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Biomedical subjects

D S Janowsky

Publications and source records attributed to D S Janowsky.

At least 91 records · Page 5Linked to original sources
PubMed1986

Psychobiology and psychopharmacology: issues in clinical research training.

Although the scope of basic studies in psychopharmacology and psychobiology has been expanding steadily for about 30 years, relatively few clinical psychiatrists, psychologists, and psychopharmacologists now choose to become researchers or teachers in these disciplines. Such training is crucial to the future vitality of both academic and private-practice psychiatry, and in view of increasing constraints on training funds, student researchers may well be an endangered species. With these concerns in mind, at its 1984 meeting, the American College of Neuropsychopharmacology's Education and Training Committee organized a symposium of investigators, administrators, and former trainees to explore aspects of effective clinical research training in psychobiology and psychopharmacology. Aspects discussed included mentoring, settings and content of training, depth versus breadth of curriculum, and the effect of a critical mass of colleagues at various stages of professional development. Following a brief overview, selected panelists addressed the issues from their individual perspectives.

National Institute of Mental Health (U.S.)↗
PubMed1985

Physostigmine effects on serotonin uptake in human blood platelets.

Platelet serotonin (5HT) uptake was measured in 18 subjects administered physostigmine salicylate in a double-blind, placebo crossover design. In comparison to placebo, the drug caused a significant transient depression in mood, as measured by self- and observer-rated depression scores. In addition, physostigmine significantly increased platelet counts while independently decreasing the maximum velocity (Vmax) of platelet serotonin uptake. Physostigmine administration did not significantly affect the affinity constant (Km) for platelet serotonin uptake. The data are interpreted as being consistent with the postulate that platelet serotonin uptake may be decreased in depressed patients via cholinergic mechanisms.

Blood Platelets↗
PubMed1985

Antagonism of physostigmine induced lethality by a combination of scopolamine and methscopolamine.

The antagonistic effects of scopolamine, methscopolamine, and a combination of methscopolamine and scopolamine were evaluated in preventing physostigmine induced lethality in Swiss Webster mice. Low dose scopolamine was found to be highly effective in reversing high dose (3 X the LD100) physostigmine induced lethality, in contrast to methscopolamine, which was ineffective except in very high doses. A combination of scopolamine and methscopolamine was more effective than either drug alone.

Animals↗
PubMed1985

Effects of physostigmine on pulse, blood pressure, and serum epinephrine levels.

In this study, the infusion of physostigmine in 14 patients with affective disorder who were pretreated with methscopolamine caused significant and often profound increases in the patients' epinephrine levels, pulse rates, and blood pressure. Since physostigmine is being used experimentally in the treatment of elderly subjects who have Alzheimer's disease, these cardiovascular effects may have clinical importance.

Adult↗
PubMed1985

Dose-related physostigmine-induced ventricular arrhythmia: case report.

Physostigmine, a centrally-acting cholinesterase inhibitor, has been shown to have potential as a treatment for primary degenerative dementia. In an experiment to test its effects, i.v. physostigmine caused the onset of unifocal premature contractions and runs of bigeminy in an 85-year-old man.

Aged↗
PubMed1985

The dexamethasone suppression test and unipolar/bipolar distinctions.

In an attempt to validate several subtypes of affective disorders, 52 consecutive patients hospitalized at a clinical research center were comprehensively classified along several diagnostic and phenomenologic axes. Cortisol levels of each patient were evaluated at baseline and after the administration of 0.5 and 1.0 mg dexamethasone. None of the depressive subtypes responded significantly differently to the 1.0 mg dose. However, the bipolar subtype was associated with significantly different DST responses to the 0.5 mg dose. Patients with bipolar affective disorder, both manic and depressed, had higher postdexamethasone mean cortisol levels than all other groups. The results support the distinctiveness of the bipolar diagnosis.

Adolescent↗
PubMed1984

Comparative effects of tetrahydrocannabinol on psychostimulant-induced behaviors.

The behavioral effects of delta-9-tetrahydrocannabinol (THC), one of the major psychoactive cannabinoids in marijuana, were tested in two models of psychostimulant-induced behaviors in rats (locomotor behavior and stereotyped gnawing) induced by amphetamine (AMPH) and methylphenidate (MEPH). Pretreatment with THC (10 mg/kg gavage) almost doubled the amount of AMPH-induced gnawing but produced no effect on AMPH-induced locomotor behavior. In contrast to AMPH, THC produced no direct effect on MEPH-induced gnawing but caused a strong suppression of MEPH-induced locomotor activity. In addition, there was no additional interaction between THC and reserpine as measured by suppression of MEPH-induced gnawing. This result was unexpected in view of the powerful interaction between THC and reserpine reported previously. Because of the clear THC-induced dissociation of the behavioral effects of these two psychostimulants (AMPH and MEPH), our working hypothesis is that THC affects motor behaviors by some non-dopaminergic mechanism.

