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At least 937 records · Page 52Linked to original sources
PubMed1990

Dopaminergic mechanism of imipramine action in an animal model of depression.

Rats, subjected chronically (10-12 weeks) to a variety of mild, unpredictable stressors, showed a decrease in their consumption of weak sucrose solutions; normal behavior was restored by chronic (5-9 weeks) treatment with the tricyclic antidepressant imipramine. Acute administration of the dopamine receptor antagonist pimozide or the specific dopamine D2 receptor antagonist raclopride had no effect in nonstressed animals and in vehicle-treated stressed animals, but both drugs selectively reversed the improvement of performance in imipramine-treated stressed animals. The 5HT antagonist metergoline increased sucrose consumption in all groups. The data suggest that the mechanism of action of imipramine in this model is an increase in functional activity at dopamine (DA) synapses.

Animals↗
PubMed1992

Platelet imipramine binding and plasma cortisol levels in Israeli civilians during the Gulf War.

[3H] Imipramine binding to platelets and plasma cortisol levels were measured in nine Israeli civilians before, during, and after repeated missile attacks. Hamilton Anxiety Rating Scale (HARS), and Beck Depression Inventory (BDI) were similar before and during the war and decreased significantly after the war. A trend toward increase in platelet imipramine binding values was observed during the war when compared with the postwar values (19%; p = 0.056), and/or when compared with prewar values (26%; p = 0.063). However, one-way analysis of variance with repeated measures did not reveal a significant statistical difference [F (2,6) = p = 2.07; NS] among the three time points. A significant correlation was found between HARS score, but not BDI, and imipramine binding values in the prewar and postwar time points (r = 0.87; 0.71, respectively). Plasma cortisol levels did not alter significantly during the study period.

Adjustment Disorders↗
PubMed1994

Effects of treatment with imipramine and clonazepam on an animal model of panic disorder.

Tonic GABAergic inhibition in the dorsomedial hypothalamus (DMH) has been shown to regulate a constellation of behavioral and physiological responses that resemble a human panic attack. The present study was aimed at testing if the panic-like response elicited by injecting gamma-aminobutyric acid (GABA) antagonists into the DMH can be blocked by pretreating the animals with the antipanic drugs, imipramine and clonazepam. Rats were fitted with arterial catheters and bilateral chronic microinjection cannulae in the DMH. Their baseline heart rate, respiratory rate, blood pressure and "anxiety" (measured by the social interaction test) responses to injection of the GABAA antagonist bicuculline methiodide (BMI) into the DMH were recorded. After treatment in a double-blind manner with vehicle, imipramine (5 and 15 mg/kg, 7 days), and clonazepam (5 mg/kg, 3 days), the response to BMI microinjection into the DMH was once again recorded. Both imipramine and clonazepam, but not vehicle treatments blocked the BMI response.

Analysis of Variance↗
PubMed1994

Studies of a neurochemical link between depression, anxiety, and stress from [3H]imipramine and [3H]paroxetine binding on human platelets.

We measured platelet [3H]imipramine and [3H]paroxetine binding in patients with major depression (n = 11), dysthymia (n = 9), generalized anxiety (n = 18) and panic disorder (n = 10), and in healthy controls (n = 13). The [3H]imipramine binding capacity (Bmax) was lower in all patient groups; [3H]paroxetine binding was reduced in anxiety disorders, however, decreases in depression and dysthymia were not significant. There were no differences in the affinity constant (Kd) for either radioligand. We also examined the effects of examination stress on platelet binding in medical students. Compared to after vacation, when binding was similar to controls, [3H]imipramine (n = 19) and [3H]paroxetine (n = 14) Bmax values were significantly decreased during examinations and similar to patient values. Examinations were also associated with an increase in plasma cortisol levels. These findings suggest that there is a neurochemical link between depression, anxiety, and stress, and that disturbances in neurochemical functioning may be associated with specific symptomatology, independent of psychiatric diagnosis.

Adult↗
PubMed1983

The detection of specific [3H]imipramine binding in bovine retina.

Using [3H]imipramine, specific imipramine binding was demonstrable in the crude membrane homogenate of bovine retina. Scatchard analysis of the saturation experiments revealed an apparent dissociation constant (Kd) of 6.4 nM and a maximal number of binding sites of 780 fmol/mg protein. These results and the substrate specificity show that the properties of imipramine binding to retinal membranes are essentially the same as described for the rat brain.

Animals↗
PubMed1989

[3H]imipramine binding in discrete brain areas is affected by castration in male rats.

In adult male rats, castration induces a progressive decrease in the number of [3H]imipramine binding sites in the cerebral cortex and hypothalamus, and a progressive increase in the hippocampus. Testosterone completely prevents this effect of castration, but has no effect on the characteristics of brain imipramine binding sites in intact, non-castrated animals. These data suggest that threshold levels of testosterone are necessary for the maintenance of a normal number of imipramine binding sites in the rat brain, but that these binding sites are not modified by excess testosterone.

