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PubMed1985

Lack of effect of oral activated charcoal on imipramine clearance.

The effect of oral activated charcoal on the pharmacokinetics of intravenous imipramine was studied in a randomized, crossover trial. Four normal men received intravenous imipramine (12.5 mg/70 kg) on two separate occasions, followed by either water or water plus high-surface-area activated charcoal (180 gm) in divided doses over 24 hours. Serum imipramine concentrations were measured from 0 to 24 hours after the imipramine infusion. There was no difference in the mean (+/- SE) t1/2 (9.0 +/- 0.8 vs. 10.9 +/- 1.6 hours), apparent volume of distribution (11.2 +/- 2.1 vs. 12.4 +/- 2.1 L/kg), or systemic clearance (992.2 +/- 138.3 vs. 930.3 +/- 101.9 ml/min/70 kg) of imipramine after dosing without and with oral activated charcoal, respectively (P greater than 0.05; paired t test). These results suggest that multiple oral doses of activated charcoal do not increase the clearance of imipramine in man.

Absorption↗
PubMed1991

The mephenytoin oxidation polymorphism is partially responsible for the N-demethylation of imipramine.

The metabolism of imipramine in six poor metabolizers of mephenytoin was compared with the metabolism of 16 extensive metabolizers of mephenytoin from an earlier study. Each subject was given single doses of 100 mg imipramine hydrochloride and 100 mg desipramine hydrochloride on separate occasions. Imipramine demethylation clearance was 0.74 L.min-1 (mean; range, 0.31-1.24) in poor metabolizers of mephenytoin compared with 1.43 L.min-1 (mean; range, 0.61-3.81) in extensive metabolizers of mephenytoin (p = 0.01, Mann-Whitney U test). It has previously been shown that the imipramine clearance by way of other pathways and desipramine oral clearance, both largely representing 2-hydroxylation, are considerably lower in poor metabolizers of sparteine than in extensive metabolizers of sparteine. In contrast, five subjects who were poor metabolizers of mephenytoin and extensive metabolizers of sparteine and a control group of 11 subjects who were extensive metabolizers of mephenytoin and sparteine showed no statistically significant difference with regard to these parameters. One subject who was a poor metabolizer of mephenytoin and sparteine had the lowest imipramine oral clearance of all 22 subjects studied. In conclusion, this and an earlier study show that the oxidation of imipramine is mediated by means of two different polymorphic P450 isozymes, 2-hydroxylation by way of the sparteine oxygenase (P450IID6) and demethylation by way of the mephenytoin oxygenase (P450IIC8).

Adult↗
PubMed1997

Effect of ketoconazole on the pharmacokinetics of imipramine and desipramine in healthy subjects.

AIMS: The aim of the study was to characterize further the role of CYP3A4 in the metabolism of tricyclic antidepressants. METHODS: The effect of oral ketoconazole (200 mg day-1 for 14 days) on the kinetics of a single oral dose of imipramine (100 mg) and desipramine (100 mg) was evaluated in two groups of six healthy male subjects. RESULTS: Ketoconazole administration was associated with a decrease in imipramine apparent oral clearance (from 1.16 +/- 0.21 to 0.96 +/- 0.20 l h-1 kg-1, mean +/- s.d.; P < 0.02), a prolongation in imipramine half-life (from 16.7 +/- 3.3 to 19.2 +/- 5.4 h, P < 0.05) and a decrease in area under the curve of metabolically derived desipramine (from 3507 +/- 1707 to 3180 +/- 1505 nmol l-1 h, P < 0.05), whereas concentrations of 2-hydroxy-imipramine were unaffected. In the subjects given desipramine, no significant changes in desipramine and 2-hydroxy-desipramine kinetics were observed during ketoconazole treatment. CONCLUSIONS: These findings indicate that ketoconazole, a relatively specific inhibitor of CYP3A4, inhibits the N-demethylation of imipramine without affecting the 2-hydroxylation of imipramine and desipramine. This interaction, confirms that CYP3A4 plays a role in the demethylation of tricyclic antidepressants.

Administration, Oral↗
PubMed1998

Chronic imipramine administration amplifies the serotonin2A receptor-induced intracellular Ca2+ mobilization in C6 glioma cells through a calmodulin-dependent pathway.

