P Willner

Publications and source records attributed to P Willner.

At least 109 records · Page 6Linked to original sources
PubMed1986

Brief exposure to uncontrollable but not to controllable noise biases the retrieval of information from memory.

Female volunteers learned two lists containing a mixture of positive and negative trait words. Both lists were learned in a neutral mood. The first list was recalled in a neutral mood, and the second following a five-minute exposure to a tape of 'meaningful' noises, designed to simulate a busy office environment. Exposure to loud, uncontrollable noise caused a substantial increase in the proportion of negative trait words recalled from the second list, and also a worsening of mood, particularly an increase in tension. These effects were not seen in subjects exposed to controllable loud noise or to uncontrollable quiet noise. The memory bias following uncontrollable loud noise is qualitatively similar to that found in clinically depressed patients or following depressive mood induction procedures.

Adult↗
PubMed1985

Antidepressants and serotonergic neurotransmission: an integrative review.

The effects of acute and chronic antidepressant treatment on various aspects of 5-HT neurotransmission are reviewed, in order to assess the net effect of antidepressants on transmission across 5-HT synapses. Events considered include presynaptic effects of antidepressants (on autoreceptor function, uptake and turnover) and effects on postsynaptic receptor function (assessed by electrophysiological, neuroendocrine, behavioural, and receptor binding methods). Acute antidepressant treatment has variable effects: transmission may be enhanced, unchanged or reduced, depending mainly upon the relative contributions of 5-HT uptake blockade and 5-HT receptor antagonism. However, on chronic administration, most antidepressants appear to enhance 5-HT transmission. This effect is clearest in the case of ECS, which has little effect on 5-HT turnover, but reduces uptake and increases postsynaptic receptor function. MAOIs may be an exception: there is little evidence that MAOIs enhance 5-HT transmission following chronic treatment. Most other antidepressant drugs, including some which are powerful receptor antagonists on acute administration, reduce 5-HT receptor function briefly, but enhance receptor function if several hours elapse between the final injection and testing. Zimelidine has little effect on postsynaptic receptor function, but enhances 5-HT transmission by its powerful blockade of 5-HT uptake. Chronic treatment with antidepressant drugs has usually been found to reduce binding to 5-HT2 receptors; it is difficult to reconcile these observations with the functional studies. In general, with the possible exception of MAOIs, chronic administration of antidepressants may enhance 5-HT transmission by both pre- and post-synaptic effects, and the relative contributions vary. This conclusion supports the classical "indoleamine hypothesis of depression" rather than the more recent "hypersensitive serotonin receptor" theory.

Animals↗
PubMed1985

Apomorphine anorexia: a behavioural and neuropharmacological analysis.

Anorectic effects of apomorphine were studied in a microstructural analysis paradigm. Low doses of apomorphine (less than 0.1 mg/kg SC) reduced food intake, by reducing both the rate of eating and eating time. The neuroleptics haloperidol and thioridazine blocked the effect of apomorphine on eating time, but not on eating rate. Anorectic effects elicited by apomorphine administration to the ventral tegmental area and, to a lesser extent, the substantia nigra were mediated by a selective reduction of eating time. Effects of apomorphine on eating time appear to result from an action at presynaptic dopamine receptors; the mechanism of the effect of apomorphine on eating rate is unclear.

Animals↗
PubMed1985

Central and peripheral contributions to the enhancement of amphetamine anorexia by desmethylimipramine (DMI).

Intrahypothalamic administration of amphetamine to rats increased food intake, but pre-treatment with the alpha-receptor antagonist phentolamine unmasked an anorexic effect commensurate with that seen after peripheral amphetamine administration. Pretreatment with systemic DMI increased anorexia after peripheral or central amphetamine administration, but the enhancement of centrally-induced anorexia was small. It is concluded that enhancement of the anorexic effect of peripherally administered amphetamine by DMI is primarily a peripheral phenomenon, with interactions within the central nervous system making a relatively minor contribution.

