Search PubMed⌕ Search

Biomedical subjects

D L Murphy

Publications and source records attributed to D L Murphy.

At least 415 records · Page 23Linked to original sources
PubMed1982

Segregation and linkage studies of plasma dopamine-beta-hydroxylase (DBH), erythrocyte catechol-O-methyltransferase (COMT), and platelet monoamine oxidase (MAO): possible linkage between the ABO locus and a gene controlling DBH activity.

Measurements of dopamine-beta-hydroxylase (DBH), catechol-O-methyltransferase (COMT), and monoamine oxidase (MAO) along with 27 polymorphic marker phenotypes were available for 162 patients with major affective disorders and 1,125 of their relatives. Levels of enzymes were previously found not to be associated with illness. Pedigree analysis methods for quantitative traits are used to test single-gene hypotheses for segregation of DBH in 32 families with 411 individuals. COMT in 30 families with 351 individuals, and MAO in 50 families with 309 individuals. The familial distribution of both DBH and COMT are consistent with two codominant alleles at the same locus that account for 56% and 59% of the total variance, respectively. MAO activity cannot be shown to be segregating as a single major gene, but a purely nongenetic hypothesis is also rejected. A possible linkage of a locus for DBH to the ABO locus is indicated by a maximum lod score of 1.82 at 0% and 10% recombination fractions for males and females, respectively. A lod score of 0.61 at 0% recombination for a similar analysis in a single large pedigree was reported by Elston et al., making the combined lod score for the two studies equal to 2.32 at 0% recombination.

Adult↗
PubMed1981

Cognitive processes in depression.

During depressive episodes, patients show both qualitative and quantitative changes in how information is processed. Depressed patients appear to use weak or incomplete encoding strategies to organize and transform events to be remembered. This makes these events less memorable. If the depressed patient is provided organization and structure, then learning-memory deficits are not apparent. Disruptions in arousal-activation in depression can account for these cognitive impairments.

Adult↗
PubMed1981

Tyramine infusions and selective monoamine oxidase inhibitor treatment. I. Changes in pressor sensitivity.

The enhanced sensitivity to the pressor effects of tyramine, an indirect-aging sympathomimetic found abundantly in the diet, is a well-known potentially dangerous side effect occurring during treatment with commonly used non-selective monoamine oxidase (MAO) inhibitors. The effects of treatment with the selective MAO-A inhibitor clorgyline and the partially selective MAO-B inhibitors pargyline and deprenyl on tyramine's pressor effects were studied in depressed patients using an IV steady-state tyramine infusion technique. After 4 weeks of treatment, clorgyline produced a significantly greater increase in tyramine sensitivity in comparison to a medication-free baseline (29-fold) than did pargyline (12-fold) or deprenyl (1.7-fold). The pressor effects of tyramine were significantly prolonged after cessation of infusion during both clorgyline and pargyline, but not deprenyl treatment. These data from IV tyramine administrations suggest that intestinal MAO inhibition is not the major determinant of the enhanced tyramine pressor sensitivity produced by clorgyline and pargyline.

Blood Pressure↗
PubMed1981

Tyramine infusions and selective monoamine oxidase inhibitor treatment. II. Interrelationships among pressor sensitivity changes, platelet MAO inhibition, and plasma MHPG reduction.

The relationship between changes in IV tyramine pressor sensitivity accompanying selective monoamine oxidase (MAO) inhibitor treatment and estimates of MAO-A and MAO-B inhibition in vivo were studied. Reductions in platelet MAO activity provided an index of MAO-B inhibition, while changes in plasma 3-methoxy-4-hydroxyphenethylene glycol (MHPG) were used as an hypothesized reflection of MAO-A inhibition. Chronic treatment with the MAO-A inhibitor clorgyline and the MAO-B inhibitor pargyline showed significant inhibition of the alternate MAO enzyme as well, although this crossover effect was greater for pargyline than clorgyline. The MAO-B inhibitor deprenyl appeared to maintain the greatest degree of MAO inhibition selectivity in vivo. Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition. Changes in plasma MHPG are suggested to provide a potentially useful clinical index of in vivo MAO-A inhibition.

Blood Platelets↗
PubMed1981

Age-related changes in sleep in depressed and normal subjects.

All-night electroencephalographic (EEG) sleep data were examined a function of age in normal control subjects and hospitalized, unmedicated depressed patients with primary affective illness. By analysis of variance, Total Sleep time, Delta Sleep, Sleep Efficiency, Rapid Eye Movement (REM) Sleep, and REM Latency decreased as a function of age, whereas Early Morning Awake time and Intermittent Awake time increased. Compared with normal controls, after the effects of age were covaried out, depressed patients had a greater Sleep Latency, Early Morning Awake time, Intermittent Awake time, Duration and REM Density of the first REM period, and average REM Density for the night, as well as less Sleep Efficiency, less Delta Sleep, and shorter REM Latency, Early Morning Awake time increased with age in depressives but not in normals.

