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PubMedDate not supplied

Interaction between thyroxine and tricyclic antidepressant drugs on cardiac neurotransmitter receptors.

The effect of chronic administration of desmethylimipramine (DMI) and iprindole on cardiac neurotransmitter receptors was studied. In addition, the influence of these drugs on the action of thyroxine (T4) on myocardial receptors was investigated. Administration of iprindole (10 mg/kg i.p., twice daily for 11 days) markedly increased the number of beta- adrenergic receptors in the heart and significantly reduced the affinity of these receptors for (-)[3H]dihydroalprenolol ([3H]DHA). Injection of T4 (500 mg/rat i.m., for 5 days) concomitantly with iprindole resulted in a lower beta-adrenergic receptor density that with iprindole treatment alone, but significantly higher than that measured in control rats. Affinity of the receptors for (-)[3H]quinuclidinyl benzilate ([3H]QNB) in heart membrane preparations of animals pretreated with T4 alone or with T4 plus iprindole was not different from control. Neither pretreatment with DMI nor with iprindole affected the density of cholinergic muscarinic receptors in the heart or their affinity for [3H]QNB. The decrease in cardiac cholinergic receptors induced by administration of T4 was not prevented by simultaneous injections of DMI. Combined administration of iprindole and T4 caused a reduction in the affinity of myocardial cholinergic muscarinic receptors, but restored the number of these receptors to normal. The results demonstrate distinct differences between DMI and iprindole in their effects on cardiac neurotransmitter receptors and in the influence of these drugs on the actions of T4 on receptors in the heart.

Animals↗
PubMed1984

Antidepressant drugs with varying pharmacological profiles alter rat pineal beta adrenergic-mediated function.

The effects of acute and chronic administrations of two antidepressant drugs with differing pharmacological profiles on pineal beta adrenergic receptor-mediated functions were examined in the rat. Animals were treated with control powdered food or with either imipramine or iprindole-containing diets (0.067%, w/w) for various time intervals. Animals were sacrificed during different phases of the light/dark cycle and pineal [3H]dihydroalprenolol (DHA) binding, N-acetyltransferase (NAT) activity, N-acetylserotonin (NAS) and melatonin levels were measured. Plasma drugs and metabolite concentrations were also assessed. A 3-day treatment with imipramine resulted in an unchanged pineal [3H] DHA binding and an increase in pineal serotonin (5-HT), NAS and melatonin. A comparable treatment with iprindole did not alter any pineal measures. Three weeks of imipramine treatment resulted in therapeutic plasma drug and metabolite concentrations and elicited a reduction (31%) in the density of pineal [3H] DHA binding. This treatment, in addition, suppressed the dark-induced activation of the intracellular enzyme NAT (38%) and the concentrations of NAS (25%) and melatonin (23%) without altering pineal 5-HT rhythm. No apparent shift was observed in the NAT, NAS and melatonin rhythms. Chronic treatment with the atypical antidepressant iprindole for 3 weeks resulted in-plasma iprindole concentrations of 76 ng/ml and a significant reduction (24%) in pineal 5-HT levels 5 hr into the dark phase of the light/dark cycle. Pineal NAT activity and NAS and melatonin content were not significantly reduced by this treatment. However, 4 weeks of iprindole ingestion produced plasma drug concentrations of 141 ng/ml and significantly reduced pineal [3H] DHA binding density (18%) without changing binding affinity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyltransferases↗
PubMed1982

The effect of some antidepressants on prejunctional muscarinic receptors on the sympathetic nerves of the isolated rabbit ear artery.

The antimuscarinic activity of amitriptyline, desipramine, iprindole, mianserin and viloxazine on prejunctional sympathetic nerve endings were compared in the isolated rabbit ear artery. In the presence of cocaine (10 micro M) and yohimbine (1 micro M), amitriptyline (0.5-1 micro M), desipramine (1-3 micro M) and iprindole (5-10 micro M) produced parallel rightward shifts of the concentration-response curve for the inhibitory effect of carbachol (CCh) on responses to electrical stimulation of the preparation at 3 Hz. Mianserin (3 micro M) produced some inhibition but altered the slope of the concentration-responses curve to CCh while viloxazine (less than or equal to 10 micro M) produced no inhibition. The depression of tritium efflux by CCh from arteries preincubated in 3H-noradrenaline was inhibited significantly (P less than 0.05) by amitriptyline (0.1 micro M) and desipramine (1 micro M) and not by iprindole (17 micro M), mianserin (3 micro M) or viloxazine (10 micro M). Amitriptyline was 10-fold more active than desipramine and at least 30-fold more active than the other antidepressants as a muscarine receptor blocking drug in this preparation. Thus, mianserin, viloxazine and iprindole exhibit much weaker antimuscarinic activity relative to amitriptyline on prejunctional muscarine receptors on sympathetic nerve endings compared with that observed by others for excitatory muscarine receptors in sympathetic ganglia. The findings support an earlier suggest that these receptors differ.