Amphetamine↗
PubMed1984

Changes in amphetamine-induced anorexia and stereotypy during chronic treatment with antidepressant drugs.

Amphetamine-induced anorexia and stereotyped behaviour were studied in rats, following pretreatment with the antidepressants DMI, inprindole and mianserin. A complex drug-dependent and dose-dependent pattern of results was obtained. Acute pretreatment with DMI and iprindole enhanced amphetamine anorexia and stereotypy; at high doses only, the enhancement of anorexia disappeared during chronic treatment. Mianserin had no effects acutely, but chronic treatment with high doses attenuated anorexia and enhanced stereotypy. High doses of all three drugs attenuated anorexia and enhanced stereotypy during withdrawal. The most parsimonious account of these results is that the acute affects of DMI and iprindole are artefactual, and that chronic administration of all three antidepressants increased dopaminergic function and decreased beta-adrenergic function.

Animals↗
PubMed1984

The validity of animal models of depression.

Eighteen animal models of depression are reviewed in relation to three sets of validating criteria. Of the 18 models, five could only be assessed for predictive validity, seven could be assessed for predictive and face validity, and six could potentially have predictive, face and construct validity. Some traditional models (reserpine reversal, amphetamine potentiation) are rejected as invalid; the models with the highest overall validity are the intracranial self-stimulation, chronic stress and learned helplessness models in rats, and the primate separation model.

5-Hydroxytryptophan↗
PubMed1984

The ability of antidepressant drugs to desensitize beta-receptors is inversely correlated with their clinical potency.

The relative clinical potencies of a range of antidepressant drugs and their relative ability to desensitize beta-adrenergic receptors were compiled from published sources and found to be inversely correlated. This findings strongly suggest that desensitization of beta-receptors is not responsible for the clinical effects of antidepressants. This conclusion is supported by a discussion of the effects of steroid hormones on beta-receptors.

Antidepressive Agents↗
PubMed1984

Cognitive functioning in depression: a review of theory and research.

This paper reviews recent research into cognitive functioning in depression, with particular reference to the theories of Lewinsohn, Beck, Seligman and Klein. The major cognitive changes in depression are a decrease in the ability to maintain concentration and effort, and an increase in the relative salience of aversive events and memories, with a corresponding decrease in the salience of pleasant events. There is as yet little evidence to support the view that depressions arise out of pre-existing depressive attitudes. Attention is drawn to the heterogeneity of depressive disorders, and the significance of the endogenous/non-endogenous distinction is discussed.

Bipolar Disorder↗
PubMed1983

Dopamine and depression: a review of recent evidence. I. Empirical studies.

This paper reviews evidence from human, predominantly clinical, studies, relevant to the hypothesis that depression involves reduced levels of dopamine (DA) function. With the exception of Parkinson's disease, there is little evidence that treatments which decrease DA function are potent inducers of depression, but it is argued that such a relationship might not necessarily be expected. There is good evidence that the nigro-striatal DA system is underactive in retarded depressions, and some evidence that DA agonists are therapeutically effective in these cases. It remains unclear whether changes in DA function are primary or secondary.

Amphetamine↗
PubMed1983

Dopamine and depression: a review of recent evidence. II. Theoretical approaches.

This paper discusses 3 behavioural approaches to depression, 'learned helplessness', reward system dysfunction and reduced responsiveness to the environment, and the role of dopamine (DA) in their related animal models. The meso-limbic and nigrostriatal DA system appears to be related primarily to responsiveness to the environment. This conclusion is discussed in relation to the clinical symptomatology of depression.

Animals↗
PubMed1983

Dopamine and depression: a review of recent evidence. III. The effects of antidepressant treatments.

This paper reviews the effects of antidepressants on brain dopamine (DA) function in people and animals. Acute antidepressant treatments have no consistent effect on DA. Chronic treatment does not appear to change DA synthesis or turnover, or to affect post-synaptic DA receptors. However, there is considerable evidence of increased DA function following chronic antidepressant treatments; the site of these effects is at present unclear, but appears to be beyond the DA receptors. There is also evidence for decreased sensitivity of pre-synaptic DA autoreceptors, though this effect is less well established.

