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PubMed1983

Subcellular distribution of high affinity [3H]imipramine binding and [3H]serotonin uptake in rat brain.

The binding of [3H]imipramine to various subcellular fractions of rat brain was investigated. Using sodium free buffer or 0.5 microM chlorimipramine to define nonspecific binding, the specific binding was found to be associated with the synaptosomal fraction, as was the uptake of [3H]serotonin. A significant quantity of 'displaceable' binding was observed in the myelin and nuclear fractions when 'specific' binding was defined using only one concentration of [3H]imipramine and a large molar excess of chlorimipramine. This 'pseudospecific' binding was of low affinity and was not affected by the presence or absence of sodium.

Animals↗
PubMed1983

(-)-Deprenyl a selective MAO "B' inhibitor, increases [3H]imipramine binding and decreases beta-adrenergic receptor function.

In rats, a selective inhibition for 3 weeks of monoamineoxydase (MAO) type B elicited by daily doses of pargyline (2.5 mumol/kg) or (-)-deprenyl (1 mumol/kg) attenuated the NE dependent stimulation of cortical adenylate cyclase and reduced the number of brain recognition sites for beta-adrenergic receptor ligands. Similar actions were not elicited by a comparable dose regimen of (+)-amphetamine. Hence the inhibition of MAO B mimicks responses that are typically elicited by antidepressants. The molecular nature of the mechanisms involved cannot be understood, however, these mechanisms may not be identical for pargyline and (-)-deprenyl because this drug but not pargyline increased the number of [3H]imipramine recognition sites. Even high daily doses of pargyline (100 mumol/kg, for 3 weeks) failed to change [3H]imipramine binding though they still down regulated beta-adrenergic recognition sites, the NE stimulation of adenylate cyclase and the Bmax of [3H]mianserin and [3H]spiroperidol binding.

Animals↗
PubMed1985

Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim.

The suppressive effect of systemic injection of desipramine and imipramine on the duration of immobility in rats forced to swim was inhibited by 6-hydroxydopamine given into the medial amygdaloid nucleus as a pretreatment. Pretreatment with 5,7-dihydroxytryptamine given into the medial amygdaloid nucleus had no effect on the immobility-reducing effect of tricyclic antidepressants. The concentrations of catecholamines and serotonin in 6-hydroxydopamine- and 5,7-dihydroxytryptamine-pretreated rats, respectively, were significantly lower than those in the saline-injected rats. These results suggest that the suppressive effect of systemic injection of desipramine and imipramine on the duration of the immobility of rats forced to swim was mediated by the catecholaminergic but not the serotonergic mechanisms in the medial amygdaloid nucleus.

5,7-Dihydroxytryptamine↗
PubMed1985

Effect of ovariectomy and estrogen on [3H]imipramine binding to different regions of rat brain.

In rats, 35 days after ovariectomy, the number of [3H]imipramine binding sites increased more than 200% in striatum, hippocampus and hypothalamus but it did not change in cerebral cortex and brain-stem. Estradiol-17 beta acting in vitro inhibited [3H]imipramine binding in control membranes of striatum, hippocampus and hypothalamus, but not in the same regions from ovariectomized rats.

Animals↗
PubMed1986

Chronic imipramine administration reduces apomorphine inhibitory effects.

Changes in activity of dopaminergic and serotonergic systems were assessed after acute and chronic (14 days) imipramine (10 mg/kg) administration in mice. For this purpose, biochemical and behavioural tests were performed at different intervals of time after withdrawal of treatment. Brain levels of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid, homovanillic acid and 3,4-dihydroxyphenylacetic acid were assayed by a fluorometric method. Locomotion and stationary behaviour were investigated in the open-field test. The results of the experiments suggest that chronic imipramine reduces the inhibitory effects of apomorphine upon the dopaminergic system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Effect of adrenalectomy and corticosterone on [3H]imipramine binding in rat blood platelets and brain.

The effect of adrenalectomy and administration of glucocorticoids on [3H]imipramine binding (IB) of rat blood platelets and brain was investigated. Adrenalectomy significantly increased both Kd and Bmax of IB in the blood platelets but not the brain of male Sprague-Dawley rats. Administration of corticosterone acetate, 1 mg/kg i.p. for 7 days, decreased both Kd and Bmax in the blood platelets of sham-operated rats, but only Bmax in adrenalectomized rats. Corticosterone administration also decreased Bmax in frontal cortex and hypothalamus of sham and adrenalectomized rats but had no effect on Kd. These results suggest that glucocorticoids may modulate imipramine binding.