Animals↗
PubMed1997

Atypical antidepressants inhibit depolarization-induced calcium uptake in rat hippocampus synaptosomes.

The effect of the atypical antidepressants mianserin, iprindole, and fluoxetine on synaptosomal calcium uptake was tested under conditions where a selective action on voltage-dependent calcium channels can be documented. Synaptosomes from rat hippocampus were incubated with 45calcium either in choline-rich medium or in depolarizing (60 mM K+) choline-rich medium, and drug effects on calcium uptake in these two conditions, as well as on the net depolarization-induced calcium uptake, were studied in the range of concentrations 0.6-200 microM. A concentration-dependent marked inhibition of uptake in depolarizing choline medium was observed for the three antidepressants, whereas only a minor degree of inhibition of uptake in resting choline medium was present at the highest drug concentration; as a result, the concentration-effect relationships exhibited a strong concentration-dependent inhibition of net depolarization-induced calcium uptake. The IC50 values, calculated by interpolation of the last three or four points of the concentration-effect relationships, were 27, 39, and 68 microM for fluoxetine, iprindole, and mianserin, respectively. Significant degrees of calcium channel inhibition are not expected at brain concentrations of mianserin and iprindole that are likely to be encountered during clinical use; however, the fluoxetine concentration-effect relationship established in the present study, coupled with the published ratio of 20:1 for brain:plasma concentrations of fluoxetine-norfluoxetine in humans, suggests that brain calcium channel function could be appreciably reduced in some patients treated with this atypical antidepressant.

Animals↗
PubMed1985

Evidence of dopamine involvement in the effect of repeated treatment with various antidepressants in the behavioural 'despair' test in rats.

Daily treatment for 7 days with 5 mg/kg nomifensine, 20 mg/kg amineptine, 10 mg/kg mianserin or 20 mg/kg iprindole reduced the immobility time in the behavioural 'despair' test in rats. No stimulation of motor activity was found with any of the drugs, and iprindole and mianserin actually reduced the activity of rats in an open field. The anti-immobility effect of the various antidepressants was significantly counteracted by 0.5 mg/kg haloperidol or 100 mg/kg sulpiride. These doses of neuroleptics alone did not significantly modify the immobility time of rats not treated with the antidepressant compounds. As previously found for desipramine and amitriptyline, the data suggest that dopamine is involved in the anti-immobility effect in rats of repeated treatment with nomifensine, amineptine, mianserin and iprindole.

Animals↗
PubMed1986

Chronic treatment with antidepressant drugs and the analgesia induced by 5-methoxy-N,N-dimethyltryptamine: attenuation by desipramine.

The effect of chronic and acute oral or intraperitoneal treatment with the antidepressant drugs, desipramine, amitriptyline, alaproclate and iprindole, upon pain thresholds in the tail flick, hot plate and shock titration tests of nociception in saline- and 5-MeODMT-treated rats was studied. Chronic desipramine treatment increased the pre-test tail flick latencies. In the saline-treated rats, chronic oral desipramine treatment increased tail flick latencies, whereas chronic oral amitriptyline treatment decreased tail flick latencies. In 5-MeODMT-treated rats, chronic oral desipramine treatment attenuated the effects of 5-MeODMT (1 mg/kg) in all three tests of nociception, whereas chronic amitriptyline caused a potentiation in the tail flick and hot plate tests. Chronic oral iprindole treatment attenuated 5-MeODMT-induced analgesia in the hot plate test. Chronic intraperitoneal desipramine treatment attenuated 5-MeODMT analgesia in the tail flick and shock titration tests. In a different chronic treatment experiment, oral desipramine treatment attenuated 5-MeODMT analgesia in the tail flick test and zimeldine did for both the tail flick and hot plate tests, whereas mianserin potentiated 5-MeODMT-induced analgesia in both the tail flick and hot plate tests. In the saline-treated rats, acute treatment with all four drugs, desipramine, amitriptyline, iprindole and alaproclate, elevated the shock thresholds, whereas in 5-MeODMT-treated rats, desipramine and amitriptyline elevated shock thresholds. Two main conclusions can be drawn: chronic desipramine caused a quite consistent attenuation of 5-MeODMT-induced analgesia and the effects of acute treatment differed strongly from that of the chronic treatment. The effects of chronic administration with these antidepressants were compared with other findings using different measures of behavioural and receptor function.

