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PubMed1985

Clomipramine and imipramine in obsessive-compulsive disorder.

Twenty-three outpatients with primary obsessive-compulsive disorder (OCD) were started in a 12-week double-blind clinical trial of clomipramine (CLI) (n = 11) and imipramine (IMI) (n = 12). There was no placebo and no crossover. After 6 weeks of treatment, data on 19 subjects (9 CLI, 10 IMI) were available. After week 12, the sample was reduced to 16 patients (8 CLI, 8 IMI). At both time points, OCD symptoms showed modest reductions (in comparison with the pretreatment baseline) in both CLI and IMI groups. Both drugs showed a major antidepressant effect. Analyses accounting for the differences in the baseline levels indicated a somewhat superior effect of CLI over IMI on OCD as well as depression. The effect of CLI and IMI on OCD was independent of the initial severity of depression. There were no clear differences in the safety of the treatments.

Adult↗
PubMed1986

Platelet 3H-imipramine binding in bipolar patients.

Platelet 3H-imipramine binding was investigated in 31 control subjects and 19 hospitalized bipolar patients, either in the hypomanic or the depressed phase of illness. The mean Bmax value in the bipolar depressed patients did not differ significantly from that in the control subjects or the hypomanic patients. Differences in timing of the assay after blood collection, membrane preparation, protein content used in the assay, or binding of radioactive ligand to the equipment do not appear to explain the discrepancy between these results and previous findings.

Adult↗
PubMed1986

Inhibition of 3H-imipramine binding by plasma from depressed and normal subjects.

The inhibition by human plasma of 3H-imipramine (3H-IMI) specific binding to rat cerebral membranes was investigated using platelet-free plasma (PFP) from normal and depressed subjects. The specific binding of 3H-IMI at a ligand concentration of 4 nM decreased with increasing PFP volumes, reaching 50% inhibition following the addition of 10-13 microliters PFP to a final incubation volume of 250 microliters. The extent of this inhibition was the same using PFP from controls or depressed patients. The inhibitory activity was associated with plasma proteins. Scatchard analysis of 3H-IMI binding in the presence and absence of PFP indicated that the inhibitory effect was associated with an increased Kd without an appreciable change in Bmax. It is suggested that an endogenous acceptor in the PFP, such as alpha 1-acid-glycoprotein may be responsible for the observed inhibition of 3H-IMI binding to the cerebral membranes.

Adolescent↗
PubMed1986

How blind is blind? Assessment of patient and doctor medication guesses in a placebo-controlled trial of imipramine and phenelzine.

The purpose of the double blind is to protect the internal validity of a clinical trial by preventing knowledge of treatment conditions from influencing outcome or its assessment. We studied medication guesses of 137 depressed patients and/or their doctors at the end of a 6-week randomized trial of placebo, imipramine, and phenelzine. Overall, 78% of the patients and 87% of the doctors correctly distinguished between placebo and active medication. Clinical outcome, treatment condition, and their interaction each contributed to guessing accuracy, while medication experience and side effects assessed only in week 6 did not. Accuracy was high, however, even when cases were stratified for clinical outcome, indicating that other cues were available to the patients and doctors. These may include patterns and timing of side effects and clinical response not detectable in this end-point analysis.

Adolescent↗
PubMed1987

Differential 3H-imipramine platelet binding in patients with panic disorder and depression.

3H-Imipramine (3H-IMI) binding to platelet membranes was measured in 19 patients with agoraphobia with panic attacks, 9 patients with major depression, and 22 healthy subjects. In comparison to healthy subjects, the maximal number of binding sites (Bmax) was significantly decreased in depressed patients but not in panic disorder patients, and the apparent affinity of binding was slightly decreased in depressed patients but not in panic disorder patients. The Bmax and Kd of 3H-IMI platelet binding did not differ between panic disorder patients with and without a history of a major depressive episode. Thus, 3H-IMI platelet binding is clearly different in patients with panic disorder compared to those with an active depression. Because 3H-IMI binding is associated with the serotonin reuptake site in platelet and brain membranes, these findings give further support to abnormalities in serotonergic function in patients with major depression.