Adrenalectomy↗
PubMed1989

Chronic imipramine reduces [3H]SCH 23390 binding and DA-sensitive adenylate cyclase in the limbic system.

[3H]SCH 23390 binding and dopamine (DA)-stimulated adenylate cyclase activity were measured in brain membrane preparations from rats chronically treated with imipramine (10 mg/kg twice daily for 14 days). [3H]SCH 23390 binding sites were decreased by 27% in the limbic system but only 14% in the striatum. The responsiveness of adenylate cyclase to DA was reduced by 38% in the limbic system but was not modified in the striatum. Concomitant treatment with alpha-methyltyrosine (alpha-MPT) (50 mg/kg daily for 14 days) prevented the imipramine-induced reduction in both [3H]SCH 23390 binding sites and the responsiveness of adenylate cyclase to DA.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Long-term verapamil treatment increases [3H]imipramine binding in human platelets.

The effect of long-term verapamil treatment on [3H]imipramine binding to the serotonin transporter in human platelets was studied. A significant increase (24%, P less than 0.05) in the density of high-affinity imipramine binding sites was observed in platelets of cardiac patients maintained exclusively on verapamil. The up-regulation of the serotonin transporter may be relevant to the previously reported beneficial effect of verapamil in affective disorders.

Blood Platelets↗
PubMed1990

Picrotoxin changes the effects of imipramine and desipramine in rats in the forced swimming test.

The aim was to find whether the chloride channel blocker, picrotoxin, at subconvulsant doses could affect the activity of imipramine or desipramine in the 'forced swimming' test with rats. It was found that picrotoxin enhanced the anti-immobility effects of imipramine and desipramine whereas open field activity remained unaffected or was even decreased by the same treatments. The results seem consistent with recent reports showing direct interactions between several antidepressant drugs and the GABAA receptor/benzodiazepine receptor/chloride ionophore complex (GABAA/benzodiazepine/Cl complex). The results also conform with the hypothesis that a reduction in the functionality of this complex could be related to the clinical effects of antidepressant drugs.

Animals↗
PubMed1992

The NMDA receptor antagonist MK-801 prevents imipramine-induced supersensitivity to quinpirole.

Chronic treatment with imipramine enhanced the locomotor stimulant response to quinpirole (0.3 mg/kg s.c.), a dopamine D2/D3 receptor agonist. Chronic, but not acute, blockade of the NMDA receptor with the non-competitive antagonist MK-801 (0.3 mg/kg i.p.) prevented the imipramine-induced potentiation of the quinpirole effect. The results suggest that NMDA receptors play a role in the development of supersensitivity to dopamine receptor agonists produced by chronic antidepressant treatment.

Animals↗
PubMed1993

Depletion of mesolimbic dopamine during behavioral despair: partial reversal by chronic imipramine.

Exposure of rate to the behavioral despair test (an animal model of depression) for 40 min resulted in a long-lasting depletion of mesolimbic dopamine output to about 40% of baseline values. The decrease in extracellular dopamine was partially prevented by chronic pretreatment with imipramine (20 mg/kg per day i.p. for 21 days). The results suggest that a fall in mesolimbic dopamine output may be associated with depressive states and indicate that changes in the functional status of the dopamine system contribute to the mechanism of action of imipramine.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Inhibition of neuronal nicotinic acetylcholine receptors by imipramine and desipramine.

The actions of two structurally related tricyclic antidepressants on neuronal nicotinic acetylcholine receptors were investigated in human neuroblastoma (SY-SY5Y) cells, using whole-cell patch-clamp recordings. Both desipramine and imipramine reversibly inhibited inward currents evoked by application of the nicotinic receptor agonist dimethylphenylpiperazinium iodide (30-300 microM) with IC50 values of 0.17 microM and 1.0 microM respectively (holding potential -70 mV). The degree of current inhibition caused by either tricyclic compound was unaffected by agonist concentration (30-300 microM). The effects of desipramine were voltage-independent over the range -40 mV to -100 mV, and inhibition caused by imipramine only increased very slightly with membrane hyperpolarization over the same range. These results indicate that tricyclic antidepressants can inhibit neuronal nicotinic acetylcholine receptors by mechanisms which are distinct from their actions at non-neuronal nicotinic acetylcholine receptors.

Desipramine↗
PubMed1994

The immobility response in the forced swim test: paradoxical effect of imipramine.