Analgesics↗
PubMed1990

Recent studies on the MAO inhibitor phenelzine and its possible metabolites.

Although N2-acetylphenelzine (N2AcPLZ) appears to be only a minor metabolite of phenelzine (PLZ), other investigations have demonstrated that it may be worthy of study as an antidepressant in its own right. In the present report, the possibility of ring hydroxylation as a metabolic route for PLZ was investigated in the rat. Indirect evidence for such a route was obtained using iprindole, a drug known to block ring hydroxylation. Treatment of rats with iprindole followed by PLZ was demonstrated to result in increased brain levels of PLZ and beta-phenylethylamine (control rats were treated with vehicle and then PLZ). The possibility that hydroxylation in the para-position might be a metabolic route for PLZ has led to interest in the possible use of analogues in which this position is blocked with a substituent. In preliminary acute studies at a dose of 0.1 mmol/kg p-chloro-PLZ was found to have a similar effect to PLZ on the inhibition of MAO and to lead to an elevation of catecholamines and 5-hydroxytryptamine (5-HT) in rat whole brain.

Animals↗
PubMed1975

Behavioral effects of thymoleptics in vervet monkeys (Cercopithecus aethiops).

Desmethylimipramine (DMI) exerts diverse quantitative effects on the gross behaviour of monkeys. Excitatory as well as sedative effects were observed, which varied according to the general animal temperament. Results resembling those obtained with DMI were observed using chlorimipramine and iprindole, although the effects of iprindole were less marked. Chlorimipramine also produced immobilization and postural change. The results are discussed in relation to behavioral effects of thymoleptics in humans, and the use of monkeys in preclinical testing of thymoleptic drugs is suggested.

Animals↗
PubMed1982

Adrenocortical function of rats under prolonged administration of lipidosis-inducing drugs.

The influence of three potent lipidosis-inducing agents, i.e. iprindole, triparanol and chloroquine, on the rat adrenal cortex was investigated by determination of the corticosterone excretion in the urine, the responsiveness to ACTH and by determination of the corticosterone content of the adrenals and of the corticosterone concentration in plasma. Administration of iprindole and triparanol left the function of the adrenal cortex unaffected, while under chloroquine treatment an activation with time was observed. Morphologically, similar degrees of lipidosis were found in all experiments. The results demonstrate that the functional capacity of the rat adrenal cortex is not directly correlated to lipidotic alterations.

Adrenal Cortex↗
PubMed1976

A possible common mechanism of action of antidepressant treatments: reduction in the sensitivity of the noradrenergic cyclic AMP gererating system in the rat limbic forebrain.

The response of the noNEpinephrine (NE) sensitive cyclic AMP generating system in slices of the rat limbic forebrain after both the acute and chronic administration of the tricyclic antidepressants desipramine (DMI) and iprindole as well as electro-convulsive treatment (ECT) was investigated. Neither the basal level of cyclic AMP nor the hormonal response to NE were altered after administration of a single dose of short term treatment with DMI and iprindole. However, the administration of the antidepressants on a clinically more relevant time basis markedly reduced the sensitivity of the cyclic AMP generating system to NE. This change in sensitivity was not related to the levels of the drugs in brain. The response of cyclic AMP to NE was also reduced by ECT, but the onset of this action was shorter than that observed with the antidepressants. ECT also antagonized the enhanced response of cyclic AMP to NE following destruction of central adrenergic nerve terminals with 6-hydroxydopamine. It thus appears that the therapeutic action of tricyclic antidepressants could be related to postsynaptic adaptive changes in the sensitivity of the noradrenergic adenylate cyclase receptor system rather than to acute presynaptic events.

Animals↗
PubMed1981

Alpha 2-adrenoreceptors on human platelets: selective labelling by [3H]clonidine and [3H]yohimbine and competitive inhibition by antidepressant drugs.