Adolescent↗
PubMed1981

Physostigmine induction of depressive symptomatology in normal human subjects.

Nine normal volunteers, screened for the absence of a personal or family history of affective disorders and free of concurrent marijuana usage, received intravenous infusions of high dose physostigmine or saline in a randomized, double-blind, counterbalanced paradigm. Self-rating and observer ratings both demonstrated a statistically significant, physostigmine associated increase in depressive-type symptoms in the group as a whole, particularly pronounced in certain individuals. These results are the first report of physostigmine associated depressive symptomatology in normal subjects. While our findings are discrepant with two previous studies, our use of multiple self-ratings, and some differences in physostigmine dosage and infusion times might have contributed to this difference. These findings suggest that high dose physostigmine may represent a pharmacological model of depression in normal subjects, or alternatively may be diagnostic of vulnerability to affective disorder in certain subjects free of a previous history of affective disturbances.

Adolescent↗
PubMed1981

Use of dexamethasone suppression test in clinical psychiatry.

The dexamethasone suppression test (DST) has been used in clinical medicine to evaluate overactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Consistent evidence has linked a specific dysfunction of the HPA axis to depressive illness. This article will review the physiology of the HPA axis and the method of the DST. After a critical review of the studies using the DST in psychiatric patients, the authors conclude that the overnight low dose DST can be a useful tool for the practitioner involved in the diagnosis and treatment of psychiatric illness.

Depression↗
PubMed1981

Neurochemical mechanisms in the affective disorders and neuroendocrine correlates.

This symposium offers the practicing clinician a general overview of ongoing research strategies exploring possible functional alterations in neurotransmitters, neuroreceptors, and regulatory neuropeptides in subjects with major affective disorders. Such alterations, if demonstrable, might provide new mechanistic insights into the pathophysiology of these illnesses and suggest novel therapeutic approaches to their pharmacological management. Rather than attempting to describe all neurobiological research strategies, we have selectively focused on strategies using specific pharmacological challenges attempting to perturb discrete central nervous system neurotransmitter pathways while recording the behavioral and neuroendocrine correlates of such manipulations. This introductory manuscript will describe the advantages as well as the limitations of such strategies and, in addition, will attempt to provide a general overview of neuroanatomical, neurochemical, and neuroendocrine mechanisms relevant to a conceptual understanding of the putative psychiatric relevance of such strategies.

Brain Chemistry↗
PubMed1981

Involvement of the central serotonergic system in affective illness.

This paper reviews the neuroanatomy and neuropharmacology of the central serotonergic system. Clinical evidence implicating altered serotonergic function in patients with affective disorders is summarized, as are the attempts to uncover central serotonergic dysfunction in these patients using pharmacological challenges. The authors conclude that the function of the brain serotonergic system in patients with affective disorders is relatively unexplored and would be a fruitful area of study for both the clinician and researcher.

Brain↗
PubMed1981

The psychopharmacological treatment of obsessive-compulsive disorder: a review.

This article reviews the literature concerning obsessive-compulsive disorder (OCD) and its treatment with drugs. We survey the differential diagnosis of OCD and the problems involved in evaluating its severity in a research setting. Pharmacological treatment of OCD has usually involved antidepressants, especially clomipramine, with equivocal but nevertheless encouraging success. Anxiolytic and neuroleptics have also been tried, but the results are inconsistent. We discuss the implications of these findings for treatment of patients with OCD and for future research.

Anti-Anxiety Agents↗
PubMed1981

Anomalous compartmentation of 5-hydroxytryptamine in intact human platelets.

1 The movement of radiolabelled 5-hydroxytryptamine (5-HT) between the extracellular medium, the thrombin-releasable (vesicular) compartment, and a non-thrombin-releasable compartment has been investigated in washed human platelets. 2 Appreciable amounts of extracellular 5-HT can accumulate in a non-releasable compartment. Depending on the incubation conditions and the amount of 5-HT already present inside the cell, non-releasable 5-HT can either remain non-releasable or rapidly migrate into the vesicular compartment. 3 Measurable amounts of vesicular 5-HT can also enter a non-releasable compartment. However, vesicular 5-HT which becomes non-releasable does not appear to mix with 5-HT becoming non-releasable following uptake from the extracellular medium. 4 Extracellular 5-HT can be added to vesicles and to the non-releasable compartment in the presence of appreciable quantities of 5-HT already in one or both compartments. 5 The vesicular and non-releasable compartments appear to accumulate 5-HT independently of one another. Furthermore, most vesicular accumulation of 5-HT occurs from the extracellular medium, rather than by translocation of non-releasable 5-HT into the vesicular compartment.

Biological Transport↗