Rats immersed in a modified version of the forced swim test in which they are unable to touch the bottom of the cylinder with their feet while keeping their noses above water, initially paddle vigorously but eventually become relatively immobile. In the present study, we show that chronic treatment with imipramine and alprazolam increases rather than decreases the immobility response of rats in this test, whereas chronic treatment with propranolol is less effective. The results of this study indicate that the interpretation of the immobility response as 'behavioral despair', which is based on the response to the antidepressant drugs such as imipramine, needs to be reevaluated.

Alprazolam↗
PubMed1993

Immunoassay reagents for psychoactive drugs. II. The method for the development of antibodies specific to imipramine and desipramine.

Imipramine and desipramine were structurally modified by the attachment of spacer arms to the aromatic ring which were subsequently attached to bovine serum albumin. This approach utilized novel spacer arms and conjugation methods. This method yielded antisera with excellent selectivity and good titers. Rabbits were used to raise the antisera and the antibodies produced were characterized with respect to their cross-reactivity with imipramine, desipramine and hydroxy metabolites as well as selected structurally related compounds.

Animals↗
PubMed1988

Inhibition of platelet [3H]-imipramine binding by human plasma protein fractions.

Inhibition of high-affinity [3H]-imipramine binding to platelet membranes by human plasma fractions and isolated plasma proteins was investigated. Several plasma proteins were found to contribute to the observed apparent inhibition and this contribution was assessed in terms of inhibitor units. Alpha 1 acid glycoprotein, high density and low density lipoprotein, IgG and alpha 1-antitrypsin were identified as effective non-specific inhibitors. Alpha-1-acid glycoprotein was confirmed to be the most potent plasma protein inhibitor. Cohn fractions were evaluated for the presence of the postulated endocoid of [3H]-imipramine binding site.

Binding Sites↗
PubMed1991

Effects of thyroid status on the characteristics of alpha 1-, alpha 2-, beta, imipramine and GABA receptors in the rat brain.

The effects of a chronic treatment with L-triiodothyronine (T3; 100 mg/rat/day s.c. for 7 days) or with propylthiouracil (PTU; 50 mg/rat/day for 35 days by stomach tube) on the characteristics of alpha 1, alpha 2, beta, imipramine and GABA binding sites in different brain areas of the adult rat have been studied. T3-treatment caused an increase in the number of [3H]dihydroalprenolol and a decrease in the number of [3H]muscimol binding sites in the cerebral cortex. PTU-treatment caused a decrease in the number of [3H]prazosin, [3H]yohimbine and [3H]dihydroalprenolol binding sites in the cerebral cortex, while the number of [3H]imipramine binding sites was reduced in the cerebral cortex and hypothalamus, and increased in the hippocampus. Affinity constants were never modified. Concurrent experiments showed that the "in vitro" addition of T3 and PTU did not influence the binding of any of the ligands employed to control rat brain membranes. The present data further support the view that neurotransmission in the CNS is influenced by the thyroid status.

Animals↗
PubMed1992

An assay to measure the simultaneous uptake of [3H]dopamine and [14C]serotonin by the human platelet reveals an imipramine-insensitive [3H]dopamine uptake mechanism.

To determine whether a specific dopamine uptake mechanism is present on the human platelet the simultaneous uptake of [3H]dopamine and [14C]serotonin by platelets was measured. Utilising a dual radiolabel uptake technique, platelets have been shown to take up serotonin more rapidly and to a greater extent than they take up dopamine. Furthermore, at high concentrations serotonin was able to reduce dopamine uptake by platelets by 60% whereas dopamine had no effect on serotonin uptake. Similarly, imipramine and reserpine reduced (97% and 74% respectively) serotonin uptake by platelets in a dose-dependent manner, but did not affect the uptake of dopamine. Our data show that platelets take up dopamine by a mechanism independent of the imipramine-sensitive serotonin uptake mechanism. Furthermore, the increased capacity of platelets to store serotonin is because serotonin, unlike dopamine, is transported into the dense granules of the platelet.

Biological Transport↗
PubMed1977

The in vitro effects of imipramine on human chromosomes.

The clastogenic effects of imipramine on chromosomes have been investigated in leukocyte cultures from seven healthy blood donors (2 mlae and 5 female), repeat cultures being initiated at intervals of 6 to 12 weeks. At various times prior to harvesting nine different doses of imipramine were added in vitro, the three lowest concentrations being within the range of plasma levels reported in psychiatric patients reveiving the drug therapeutically. In addition, streptonigrin was used as a positive control. No increase in chromosome breaks was found at any concentration for any duration of exposure even in those cultures where high concentration and/or long duration of exposure significantly suppressed cell growth. Only cultures to which streptonigrin had been added showed a significant increase in chromosome breaks.

Adult↗