Animals↗
PubMed1979

Trazodone and imipramine: comparative effects on canine cardiac conduction.

Lead II EKG and His bundle electrograms were recorded in closed-chest pentobarbital-anesthetized dogs. Trazodone, a structurally distinct, new antidepressant agent, had no effect on His--Purkinje (HV interval) or intraventricular (HS interval) conduction following intravenous injection at graded doses between 1 and 30 mg/kg. In contrast, the tricyclic psychotropic agent imipramine (0.5--5 mg/kg) significantly slowed impulse conduction as indicated by increases in both the HV and HS intervals. Imipramine (5 mg/kg) also slowed impulse transmission across the atrium (PA interval). These responses to imipramine were associated with a concurrent prolongation of both the PR interval and QRS duration. In the anesthetized dog, trazodone administration promoted no evidence of heart block or sign of rhythm disturbances other than slowing in normal sinus rhythm.

Animals↗
PubMed1982

Effects of chronic lithium, clorgyline, imipramine, fluphenazine and constant darkness on the alpha-melanotropin content and circadian rhythm in rat brain.

The effects of constant darkness, chronic lithium, clorgyline, imipramine and fluphenazine treatment on the content and diurnal rhythm of alpha-MSH in rat forebrain were investigated. The persistence of the alpha-MSH rhythm in constant darkness demonstrated that the rhythm was circadian in nature. Constant darkness increased the 24 h mean alpha-MSH concentration in brain while lithium, fluphenazine and imipramine decreased it. In addition, imipramine and clorgyline delayed the phase of the alpha-MSH circadian rhythm while lithium advanced it.

Animals↗
PubMed1983

In vitro and in vivo inhibition of [3H]imipramine binding by cadmium.

Chronic exposure of rats to CdCl2 altered the specific binding of [3H]imipramine to membranes from platelets and hypothalamus. There was a decrease in Bmax of 10-40% and a decrease in KD values of 30-40% as compared to the control group. In vitro studies on the inhibition of [ 3H ]imipramine binding to membranes from human and rat platelets and hypothalamus by CdCl2 corroborate the in vivo results which imply that the imipramine binding protein contains Cd2+-sensitive groups.

Animals↗
PubMed1983

Temperature-sensitive conformational changes in membrane-bound and solubilized [3H]imipramine binding sites.

[3H]Imipramine binding sites are located on serotonergic nerve terminals and on blood platelets. Previous studies on our laboratories have indicated temperature-sensitive conformational changes in [3H]imipramine binding sites in hippocampal and cerebral cortex membranes. We now report that similar changes are observed in both membrane-bound and digitonin-solubilized [3H]imipramine binding sites of human blood platelets. This may indicate integrity of the solubilized binding site.

Animals↗
PubMed1984

[3H]Imipramine binding and [3H]5HT uptake in human blood platelets: changes after one week chlorimipramine treatment.

In platelets of normal volunteers taking chlorimipramine (50 mg/day) for one week, the saturable uptake of [3H]5HT was fully inhibited at day 8, but returned to control values at day 15. The Bmax of [3H]imipramine binding was decreased by 65% at day 8 and remained significantly below control values at day 15. If the present findings can be extrapolated to other antidepressants, the reported decreases in [3H]imipramine binding in depression may partly reflect residual treatment effects. It cannot be excluded that, in depression, the platelet [3H]imipramine receptor already is down-regulated maximally which would preclude a further down-regulation due to antidepressant drug therapy.

Adult↗
PubMed1984

Human platelets possess multiple [3H]imipramine binding sites.

Scatchard analysis of [3H]imipramine binding to human platelets over the concentration range of 0.1-250 nM revealed a biphasic concave upward curve. Computer-assisted analysis indicated the best fit of the data by a two-site model with apparent Kd values of 0.68 and 293 nM and apparent Bmax values of 802 fmol/mg protein and 12.72 pmol/mg protein for the high- and low-affinity components, respectively. These results demonstrate the complex manner in which [3H]imipramine binding to human platelets, suggesting a reason for inconsistencies in Bmax values reported in the literature. Further studies of these low- as well as high-affinity sites may help elucidate the functional role of [3H]imipramine binding sites in affective disorders.

Blood Platelets↗
PubMed1984

Size determination of binding polymers for [3H]imipramine and [3H]paroxetine in human platelet membranes.

Imipramine and paroxetine both inhibit the transport of serotonin in serotonergic neurons and in platelets; furthermore specific high affinity binding sites for [3H]imipramine and [3H]paroxetine are located in these two cell types, probably on the serotonin transport mechanism. However, previous studies indicated that the binding site for [3H]imipramine was different from the binding site for [3H]paroxetine. We now report that the polymers on which the two binding sites are located have different molecular weights.