In the present study, we examined whether chronic exposure of C6BU-1 cells to 100 nM of several different types of antidepressants directly influences serotonin2A (5-HT2A) receptor-stimulated intracellular Ca2+ mobilization. Imipramine, desipramine, clomipramine, and maprotiline amplified the 5-HT response at 48, but not at 2, h. Imipramine increased the maximum response to 5-HT without altering the EC50 of the dose-response curve. This effect was time dependent and cycloheximide blocked the maximal induction, suggesting an essential role for protein synthesis in this process. Previous exposure of the cells to thrombin or isoproterenol did not influence 5-HT2A receptor function and pretreatment with imipramine did not alter the thrombin- or bradykinin-induced Ca2+ mobilization, which indicates that the effects of imipramine appear to be specific to the 5-HT2A receptor. The effect of imipramine was potently suppressed by a calmodulin antagonist, W-13, in a dose-dependent manner. Furthermore, this amplified 5-HT response was blocked by KN-93, but not by H-7. Taken together, these results suggest that imipramine has a modulatory effect on the 5-HT2A receptor-coupled intracellular Ca2+ in C6 cells through a calmodulin-dependent pathway, possibly involving Ca2+/calmodulin kinase activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Interactions between imipramine and morphine on motility in rats: possible relation to antidepressant effects?

The aim of the present study was to evaluate whether morphine and the more modern antidepressant drug imipramine have common effects on behavior after both acute and chronic administration, and, in particular, to establish whether they act synergistically. In rats, morphine (15 mg/kg i.p.) produced a pronounced hypokinesia, followed by locomotor activation and stereotyped behavior. After repeated administration (eight times), tolerance to the hypokinesia developed, whereas locomotor activation and stereotypies occurred earlier and were more pronounced. Subacute pretreatment with imipramine (twice daily 10 mg/kg i.p. for eight days) enhanced and prolonged hypokinesia and delayed the manifestation of stereotypies and locomotor activation. In contrast, chronic treatment with imipramine (for 29 days) no longer inhibited morphine-induced stereotypies and locomotor activation, but seemed to enhance them when they were tested in rats repeatedly treated with morphine. When the same rats were tested with morphine (15 mg/kg) seven days after withdrawal of morphine and imipramine, morphine produced increased stereotypies and a slight enhancement of locomotion. The experimental conditions used excluded the possibility that conditioning phenomena might explain the enhancement of (probably dopamine-mediated) behavior. Furthermore, the results demonstrated that 1) acute administration of morphine and subacute administration of imipramine may act in a synergistic way, and 2) repeated administration of morphine and chronic treatment with imipramine also act synergistically, although contrary to the acute actions of both drugs. These interactions might be of therapeutic or toxicological relevance.

Animals↗
PubMed1999

Depressed in-patients respond differently to imipramine and mirtazapine.

Tricyclic antidepressants and more recent antidepressants are generally considered to have equivalent efficacy in the treatment of depression. After a previous report of a marked difference in the response to mirtazapine compared to imipramine, we report here an analysis of different symptom clusters. One hundred seven consecutive in-patients with major depression (Diagnostic and Statistical Manual III-R, DSM-III-R) and a Hamilton Rating Scale for Depression (HRS-D) score of 18 points or more were randomly assigned to double-blind treatment. Two and four weeks after predefined blood levels had been obtained, the severity of depression was assessed using the HRS-D. The mean dosages used were 235 mg/day of imipramine and 77 mg/day of mirtazapine, the latter being in excess of the 15-45 mg/day range currently advised. Total HRS-D scores and seven symptom clusters were analyzed in the 85 patients (79%) who were not receiving any co-medication. Imipramine was more effective against the clusters related to core symptoms of depression: "depression and guilt", "retardation", and "melancholia", respectively. Mirtazapine showed a biphasic response with regard to the clusters "sleep" and "anxiety/agitation", respectively, which consisted of a marked response after two weeks of predefined blood level, but with a waning of this effect at four weeks. Imipramine produced a more gradual response on these clusters, which was more pronounced at four weeks than with mirtazapine. Two aspects of the present study could be related to this finding: blood level control resulted in optimal treatment with imipramine but not mirtazapine, and - most importantly - the patients were not receiving any anxiolytic or hypnotic co-medication. These findings suggest that mirtazapine may have anxiolytic and sedative properties and fewer antidepressant properties than imipramine in severely depressed in-patients.