[3H]Clonidine and [3H]yohimbine have been used to characterize alpha 2-adrenoreceptors on human platelets. At 25 degrees C binding was rapid (t 1/2 of association, 1.8 and 2.7 min) and reversible (t 1/2 of dissociation, 0.5 and 8.2 min). The binding sites for [3H]clonidine and ]3H]yohimbine showed the specificity required for an alph 2-adrenoreceptor. The rank order of potency of inhibitors of [3h[clonidine binding was clonidine greater than yohimbine greater than phenylephrine greater than prazosin and of [3H]yohimbine binding was yohimbine greater than clonidine greater than phenylephrine greater than prazosin. Scatchard analysis of [3H]yohimbine binding indicated the existence of a single population of noninteracting sites (KD = 3.0 nM; Bmax = 188 fmol/mg protein). The high-affinity binding of [3H-clonidine had a lower affinity and a lower number of sites (KD = 5.0 nM; Bmax = 35 fmol/mg protein). [3H]Clonidine binding also showed evidence of a second site of much lower affinity and greater number (KD = 18.6 nM; Bmax = 77 fmol/mg protein) in 40% of the normal population. In vitro, antidepressant drugs competed with [3H]clonidine and [3H]yohimbine for the platelet alpha 2-adrenoreceptor. The rank order of potency of inhibitors of [3H]clonidine binding was mianserin greater than amitriptyline greater than iprindole greater than desipramine and of [3H]yohimbine binding was mianserin greater than amitriptyline greater than desipramine greater than iprindole. The inhibition constants (Ki) of adrenergic drugs and of various antidepressant drugs in competing with [3H]clonidine were correlated with the inhibition constants of these drugs in competing with [3H]yohimbine (r = 0.970; P less than 0.001) which suggests that both radioligands labelled the same alpha 2-adrenoreceptor on the human platelet. The inhibition of binding induced by all antidepressant drugs was competitive. In contrast, long-term administration of tricyclic antidepressant drugs to patients was recently found to be associated with a decrease in the number of binding sites for [3H]clonidine on platelet membranes. The present results indicate that both [3H]clonidine and [3H]yohimbine are useful tools for the quantification of alpha 2-adrenoreceptors on blood platelets and suggests that the specific binding of radiolabelled alpha 2-adrenoreceptor ligands to human platelet membranes might be used to monitor changes in alpha 2-adrenoreceptors during tricyclic antidepressant drug treatment.

Adult↗
PubMed1984

Changes in amphetamine-induced anorexia and stereotypy during chronic treatment with antidepressant drugs.

Amphetamine-induced anorexia and stereotyped behaviour were studied in rats, following pretreatment with the antidepressants DMI, inprindole and mianserin. A complex drug-dependent and dose-dependent pattern of results was obtained. Acute pretreatment with DMI and iprindole enhanced amphetamine anorexia and stereotypy; at high doses only, the enhancement of anorexia disappeared during chronic treatment. Mianserin had no effects acutely, but chronic treatment with high doses attenuated anorexia and enhanced stereotypy. High doses of all three drugs attenuated anorexia and enhanced stereotypy during withdrawal. The most parsimonious account of these results is that the acute affects of DMI and iprindole are artefactual, and that chronic administration of all three antidepressants increased dopaminergic function and decreased beta-adrenergic function.

Animals↗
PubMed1987

Regulation of high- and low-affinity [3H]imipramine recognition sites in rat brain by chronic treatment with antidepressants.

Specific binding of [3H]imipramine to its recognition sites in frontal cortex and levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE) as well as uptake of serotonin by crude synaptosomal (P2) fraction were determined in a group of rats chronically (for 21 days) treated with different types of antidepressant drugs: nortriptyline, fluoxetine, iprindole, phenelzine (10 mg/kg per day), maprotiline (20 mg/kg per day) and vehicle only (controls). Quantitative analysis of imipramine competition curves confirmed the existence of two classes of [3H]imipramine sites: high-affinity with IC50 and 11.2 nM and low-affinity with IC50 of 630 nM for the competing ligand. The proportion of high- and low-affinity sites was 73 +/- 4 and 26 +/- 4%, respectively. Chronic treatment with all antidepressant drugs except iprindole significantly decreased the affinity but not the proportion of high-affinity sites for imipramine. IC50 of imipramine at low-affinity sites was even more markedly increased at low-affinity sites by all treatments except for phenelzine. Fluoxetine was by far the most effective in altering the affinity of both high- and low-affinity [3H]imipramine recognition sites. Both NE and 5-HT levels were significantly enhanced only by phenelzine treatment, whereas 5-HT and 5-HIAA levels were found to be lower after fluoxetine. Kinetics of 5-HT uptake were altered significantly only in rats treated with fluoxetine: rate of 5-HT uptake (Vmax) was decreased by 43% and Km value increased from 104 to 184 nM. Changes in affinity of imipramine for its binding sites were not found to be associated with the effect of tested drugs on 5-HT levels or uptake. They may be due to adaptive alterations in physico-chemical properties of binding proteins although the presence of residual drug interfering with the binding assay cannot be excluded. The observed changes are likely to represent the condition during chronic administration of these drugs in clinical therapy of depression.