Blood Platelets↗
PubMed1988

Inhibition of sodium-dependent [3H]imipramine binding in rat brain by serotonin and serotonin uptake inhibitors.

The sodium-dependent component of [3H]imipramine binding in rat cerebral cortex was completely displaced by serotonin and non-tricyclic (fluoxetine) as well as tricyclic (clomipramine) serotonin uptake inhibitors. The competition curves were monophasic yielding pseudo-Hill coefficient close to unity and IC50 values of 89, 10 and 6 nM, respectively for serotonin, fluoxetine and clomipramine. The Ki of serotonin for the sodium-dependent [3H]imipramine binding was within the range of its Km for the uptake process. These results suggest that sodium-dependent [3H]imipramine sites relevant for serotonin uptake may be the same as the substrate recognition sites on the serotonin transporter.

Animals↗
PubMed1989

Effects of dihydropyridine drugs on reversal by imipramine of helpless behavior in rats.

The present study was undertaken in order to determine the effects of the dihydropyridine calcium channel blocker, nimodipine and the dihydropyridine calcium channel activator BAY k 8644, in the learned helplessness test in the rat. Nimodipine dose dependently (0.5-2 mg/kg per day) reversed the behavioral deficit induced by inescapable shocks. The reversal of helpless behavior by imipramine (32 mg/kg per day) was antagonized by BAY k 8644 (0.5 and 1 mg/kg per day), and the effects of imipramine 8 and 16 mg/kg per day) were potentiated by a subeffective dose (0.5 mg/kg per day) of nimodipine. These results suggest that central dihydropyridine binding sites may be specifically involved in the modulation of the imipramine reversal of helpless behavior and favor a physiological role for dihydropyridine binding sites in the brain.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

In vivo action of phosphatidylserine, amitriptyline and stress on the binding of [3H]imipramine to membranes of the rat cerebral cortex.

Liposomes of bovine brain phosphatidylserine and of phosphatidylcholine were prepared and injected i.p. into rats for 5 days. Another group received i.p. injections of amitriptyline in addition to phosphatidylserine. Subgroups of control and phosphatidylserine-injected rats were submitted to an acute swimming stress for 15 min. The number of [3H]imipramine binding sites in the phosphatidylserine-injected rats, decreased 23% whereas there was no change in the phosphatidylcholine-injected rats. The combination of amitriptyline and phosphatidylserine produced a more marked reduction in [3H]imipramine binding (-47%). Control rats undergoing acute stress showed a 30% decrease in [3H]imipramine binding whereas the stress did not significantly change the control values of the phosphatidylserine-treated animals. These findings are discussed in relation to the known action of phosphatidylserine on several neurotransmitter systems and on the potentiation of antidepressant effects.

Amitriptyline↗
PubMed1989

Imipramine and tetrabenazine: effects on monoamine receptor binding sites and phosphoinositide hydrolysis.

Treatment of rats for 21 days with tetrabenazine, a drug which depletes monoamines and is used behaviorally to screen for antidepressants, significantly decreased 5-HT2 receptor density, increased alpha 1-adrenoceptor density but did not alter beta-adrenoceptor density in homogenates of frontal cortices labeled with [3H]ketanserin, [3H]prazosin and [3H]dihydroalprenolol, respectively. These effects were not opposite to those of the antidepressant drug imipramine which decreased both 5-HT2 and beta-adrenoceptor density and did not alter alpha 1-adrenoceptor density. Some evidence for antagonistic interactions between the two drugs was found in that imipramine partially prevented the tetrabenazine-induced increase in alpha 1-adrenoceptor density and tetrabenazine partially prevented the imipramine-induced decrease in beta-adrenoceptor density. Neither drug altered phosphoinositide hydrolysis coupled to alpha 1-adrenoceptors. While the effects of tetrabenazine are frequently attributed to its reserpine-like action of depleting monoamines, these results provide the first indication that tetrabenazine alters 5-HT2 and beta-adrenoceptor density in a manner different from that of reserpine.

Animals↗
PubMed1989

Antidepressant action of imipramine and iprindole in mice is enhanced by inhibitors of enkephalin-degrading peptidases.

The implication that opioid peptides are involved in the action of the antidepressants imipramine and iprindole was investigated in mice by using the forced swimming test as an experimental model of depression. Both the drugs were found to shorten the immobility time in this test. This effect of imipramine and iprindole was reversed by the opiate antagonist naloxone. Moreover, when subeffective doses of either imipramine or iprindole were given together with an intracerebroventricular injection of an inhibitor of their degradation (thiorphan or bestatin), the immobility time was again decreased. Interestingly, the reduction of the time of immobility was found to be not related to the effect of the drugs on locomotor activity. These data might be taken as further evidence for the involvement of opioid peptides in the pharmacological action of antidepressant drugs.

Animals↗