PubMed Health⌕ Search

Biomedical subjects

S C Dilsaver

Publications and source records attributed to S C Dilsaver.

At least 109 records · Page 6Linked to original sources
PubMed1988

Bright artificial light produces subsensitivity to clonidine.

The authors used a thermoregulation paradigm to test the hypothesis that chronic treatment with bright artificial light produces subsensitivity to the hypothermic effects of clonidine, an alpha 2-agonist. One week of treatment produced blunting of the hypothermic response to clonidine (p less than 0.00001). These findings are consistent with previous reports that somatic treatments for depression produce subsensitivity of the alpha 2-receptor.

Animals↗
PubMed1988

Bright artificial light produces subsensitivity to nicotine.

Bright artificial light is a treatment for seasonal depression. Eleven (11) rats were exposed to bright artificial light (11,500 lux) for two consecutive weeks. The thermic response to nicotine was measured prior to light exposure and after one and two weeks of treatment. The thermic response to nicotine at baseline was -1.69 +/- 0.25 degrees C (mean +/- SEM). The thermic response to nicotine was -0.66 +/- 0.12 degrees C (p less than 0.002) after one and +0.31 +/- 0.14 degrees C (p less than 0.000025) after two weeks of light exposure. The change in temperature was different between weeks one and two (p less than 0.000025). The exposure of animals to constant light at an intensity of 300 lux did not blunt the hypothermic response to nicotine. These findings suggest that bright artificial light, like other antidepressant treatments, produces subsensitivity of a nicotinic mechanism involved in the regulation of core temperature.

Animals↗
PubMed1988

Antipsychotic withdrawal phenomena in the medical-surgical setting.

The literature describing nondyskinetic antipsychotic withdrawal symptoms is reviewed. The withdrawal of antipsychotic agents can result in nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness, and insomnia. However, the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.

Antidepressive Agents↗
PubMed1988

Amitriptyline-induced supersensitivity of a central muscarinic mechanism: lithium blocks amitriptyline-induced supersensitivity.

Chronic treatment with amitriptyline produces dose-dependent super-sensitivity of a central muscarinic cholinergic mechanism involved in the regulation of core body temperature. The authors demonstrated that chronic treatment with lithium prevents the induction of this response. The potential clinical and theoretical significance of this finding is set forth.

Amitriptyline↗
PubMed1988

Temperature as a dependent variable in the study of cholinergic mechanisms.

1. Change in core temperature over time can be used as a dependent variable when studying the effects of manipulations on neurotransmitter systems. This article focuses on the measurement of core temperature as a strategy for detecting changes in the status of cholinergic systems. 2. Cholinergic neurons participate in the process of thermoregulation and interventions affecting them alter the thermal response to cholinomimetics. For example, chronic treatment with amitriptyline, chronic swim stress and inescapable footshock supersensitize rats to the hypothermic effects of oxotremorine. 3. This is consistent with the hypothesis that the pathophysiologies of tricyclic antidepressant withdrawal phenomena and stress involve supersensitivity of muscarinic mechanisms. 4. Uses of thermoregulation paradigms for investigating the actions of lithium ion, electroconvulsive shock and substances of abuse on muscarinic mechanisms are discussed. Applications to problems in the arena of clinical research are highlighted.

Animals↗
PubMed1988

Effects of stress on muscarinic mechanisms.

Hyperactivity of muscarinic mechanisms may be involved in the patho-physiology of depressive disorders and stress. The literature emphasizes the impact of stress on aminergic networks and muscarinic mechanisms are generally not accorded a significant role in the neurobiology of stress. However, experiments in man and animals indicate that acute and chronic stress activate central muscarinic mechanisms. The literature reporting these results is reviewed.

Animals↗
PubMed1988

Antipsychotic withdrawal symptoms: phenomenology and pathophysiology.

The authors review the literature discribing non-dyskinetic antipsychotic withdrawal phenomena. Withdrawal of these agents can cause nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgia, paresthesia, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness and insomnia, but the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.

Antipsychotic Agents↗
PubMed1988

Monoamine oxidase inhibitor withdrawal phenomena: symptoms and pathophysiology.

The author reviews the literature reporting the untoward effects of withdrawing monoamine oxidase inhibitors (MAOIs). The withdrawal of these agents can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium and paranoid psychosis. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. The capacity of MAOI to exert amphetamine-like effects presynaptically, and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines, can provide a basis for the development of psychotic syndromes upon the withdrawal of MAOIs. Evidence for this hypothesis is reviewed.

Adult↗
PubMed1988

Model curriculum.

Explore the source record for details and available documents.

Curriculum↗
PubMed1988

Pharmacological perturbation of cholinergic systems: applications to the study of pathophysiological mechanisms in affective disorders.

Clinical, behavioral, physiological, biochemical and receptor binding parameters are useful as dependent measures in studies into the pathophysiology of affective disorders. Pharmacological perturbation of cholinergic mechanisms and modification of cholinergic-monoaminergic interaction mimics aspects of the neurobiology of affective disorders. The effects of these pharmacological manipulations can be quantitatively assessed by measuring their impact on variables in each of these classes. These deviations are easily and safely produced by several classes of drugs which directly or indirectly modify the function of central muscarinic cholinergic networks. Methods for inducing these changes in cholinergic systems and their application to clinical and basic research in the field of affective disorders are highlighted.

Amitriptyline↗
PubMed1988

Seasonal depression.

Seasonal affective disorders are mood disturbances that occur with a change in season. The most common form is winter depression, marked by sadness, anxiety, decreased physical activity, increased appetite, carbohydrate craving, weight gain, hypersomnia, decreased libido, worsening of premenstrual symptoms, impaired work performance and interpersonal conflict. This syndrome often responds to daily exposure to bright artificial light.

Antidepressive Agents↗