Agoraphobia↗
PubMed1988

Sleep deprivation and imipramine binding sites in depressed patients and healthy subjects.

The influence of sleep deprivation on 3H imipramine binding was investigated in blood platelets of 32 depressed patients and 15 healthy subjects. The effect of sleep deprivation was not statistically different in either group. Changes of Bmax associated with sleep deprivation were compensated for by reciprocal changes of Kd in the group of patients, suggesting altered regulatory mechanisms. A comparison of binding characteristics of responders and nonresponders to sleep deprivation revealed no difference between groups. If the patients were divided by a biological criterion (number of binding sites), a prediction of clinical response to sleep deprivation was possible.

Adult↗
PubMed1988

Platelet 3H-imipramine binding in psychogenic pain patients.

High-affinity binding of 3H-imipramine was analyzed in platelet membranes from patients with chronic psychogenic pain. The patients who in addition to the pain also showed affective symptoms such as depression and anxiety had lower binding than the pain patients without these symptoms.

Adolescent↗
PubMed1990

Subclasses of platelet 3H-imipramine binding sites.

The possible presence of multiple high affinity 3H-imipramine (3H-IMI) binding sites on blood platelets was studied using trypsin digestion and cyanoimipramine (CNIMI), a pseudo-irreversible inhibitor of 3H-IMI binding and serotonin uptake. Increasing concentrations of CNIMI resulted in a discontinuous curve with a plateau at intermediate concentrations (0.05-0.35 nM). CNIMI sensitive (0.25 nM) sites accounted for approximately half of total high affinity 3H-IMI binding as defined by displacement with 100 microM desipramine. Similar results were obtained when platelet membranes were pretreated with trypsin (0.21-0.84 mg/ml), and no additional inhibition was evident with a combination of both treatments. The present results suggest that 3H-IMI may bind to two separate types of high affinity sites. One subclass is apparently proteinaceous and sensitive to low concentrations of CNIMI, whereas the other is apparently nonproteinaceous and is CNIMI resistant.

Blood Platelets↗
PubMed1990

Seasonal changes in cyanoimipramine specific platelet 3H-imipramine binding in depression.

Seasonal variations in cyanoimipramine (CNIMI) sensitive and CNIMI resistant subclasses of platelet 3H-imipramine (3H-IMI) binding sites were studied in depressed patients and normal volunteers. Sinusoidal rhythms of the binding of both subclasses were found in patients and controls with peak levels in mid-February. Patient values of CNIMI sensitive binding fluctuated about a yearly average that was 32% lower than the average of controls. Patient deviations from the normal pattern were apparently bimodally distributed, whereas those of controls were normally distributed. CNIMI resistant binding was also normally distributed in controls, but not in depressed patients, although patient mesor values were not lower than those of controls. Platelet binding was not correlated with the severity of illness as measured by the Hamilton Rating Scale for Depression, and individual symptoms failed to discriminate between patients with high and low Bmax values.

Adult↗
PubMed1990

Methodological issues in the preparation and assay of platelet 3H-imipramine binding.