Amphetamine↗
PubMed1984

Central cholinergic stimulation causes adrenal epinephrine release.

Cholinergic drugs administered into the cerebral ventricles of animals selectively stimulate the adrenal medulla. However, the effects of central cholinergic stimulation on the sympathoadrenal system have not been studied in man. We stimulated central cholinergic activity in man by administering the cholinesterase inhibitor physostigmine to subjects pretreated with peripheral cholinergic blocking agents. A dose of 0.022 mg/kg physostigmine dramatically increased plasma epinephrine levels and slightly increased norepinephrine levels, which is consistent with selective adrenomedullary stimulation. A smaller dose of physostigmine increased epinephrine but did not alter norepinephrine levels. Subjects had increased pulse rates and blood pressures, and felt anxious while they had high plasma epinephrine levels.

Adrenal Medulla↗
PubMed1984

Plasma/RBC haloperidol ratios and improvement in acute psychotic symptoms.

In a double-blind controlled study, 20 acutely psychotic inpatients were treated with different haloperidol dosage regimens. Over a 24-hour period, 10 of the patients were treated with rapid intramuscular neuroleptization at 10 mg per dose and 10 at 2 mg per dose. The patients were then treated for 6 more days with an oral dose equivalent to that given over the first 24 hours of treatment, with doctor's choice adjustments as needed. Behavioral change was rated using the Brief Psychiatric Rating Scale (BPRS). Blood samples drawn at baseline and late in the treatment were assayed for plasma and red blood cell haloperidol levels. Although neither of these variables showed a significant correlation with behavioral improvement, the ratio of plasma/RBC haloperidol levels significantly correlated with improvement.

Acute Disease↗
PubMed1984

Desipramine: an overview.

It is proposed that factors including a long "track record," perceived lack of anticholinergic effects, suggestions of earlier onset of action, and the concept of noradrenergic specificity have contributed to the widespread clinical use of desipramine. Recent studies bearing on these clinical beliefs are reviewed, with a focus on desipramine side effects, specificity, and speed of onset as compared to other tricyclics and to new generation antidepressants.

Clinical Trials as Topic↗
PubMed1984

A cholinomimetic model of motion sickness and space adaptation syndrome.

The space adaptation syndrome is one of the more vexing problems confronted by our nation's astronauts during their journeys. This syndrome may be a variant of motion sickness, although this possibility has been questioned. Physostigmine, a centrally active cholinesterase inhibitor which increases brain acetylcholine, was found to cause a motion sickness-like syndrome--in psychiatric patients and normals--including nausea, emesis, malaise, dysphoria, increases in serum ACTH, beta-endorphin, cortisol, and prolactin, Neostigmine, a non-centrally acting cholinesterase inhibitor, and saline placebo caused no such effects. The above effects closely parallel those of motion sickness. Thus, the effects of physostigmine may be a convenient model for screening for treatments for motion sickness or space adaptation syndrome, or for predicting who will develop these syndromes.

Adaptation, Physiological↗
PubMed1984

Naloxone increases electrophysiological measures of selective information processing in humans.

The effects of the opiate antagonist naloxone on electrophysiological measures of human selective attention were examined utilizing a paradigm which dissociates selective information processing from any concurrent processes of general arousal that may be present. Subjects were injected with naloxone (2 mg, i.v.) or placebo prior to performing a three-channel selective listening task. The measure of selective attention was the difference between the auditory event-related potential (AERP) to a sequence of tones when they were attended and to the same sequence of tones when they were ignored. Typically, the AERP to attended channel tones is more negative, and this increased negativity is designated the attention effect. In this study, naloxone produced a significant augmentation of the AERP attention effect at frontal electrode sites, primarily by decreasing the negativity of AERPs to inattended tones. Naloxone had no effect on the AERPs from the undistracted and divided attention tasks or on the sensitivity of the AERP to a physical parameter of stimulus presentation, interstimulus interval. The effects of naloxone on selective attention appear to be independent of any alterations in arousal, as the drug had no effect on autonomic measures, reaction times, or auditory sensitivity, and the attention changes could be dissociated from any naloxone-induced alterations of mood. These data indicate that naloxone can have the specific effect of increasing AERP measures of selective information processing, thus suggesting a role for endogenous opioid peptides in the regulation of auditory selective attention in humans.

Adult↗