Adrenergic alpha-Antagonists↗
PubMed1997

The effect of hypericum extract on cardiac conduction as seen in the electrocardiogram compared to that of imipramine.

The electrocardiographic effects of high-dose hypericum extract were compared to the effects of imipramine hydrochloride on ECG recordings in a randomized, double-blind, multicenter treatment study of 209 patients suffering from depression. ECGs were recorded before and after a six-week treatment period with either hypericum extract or imipramine. At the end of the study ECGs of 84 patients treated with hypericum extract and 76 patients treated with imipramine were suitable for an analysis of conduction intervals and pathological findings. In the first ECG analysis comparing high dose hypericum extract with imipramine, a prolongation of the conduction intervals PR, QRS and QTc was found for imipramine. In contrast, a small acceleration of conduction was seen for the high-dose hypericum extract. The comparison of ECGs at the beginning and after six weeks of treatment showed a significant increase in first degree AV-blocks and abnormalities of repolarization under imipramine but a significant reduction of such pathological findings under treatment with hypericum extract. It should be emphasized that this favorable feature of safe cardiac activity was achieved with 1800 mg of hypericum extract. The reduction in pathological ECG features after treatment with hypericum extract may have resulted mainly from the change of medication, probably tricyclics, to hypericum extract. Our results indicate that for the treatment of patients with a pre-existing conductive dysfunction or elderly patients, high-dose hypericum extract is safer with regard to cardiac function than tricyclic antidepressants.

Adult↗
PubMed1996

Subchronic antidepressant treatment with venlafaxine or imipramine and effects on blood pressure and heart rate: assessment by automatic 24-hour monitoring.

Venlafaxine is a new nontricyclic antidepressant inhibiting the reuptake of serotonin, noradrenaline, and, to a lesser extent, dopamine without antagonizing cholinergic, histaminergic, or noradrenergic receptors. Significantly, in a first placebo-controlled safety and efficacy study, high doses of venlafaxine increased blood pressure in some study subjects. In order to investigate further the effect of subchronic antidepressant drug treatment on blood pressure and heart rate, the effects of a conventional tricyclic (imipramine) and a structurally different phenethylamine antidepressant (venlafaxine) were compared. Sixteen inpatients with major depression (melancholic type) were treated for six weeks with imipramine or venlafaxine in a randomized parallel double-blind design. Blood pressure was monitored for 24 hours before treatment and at days 14 and 28 by means of a portable, automatic blood-pressure monitoring system. Both compounds lowered systolic blood pressure by about 5% on average, while diastolic pressure was influenced neither by imipramine nor by venlafaxine. Imipramine treatment resulted in a significant 15% increase in heart rate on both day 14 and day 28, whereas heart rate tended to decrease under venlafaxine. When the data of individual patients were evaluated, a clinically significant increase in blood pressure was apparent in one venlafaxine-treated patient; a marked increase in blood pressure in one patient treated with imipramine proved to be reversible with continued treatment. Due to the relatively small sample sizes, the present data do not allow a definitive judgement as to whether venlafaxine may cause differential blood pressure alterations in comparison with imipramine. However, our results demonstrate that the blood pressure-increasing effect reported for venlafaxine from first clinical studies might be clinically significant in individual patients. Furthermore, our study shows that 24-hour monitoring of blood pressure and heart rate is a powerful tool in safety evaluations of new drugs, even in relatively small samples.

Adult↗
PubMed1994

Imipramine in patients with chest pain despite normal coronary angiograms.

