Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenously depressed patients who showed an antidepressant response to the tricyclic drug imipramine continued to show sustained well being after alpha-MPT was added whereas depression returned when small doses of PCPA were added for brief periods. In one patient the antidepressant response to imipramine occurred after pre- and continued treatment with alpha-MPT. Urinary excretion levels of MHPG in one of the patients studied longitudinally did not correspond to the direction of clinical affective state but did reflect anticipated changes during alpha-MPT treatment. Implications are that serotonergic mechanisms are likely involved in the anti-depressant effects of imipramine in man.
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PMID:Use of synthesis inhibitors in defining a role for biogenic amines during imipramine treatment in depressed patients. 13 59

1. The clinical efficacy of mianserin, a tetracyclic compound, was compared with imipramine and placebo in 47 hospitalized depressed patients. 2. The clinical ratings showed that the three treatment groups improved equivalently during hospitalization. 3. Plasma levels of mianserin correlated with changes in the Hamilton Rating Scale for depression, total score and two of its factors (anxiety/somatization, and retardation) and the item 'late insomnia'. 4. Drowsiness was a more frequent side-effect among mianserin patients on day 4; no other side-effect distinguished the treatments. 5. No relationship between MHPG levels and treatment or treatment outcome were observed.
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PMID:Clinical study of mianserin, imipramine and placebo in depression: blood level and MHPG correlations. 34 42

1. In humans, norepinephrine (NE) has been postulated to be involved in the regulation of mood and behavior and to be altered in patients with manic-depressive illness. 2. Recent methodological advances have made possible a more direct assessment of central noradrenergic activity by the accurate measurement of the small amounts of NE and of the enzyme responsible for the conversion of dopamine to NE, dopamine-beta-hydroxylase (DBH), found in cerebrospinal fluid (CSF). 3. Cerebrospinal fluid samples were obtained from depressed patients both before and after treatment with two monoamine oxidase-inhibiting antidepressant drugs, clorgyline and pargyline. 4. Patients were rated twice daily by nursing staff on a modified 15-point scale for severity of global depression and anxiety. Patients were also rated using the Hamilton depression rating scale. 5. High negative correlations were observed between the drug-related changes in CSF NE and the changes in depression ratings on both the global ratings (r = -.95, p less than .001) and the Hamilton rating scale (r = -.81, p less than .01). Changes in NE were also highly correlated with changes in global anxiety ratings (r = -.85, p less than .01) calculated on the basis of changes from baseline for each measurement. Drug-related changes in CSF DBH similarly showed negative correlations with clinical response (r = -.79, r = -.38, r = -.68 respectively). In contrast, no significant correlations were found when drug-related changes in CSF MHPG were compared to changes in clinical state.
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PMID:The central noradrenergic system and affective response to MAO inhibitors. 40 Oct 4

Indirect evidence has linked opioid reinforcement with changes in noradrenergic metabolism secondary to drug administration. Methodological precedents for biobehavioral correlations in depressive illness have suggested an important association between changes in mood and biogenic amine excretion patterns in the urines of patients during depression and recovery. This paper presents preliminary data on the possible relationship between changes in catecholamine excretion that were observed and the changes in behavior, mood, psychiatric status, and cardiorespiratory physiology secondary to heroin administration and methadone-assisted withdrawal. This study focuses on the urinary excretion of MHPG, since an appreciable fraction of this metabolite is probably derived from norepinephrine originating in the brain. The subjective changes in mood associated with heroin use, the decrease in respiratory rate, and the behavioral and mental status effects associated with opiate intoxication were observed only in the individuals whose MHPG excretion increased during the period of opiate administration.
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PMID:Opiates, catecholamines, behavior, and mood. 41 42

Erythrocyte catechol-O-methyl transferase (COMT) activity was studied in 65 patients with depressive illness and anxiety states. A hypothesis that measurement of this enzyme might have some value as an aid to diagnosis and as an index of clinical recovery has not been confirmed. In patients with endogenous depression, agitated subjects had COMT levels significantly higher than normal (P less than .01) and retarded subjects had levels significantly lower than normal (P less than .02). These observations are congruent with some reports of high and low urinary MHPG excretion in patients with depression. Further data correlating COMT assays with catecholamine metabolites in depressed patients may reveal homogeneous biochemical subgroups which could serve as a guide to rational therapy.
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PMID:Catechol-O-methyl transferase activity in patients with depressive illness and anxiety states. 62 44