Several methodological factors in the preparation of platelets and the determination of platelet 3H-imipramine (3H-IMI) binding were examined. The ionic composition of the assay significantly affected platelet 3H-IMI binding. Approximately 25% of the specific binding of 3H-IMI to intact platelet preparations was retained in the absence of sodium and chloride ions. The addition of sodium ions enhanced the specific binding of 3H-IMI, but the addition of chloride in the presence of sodium had a more pronounced effect, enhancing binding approximately five-fold over that observed with the addition of sodium. Sodium was the only cation tested that enhanced binding. Only halides enhanced binding in the presence of sodium with the following order of potency: Cl- greater than Br- greater than I- = F-. Ions increased the density of binding sites (Bmax) and did not affect the affinity of the binding sites for 3H-IMI. In the presence of sodium and chloride, the use of serotonin (5HT) to define nonspecific binding in saturation experiments resulted in lower binding densities (Bmax) than when desipramine was used to define nonspecific binding. The component of binding that was insensitive to 5HT was roughly equal to the Bmax of 3H-IMI binding obtained in the absence of sodium and chloride using desipramine to define nonspecific binding. Overall, these data suggest that not all 3H-IMI binding that is displaced by desipramine is related to serotonergic mechanisms, and suggest that 5HT is a better choice than desipramine for the determination of the nonspecific binding of 3H-IMI. In addition, the binding of 3H-IMI to different platelet preparations was compared. The binding of 3H-IMI to intact platelets was less than that obtained using lysed platelet membranes when data were expressed per mg protein. The Coomassie Blue dye-binding method to determine platelet protein resulted in greater Bmax values than were obtained with the Folin phenol reagent method. The method of platelet preparation that is commonly used to prepare platelets for 3H-IMI binding resulted in similar binding values when compared to a method that prepares the entire platelet population. The results suggest that some, but not all, variations in laboratory methods used to prepare platelets and assay for platelet 3H-IMI binding may affect clinical studies examining this measure.

Adult↗
PubMed1991

Kinetic effects of desmethylimipramine treatment on platelet serotonin uptake in depressed patients: a comparison with imipramine.

The kinetic effects of desmethylimipramine (DMI) on platelet serotonin (5HT) uptake were compared to those of imipramine (IMI) in eight DMI-treated depressed patients and seven IMI-treated depressed patients, and compared to values after patients were off drug for 19 (+/- 8 SD) and 33 (+/- 15) days. As expected, IMI was a stronger inhibitor of 5HT uptake than DMI during treatment, with the mean apparent Km in treated patients being elevated nearly threefold over that of the drug-free condition. In DMI-treated patients, the mean Km was elevated nearly twofold over that of the drug-free condition. Although DMI is considered a preferential norepinephrine uptake inhibitor, the results suggest the following: (1) Significant decreases in the apparent platelet 5HT affinity are achieved with DMI; (2) the inhibition kinetics in depressed patients are competitive; (3) there was a significant relationship between Km change and depression outcome with DMI discontinuation; and (4) DMI, as a metabolite, appears to contribute to the 5HT uptake inhibition of IMI in vivo.

Blood Platelets↗
PubMed1992

Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine.

A double-blind clinical trial was carried out to evaluate the efficacy of S-adenosyl-L-methionine (SAMe) in speeding the onset of action of imipramine (IMI). SAMe is a naturally occurring substance that has been shown to possess antidepressant activity with a rapid mode of onset and minimal side effects. Sixty-three outpatients with moderate to severe depression were included in the study. After an initial 1-week placebo period, only 40 patients entered the active treatment phase. During the first 2 weeks of the trial, half of these patients received 200 mg/day of SAMe intramuscularly, while the other half received placebo. Simultaneously, oral IMI was administered to all patients at a fixed dose of 150 mg/day. The onset of clinical response was determined by evaluating patients every second day. By the end of week 2, the parenteral treatment was suppressed and IMI was adjusted according to individual needs. Depressive symptoms decreased earlier in the patients who were receiving the SAMe-IMI combination than in those who were receiving the placebo-IMI combination.

Adult↗
PubMed1990

Influence of protein concentration on platelet 3H-imipramine binding.

1. The effects of protein concentration in the assay mixture on platelet 3H-imipramine binding were studied in normal controls. 2. Increasing protein concentrations (76-926 micrograms/ml) were found to alter estimates of binding affinity (Kd) but not the number of binding sites (Bmax). 3. Increasing Kd estimates were protein dependent at concentrations in excess of ca. 200 micrograms/ml but were not protein dependent at lower concentrations. 4. A comparison of the present results with previous reports suggests that widespread interlaboratory differences in reported Bmax values for normal controls cannot be attributed to differences in the protein content of incubated samples. Rather these differences may be due to the inclusion of non-membrane protein in the assayed material.