BACKGROUND: Ten to 30 percent of patients undergoing cardiac catheterization because of chest pain are found to have normal coronary angiograms. Because these patients may have a visceral pain syndrome unrelated to myocardial ischemia, we investigated whether drugs that are useful in chronic pain syndromes might also be beneficial in such patients. METHODS: Sixty consecutive patients underwent cardiac, esophageal, psychiatric, and pain-sensitivity testing and then participated in a randomized, double-blind, placebo-controlled three-week trial of clonidine at a dose of 0.1 mg twice daily (20 patients), imipramine at a dose of 50 mg nightly with a morning placebo (20 patients), or placebo twice daily (20 patients); this treatment phase was compared with an identical period of twice-daily placebo for all patients (placebo phase). RESULTS: Thirteen (22 percent) of the 60 patients had ischemic-appearing electrocardiographic responses to exercise, 22 of the 54 tested (41 percent) had abnormal esophageal motility, 38 of 60 (63 percent) had one or more psychiatric disorders, and 52 of 60 (87 percent) had their characteristic chest pain provoked by right ventricular electrical stimulation or intracoronary infusion of adenosine. During the treatment phase, the imipramine group had a mean (+/- SD) reduction of 52 +/- 25 percent in episodes of chest pain, the clonidine group had a reduction of 39 +/- 51 percent, and the placebo group a reduction of 1 +/- 86 percent, all as compared with the placebo phase of the trial. Only the improvement with imipramine was statistically significant (P = 0.03). Repeat assessment of sensitivity to cardiac pain while the patients were receiving treatment showed significant improvement only in the imipramine group (P = 0.01). The response to imipramine did not depend on the results of cardiac, esophageal, or psychiatric testing at base line, or on the change in the psychiatric profile during the course of the study, which generally improved in all three study groups. CONCLUSIONS: Imipramine improved the symptoms of patients with chest pain and normal coronary angiograms, possibly through a visceral analgesic effect.

Adult↗
PubMed1999

Imipramine treatment in pediatric burn patients with symptoms of acute stress disorder: a pilot study.

OBJECTIVE: Pediatric burn patients often exhibit acute stress disorder (ASD) symptoms. Information on psychopharmacological treatment of ASD symptoms in children is scarce. This pilot study used a prospective, randomized, double-blind design to test whether thermally injured children suffering ASD symptoms benefit from imipramine. METHOD: Twenty-five children, aged 2 to 19 years, received either imipramine or chloral hydrate for 7 days. A structured interview (clinically useful, but validity and reliability not yet established) was used to assess the presence and frequency of ASD symptoms both before treatment and 3 times during the treatment period. RESULTS: Eleven females and 14 males participated, with a mean total burn surface area of 45% (SD = 23%) and mean age of 8 years (SD = 6). Imipramine was more effective than chloral hydrate in treating ASD symptoms (chi 2 [1, N = 25] = 5.24, p < .02). Five of 13 were positive responders to chloral hydrate (38%). Ten of 12 were positive responders to low-dose imipramine (83%). CONCLUSIONS: This pilot study suggests a place for cautious initial use of imipramine to reduce ASD symptoms in burned children. Care must be taken to minimize cardiovascular risks in an off-label application of imipramine in children, especially those receiving additional medications.

Acute Disease↗
PubMed1993

A double-blind comparison of paroxetine with imipramine in the long-term treatment of depression.

The chronic and recurrent nature of major depression is well recognized, and recent data suggest that maintenance therapy with full-dose pharmacotherapy (i.e., the dose used to treat the index episode) is effective in preventing relapse and recurrence. We present results from a 1-year, double-blind trial of paroxetine and imipramine in patients who successfully completed a 6-week acute course of therapy. A total of 717 outpatients were included in the 6-week, randomized, double-blind, placebo-controlled comparative study of paroxetine and imipramine conducted at six centers. At the end of the acute treatment phase, patients showing a therapeutic response were eligible to enter a long-term extension of the study in which they would continue to receive the same drug (or placebo) in double-blind fashion for up to 1 year. Of the 219 patients who entered the long-term phase, 94 received paroxetine, 79 received imipramine, and 46 received placebo. During the 1-year maintenance study, both paroxetine and imipramine were more effective than placebo in maintaining euthymia among patients who had responded to short-term treatment. However, approximately twice as many imipramine-treated patients dropped out of the study prematurely because of adverse experiences compared to paroxetine-treated patients, suggesting that paroxetine is more readily tolerated than imipramine during long-term treatment.

Adult↗
PubMed1993

Moclobemide versus imipramine in depressed out-patients: a double-blind multi-centre study.