A patient with unusually regular and rapid switches from mania to depression was studied for 113 consecutive days through five switches. Average evoked responses (AERs) to four intesities of light were recorded from vertex and occipital leads; telemetered activity records and behavioral ratings were also collected. Late AER components (P200) tended to change amplitude synchronously with the switches, vertex P200 amplitude decreased and occipital P200 amplitude increased in mania. Urinary MHPG changes paralleled the changes in P200 amplitude. Early AER components (P100) and especially the amplitude/intesity slope measures for P100 decreased about 8-10 days before a switch from depression to mania. Cross-spectral and linear regression analysis helped confirm these observations. The results, taken together with AER data in recent L-dopa studies, were consistent with catecholamine potentiation prior to the switch process from depression into mania.
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PMID:Average evoked responses in a rapidly cycling manic-depressive patient. 83 24

MHPG excretion of 14 endogenously depressive patients and 5 healthy controls was investigated before, during and after a night of sleep deprivation (SD). Patients having a minimum improvement of 40% in the Cronholm-Ottoson rating scale had shown a significantly higher MHPG excretion in the night before SD ( p less than 0.02) as compared to the non-improved group. The MHPG excretion of the night before SD shows a significant negative correlation, both with the depression score according to Cronholm-Ottoson (p less than 0.05) and with the self-rating score according to von Zerssen (p less than 0.005), on the day after SD. No correlation was found between the motor activity measured by pedometer and MHPG excretion. The results are discussed in connection with values found in controls.
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PMID:MHPG excretion during sleep deprivation in endogenous depression. 89 95

In 30 patients suffering from vital depression (the syndrome of endogenous depression) a negative correlation was found between the pre-therapeutic post-probenecid CSF 5-HIAA response and the therapeutic response to clomipramine (Anafranil). Clomipramine is a tricyclic antidepressant with a strong potentiating effect on central 5-HT. The following conclusion was drawn: if the cenral 5-HT turnover is diminished in depressions, then correction of this biochemical disturbance leads to alleviation of depressive symptoms. This finding is considered to support the concept of '5-HT-deficient depression'. Five of the 8 clomipramine-resistant patients showed a favourable response to nortriptyline, a NA-potentiating anti-depressant. The pre-therapeutic CSF MHPG concentration in these patients was not related to the therapeutic efficacy of nortriptyline. So, the assumption that these patients have been NA-deficient was not confirmed. However, renal MHPG excretion was not measured and possibly this variable correlates better with cerebral NA metabilism than MHPG in lumbar CSF which is of mainly spinal origin.
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PMID:New evidence of serotonin-deficient depressions. 89 99

Binding parameters (Bmax and Kd) of alpha 2-adrenergic receptors were studied in platelets from 14 depressed patients and 18 control subjects. Using 3H-clonidine (a partial alpha 2-adrenergic agonist) as the ligand and membranes, prepared from platelets isolated under physiological conditions, we found no significant differences in Bmax and Kd between medication free patients and control subjects. Platelet binding parameters in the depressed patients did not correlate with plasma levels of norepinephrine, epinephrine or MHPG. Age had a significant positive effect on platelet alpha 2-adrenergic receptor Bmax in both groups, and may have masked the patient-control differences. Treatment with desipramine for 28 days had no effect on the binding parameters in depressed patients when compared to pretreatment values. Adding desipramine to platelets of control subjects 'in vitro' did also not affect binding parameters. Our findings suggest that receptor binding studies with a partial alpha 2-adrenergic agonist in platelet membranes are not a useful model to test the hypothesis of a central supersensitive adrenergic system in depression.
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PMID:Platelet alpha 2-adrenergic receptors in depressed patients and healthy volunteers: the effects of desipramine. 132 72

1. Monoamine neurotransmitters (epinephrine, norepinephrine, dopamine, serotonin and some of their metabolites (DOPEG, MHPG, DOPAC, 5-HIAA) were measured by HPLC in extracts from telencephalon (TEL) and diencephalon-midbrain (DM) before, during at the end of metamorphosis. 2. During metamorphosis MHPG increased and 5-HIAA decreased in TEL and DM while DOPEG decreased only in DM. 3. Monoamine levels were greater in the TEL and a larger increase in MHPG occurred there. 4. Captivity without metamorphosis also caused a significant depression of 5-HIAA in TEL and depression of DOPEG, MHPG and DOPAC in DM.
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PMID:Monoamines and their metabolites in the amphibian (Ambystoma tigrinum) brain: quantitative changes during metamorphosis and captivity. 135 51


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