Blood Platelets↗
PubMed1990

Relationship between 3H-imipramine binding, 14C-serotonin uptake, and the surface area of blood platelets.

1. The relationship between 14C-serotonin uptake, 3H-imipramine binding and surface area was studied in blood platelets. 2. Platelet rich plasma from 5 normal subjects was divided into 5 size subfractions by differential centrifugation and the total surface areas computed from platelet size profiles. 3. Linear relationships were found between both uptake and binding as a function of surface area regardless of platelet size. 4. The results suggest that platelet heterogeneity may contribute to the variability of uptake measurements which are commonly expressed on a per platelet basis. In contrast, the importance of heterogeneity to binding measurements, which are expressed per unit protein, may have been previously overestimated.

Biological Transport↗
PubMed1990

The relationship between response to fluoxetine, plasma drug levels, imipramine binding to platelet membranes and whole-blood 5-HT.

1) Thirty-four (34) out-patients with major depressive disorder as defined by Research Diagnostic Criteria were treated with fluoxetine in an open study. 2) All patients received 60 mg daily of the drug for between 18 and 21 days. 3) Of the 28 patients who completed the trial 21 showed improvement and 7 of these showed a marked change. 4) The 7 good responders had a higher fluoxetine:norfluoxetine ratio after three weeks treatment than the remaining patients; 6 of these patients were males. 5) All patients, irrespective of response, showed a decrease in imipramine binding and decrease in whole blood 5-hydroxytryptamine (5-HT) during the period of the study. 6) The response to the drug may be related to metabolism of fluoxetine.

Biomarkers↗
PubMed1994

Cumulative mean change procedure: application to a comparative trial of venlafaxine, imipramine, and placebo in the treatment of major depression.

1. A simple summary measure--namely, cumulative mean change (CMC)--is proposed for analyzing incomplete repeated measures in clinical settings. 2. A simple test statistic that uses the correlation between subject responses was derived and applied to a study comparing an investigational antidepressant, venlafaxine, with imipramine and placebo. 3. The global fashion in which CMC captured all data confirmed the efficacy advantage of venlafaxine over the two control agents.

Adult↗
PubMed1986

Effect of serotonin on the dissociation of high-affinity binding of [3H]imipramine in mouse cerebral cortex.

A low concentration of norzimelidine can be used to selectively measure the rate of dissociation of [3H]imipramine from high-affinity binding sites in the mouse cerebral cortex. Serotonin attenuates the dissociation initiated by norzimelidine. There is no difference between the half-time of dissociation in the presence of both serotonin and norzimelidine and that in the presence of serotonin alone. These effects are similar to but much less pronounced than those observed in the platelet.

Animals↗
PubMed1987

Chronic imipramine treatment reduces (+)2-[125I]iodolysergic acid, diethylamide but not 125I-neuropeptide Y binding in layer IV of rat cerebral cortex.

The effects of chronic oral (2 X 10 mumol/kg, twice daily for 14 days) imipramine treatment on (+)2-[125I]-iodolysergic acid, diethylamide (125I-LSD) and 125I-neuropeptide Y (125I-NPY) receptor binding were examined in rat cerebral cortex by quantitative receptor autoradiography. A 35% reduction of 125I-LSD binding was observed in layer IV, both in the frontal and occipital cortex, while there was no significant change in 125I-NPY binding. The observed decrease in 125I-LSD binding is probably due to a reduction in the density of 5-hydroxytryptamine (5-HT) receptors of the 5-HT2 type. This reduction may represent a disturbance in the 5-HT synapses, regulating the transmission of the specific afferents innervating layer IV of the cerebral cortex.

Animals↗