One hundred and twenty seven patients with major depressive episode were included in a double-blind, four-week, prospective, randomized, multi-centre parallel-group trial comparing moclobemide and imipramine. The dose of moclobemide was 150-525 mg/day and that of imipramine 50-175 mg/day; the mean daily doses during the last week of treatment were 307 mg and 100 mg of moclobemide and imipramine, respectively. The decrease of the total scores of the Hamilton Depression Scale (HDRS) as well as the Overall Assessment of Efficacy by the Investigators showed significant amelioration of depression in both treatment groups (p < 0.001). No significant differences were found between the moclobemide and imipramine groups with regard to treatment outcome. The onset of the antidepressant activity was faster in the moclobemide group as measured by the Assessment of the Investigators. This difference was not observed when the therapeutic index figures calculated on the basis of the changes in the HDRS scores were scrutinized. Treatment-emergent side effects were somewhat more frequent during imipramine than during moclobemide treatment. Nevertheless, a total of only four patients discontinued the trial prematurely because of poor tolerability. Imipramine-treated patients reported more anticholinergic side effects, whereas tiredness and headache were observed more frequently in the moclobemide-treated patients. Restlessness, nervousness and sleep disturbances were noted with equal incidence in both patient groups.

Adult↗
PubMed2004

Comparing the effects of 8-week treatment with fluoxetine and imipramine on fasting blood glucose of patients with major depressive disorder.

This study was designed to compare the effects of fluoxetine and imipramine on fasting blood glucose (FBG) in patients with major depressive disorder. Sixty nondiabetic patients with major depressive disorder (based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria) entered this randomized, double-blind study. Patients did not receive any medication affecting serum FBG levels for at least 2 weeks before the initiation of the study. Patients were assigned to receive 20 to 40 mg/d of fluoxetine or 75 to 200 mg/d of imipramine for 8 weeks. Pregnant women and patients with diabetes mellitus and a history of any major heart disease were excluded from this study. Additionally, none of the patients should have received electroconvulsive therapy within 6 months before the initiation of the antidepressants. FBG levels were measured at the initiation, as well as 4 and 8 weeks after starting antidepressants. Nineteen patients in the fluoxetine and 24 patients in the imipramine groups completed the study. In the fluoxetine group, FBG level was decreased from 88.5 mg/dL (baseline) to 85.0 mg/dL at week 4 (P = 0.73), and to 79.8 mg/dL at week 8 (P < 0.001). On the other hand, in the imipramine group, FBG level was increased from 86.96 mg/dL (baseline) to 89.71 mg/dL at week 4 (P = 0.079), and to 96.90 mg/dL at week 8 (P < 0.001). This 8-week study showed that FBG levels may decrease in depressive patients receiving fluoxetine and may increase in those patients treated with imipramine. Therefore, it is suggested to measure and monitor FBG before initiation and during treatment with fluoxetine and imipramine.

Adolescent↗
PubMed1983

Plasma levels and clinical response with imipramine in a study comparing efficacy with mianserin and nomifensine.

1 The comparative antidepressant efficacy of 150 mg imipramine, 60 mg mianserin and 150 mg nomifensine was studied in 45 depressed patients in a six week double-blind investigation. 2 In the efficacy analysis of 41 patients completing the study there was no overall significant difference in efficacy between the groups. Individual group comparisons showed no significant difference in response between mianserin and nomifensine, and mianserin and imipramine. There was a significant (z = 1.99, P less than 0.05) improved response in the imipramine compared with the nomifensine treated group. The imipramine treated group were significantly older. 3 No significant plasma concentration/clinical response relationships were demonstrated with nomifensine, mianserin, imipramine or desipramine. 4 Plasma level monitoring of imipramine recommended by some investigators does not seem to be appropriate.

Adult↗
PubMed1994

The role of S-mephenytoin 4'-hydroxylase in imipramine metabolism by human liver microsomes: a two-enzyme kinetic analysis of N-demethylation and 2-hydroxylation.