Amphetamine↗
PubMed1982

Evidence suggesting that DMI-induced resistance to extinction is not mediated by the dorsal noradrenergic bundle.

Rats were trained to press a lever for food rewards, then given a 5 week break, followed by a single extinction session. Animals which received 14 daily desmethylimipramine (DMI) injections, ending 4 days before the extinction session, showed resistance to extinction; no effect was seen in animals which received DMI during acquisition. The opposite pattern of results would be predicted if the effect were mediated by changes in the efficacy of the dorsal noradrenergic bundle.

Animals↗
PubMed1982

Microstructural analysis of the involvement of beta-receptors in amphetamine anorexia.

Rats were trained to take food by pushing the door of the pellet dispenser in an operant chamber. Log survivor analysis of the inter-response time frequency distribution was used to determine whether or not an animal was eating, at any time during a thirty minute session. This information was used to compute eating time, eating rate, and the mean length of bouts of eating and gaps between eating bouts. Video-recordings confirmed that the method discriminated eating from not eating with an accuracy of approximately ninety percent. Amphetamine (0.5 mg/kg) significantly reduced total food intake and eating time, and increased gap length; propranolol (5 mg/kg) significantly increased eating time and bout length. Following propranolol pretreatment, amphetamine significantly reduced eating time and bout length but also significantly increased eating rate; as a result there was no significant decrease in total food intake. The possible mediation of these effects by beta-adrenergic and dopaminergic systems is discussed.

Amphetamine↗
PubMed1981

Behavioural changes during withdrawal from desmethylimipramine (DMI). I. Interactions with amphetamine.

Amphetamine anorexia in rats was potentiated by acute pretreatment with the tricyclic antidepressant desmethylimipramine (DMI), but was not significantly different from controls following chronic DMI pretreatment. During withdrawal from DMI, amphetamine anorexia was attenuated after 2 weeks or 2 months pretreatment, but not after 1 week of treatment. The locomotor stimulant and stereotypy inducing effects of amphetamine were slightly enhanced during withdrawal from chronic DMI. The results are discussed in relation to known neurochemical actions of DMI.

Animals↗
PubMed1981

Behavioural changes during withdrawal from desmethylimipramine (DMI). II. Increased resistance to extinction.

Rats withdrawn from chronic treatment with the tricyclic antidepressant desmethylimipramine (DMI) showed increased resistance to extinction in a runway and in continuously reinforced lever pressing. Changes were not seen in animals maintained on DMI. In acquisition, in the runway, there were no significant differences between groups; in the Skinner box, animals maintained on DMI performed worse than controls, but withdrawn animals recovered to control levels of performance. It is suggested that the effect on extinction may be mediated by a decrease in the efficacy of the dorsal noradrenaline bundle, which develops during chronic DMI treatment, but is masked by the presence of DMI. The implications of the conclusion for the " revised catecholamine hypothesis of depression" are discussed.

Animals↗
PubMed1981

Subchronic treatment with the tricyclic antidepressant DMI increases isolation-induced fighting in rats.

Male rats treated with desmethylimipramine (DMI) (20 mg/kg for 7 days) were more likely than controls to attack an intruder rat placed in their home cage; they were also more likely to submit when attacked by the intruder. These behavioural changes were not seen at lower doses of DMI. Similar results were obtained in experiments in which is drugged animal and a control were placed together in a "neutral" cage; in this paradigm it was also found that lower doses of DMI were effective, provided that either the period of drug treatment was increased, or a delay of 3-4 days after withdrawal of DMI preceded behavioural testing. A dose dependent resistance to handling developed during drug treatment; drugged animals also showed weight loss and decreased open-field activity. In previous studies, acute treatment with tricyclic antidepressants has not been found to increase fighting; the present results underline the importance of chronic drug studies.

Aggression↗