1. The metabolism of imipramine (N-demethylation and 2-hydroxylation) was studied in relation to the activity of S-mephenytoin 4'-hydroxylase in human liver microsomes. 2. Eadie-Hofstee plots for the formation of despiramine and 2-hydroxyimipramine were biphasic, suggesting that at least two enzymes are involved in both the N-demethylation and 2-hydroxylation of imipramine by human liver microsomes. 3. The respective mean (+/- s.d.) kinetic parameters for the N-demethylation and 2-hydroxylation of imipramine derived from a two-enzyme kinetic analysis were: Km1 = 1.1 +/- 0.4 and 1.6 +/- 0.6 microM, Vmax1 = 0.11 +/- 0.03 and 0.15 +/- 0.07 nmol mg-1 min-1, and Vmax1/Km1 = 0.10 +/- 0.02 and 0.09 +/- 0.04 ml mg-1 min-1; Km2 = 214 +/- 84 and 257 +/- 148 microM, Vmax2 = 2.22 +/- 0.69 and 0.53 +/- 0.15 nmol mg-1 min-1, and Vmax2/Km2 = 0.011 +/- 0.001 and 0.003 +/- 0.002 ml mg-1 min-1. 4. With regard to imipramine N-demethylation and 2-hydroxylation at 2 microM (representing high-affinity reactions) and at 400 microM (representing low-affinity reactions), only N-demethylation at 2 microM showed a close correlation with the 4'-hydroxylation of S-mephenytoin (rs = 0.952, P < 0.01; n = 10 livers). 5. Concentrations up to 250 microM S-mephenytoin inhibited the N-demethylation of imipramine (2 microM), but no further inhibition was observed using concentrations from 250 to 750 microM. 6. Imipramine inhibited S-mephenytoin 4'-hydroxylation competitively with a Ki value of 12.5 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aryl Hydrocarbon Hydroxylases↗
PubMedDate not supplied

Effects of imipramine of the orthostatic changes in blood pressure, heart rate and plasma catecholamines.

The effect of imipramine on the orthostatic changes in heart rate, blood pressure and plasma catecholamines were examined in six healthy male subjects on two occasions on high sodium balance (Na+ excretion greater than 120 mmol per day) and on low sodium balance (Na+ excretion less than 110 mmol per day), respectively. Orthostatic tests were carried out before and 2 h after ingestion of 150 mg imipramine hydrochloride. Imipramine caused a moderate increase in supine systolic blood pressure, and a pronounced increase in the rise in heart rate, when the subjects assumed erect position. The orthostatic drop in systolic blood pressure was in most cases only moderately increased after ingestion of imipramine, but in three subjects pronounced orthostatic hypotension developed when the sodium balance was low, whereas no clinical symptoms were seen in the same subjects when tested after imipramine ingestion on a high sodium balance. The plasma catecholamine levels in supine and standing position were not influenced by imipramine or by the changes in sodium balance. The data may suggest that inhibition of presynaptic reuptake of noradrenaline and/or alpha 2-adrenoceptor blockade causes the moderate rise in supine blood pressure, whereas alpha 1-adrenoceptor blockade, mainly affecting the venous part of the vascular bed, may explain the orthostatic reactions.

Adrenergic alpha-Antagonists↗
PubMed1986

Chronic lithium treatment decreases [3H]-imipramine binding in rat brain.

The effect of a chronic lithium treatment on the [3H]-imipramine binding in rat brain regions was investigated. In the striatum, an oral administration of lithium for 30 days induced a decrease in the [3H]-imipramine binding at the concentration of [3H]-imipramine, 1.0 nM, compared to the control. Lithium did not affect the [3H]-imipramine binding in the cerebral cortex and hypothalamus. A Scatchard analysis in the striatum revealed a decrease in the number of [3H]-imipramine binding sites with no changes in the binding affinity. These results suggest that the chronic lithium treatment may produce subsensitivity of the [3H]-imipramine binding in man and that this effect of the ion may be closely related to the established effect of lithium in the treatment of affective disorders.

Animals↗
PubMed1983

[3H]imipramine labels sites on brain astroglial cells not related to serotonin uptake.

Brain astroglial cells, whether from a bulk isolated preparation or in culture, have been shown to take up serotonin actively. [3H]imipramine has been proposed as a specific label for serotonin uptake sites in brain. We therefore studied the binding of [3H]imipramine to C6 astroglial cells in culture to determine if some of the binding of this radioligand in brain homogenates is actually to serotonin transporting sites on glia. [3H]Imipramine binds saturably (Bmax = 202 fmol/mg protein) and with high affinity (KD = 1.72 nM) to C6 cells. This binding is competitively inhibited by other tricyclic antidepressants. The C6 cells actively transport [3H]serotonin with a Km of 2 microM and a Vmax of 1080 fmol/10(6) cells/min. However, the pharmacological profile for inhibition of serotonin uptake does not correlate with the pharmacological profile for inhibition of [3H]imipramine binding. These results suggest that the binding of [3H]imipramine to astroglial cells is not related to their capacity for active uptake of serotonin. Further, in brain homogenates, some of the binding of [3H]imipramine may not be to neuronal uptake sites but rather may be to sites on astroglial cells.

Animals↗