Animals↗
PubMed1992

Protection against amphetamine-induced neurotoxicity toward striatal dopamine neurons in rodents by LY274614, an excitatory amino acid antagonist.

LY274614, 3SR,4aRS,6SR,8aRS-6-[phosphonomethyl]decahydr oisoquinoline-3- carboxylic acid, has been described as a potent antagonist of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. Here its ability to antagonize the prolonged depletion of dopamine in the striatum by amphetamine in iprindole-treated rats is reported. A single 18.4 mg/kg (i.p.) dose of (+/-)-amphetamine hemisulfate, given to rats pretreated with iprindole, resulted in persistent depletion of dopamine in the striatum 1 week later. This prolonged depletion of dopamine in the striatum was antagonized by dizocilpine (MK-801, a non-competitive antagonist of NMDA receptors) or by LY274614 (a competitive antagonist of NMDA receptors). The protective effect of LY274614 was dose-dependent, being maximum at 10-40 mgkg (i.p.). A 10 mg/kg dose of LY274614 was effective in antagonizing the depletion of dopamine in the striatum, when given as long as 8 hr prior to amphetamine but not when given 24 hr prior to amphetamine. Depletion of dopamine in the striatum was also antagonized when LY274614 was given after the injection of amphetamine; LY274614 protected when given up to 4 hr after but not when given 8 or 24 hr after amphetamine. The prolonged depletion of dopamine in the striatum in mice, given multiple injections of methamphetamine, was also antagonized dose-dependently and completely by LY274614. The data strengthen the evidence that the neurotoxic effect of amphetamine and related compounds toward nigrostriatal dopamine neurons involves NMDA receptors and that LY274614 is an NMDA receptor antagonist with long-lasting in vivo effects in rats.

Amino Acids↗
PubMed1982

Effects of acute and subacute antidepressant treatment on kindled seizures in rats.

The effects of acute and subacute administration of the tricyclic antidepressants imipramine and amitriptyline, and the atypical antidepressants mianserin and iprindole, on seizures kindled from the amygdala and the cortex were examined. Whereas amitriptyline selectively antagonized seizures kindled from the amygdala after a single dose, neither amitriptyline nor imipramine was any more effective in antagonizing seizures kindled from the amygdala than from the cortex following subacute treatment. Both acute and subacute administration of iprindole failed to significantly alter seizures kindled from either site. Although only the highest acute dose of mianserin tested selectively attenuated amygdaloid seizures, a lower dose that was ineffective when given acutely, was selective when given subacutely. In contrast to an earlier report, the present findings suggest that kindling may not be a particularly useful model for the evaluation of potential antidepressant agents.

Amitriptyline↗
PubMed1988

Dose-dependent down-regulation of beta-adrenergic receptors after chronic intravenous infusion of antidepressants.

1. The effects of intravenous infusion of desipramine (1, 3, 10, and 60 mg/kg/day), amitriptyline, zimelidine, iprindole (3, 10, 30, 60, and 100 mg/kg/day each), imipramine (10, 30, and 100 mg/kg/day), or U-48753E (1, 3, 10, and 30 mg/kg/day) on the density of central beta-adrenergic receptors (beta-AR) were investigated in female Sprague-Dawley rats. 2. Desipramine, amitriptyline, zimelidine, iprindole, imipramine, and U-48753E dose-dependently reduced the density of beta-AR in the cerebral cortex. 3. The time of onset of down-regulation of beta-AR was negatively correlated with the doses of drugs. 4. At equipotent doses, antidepressants seem to have a similar profile for the time of onset of reduction in the density of beta-AR. 5. The results indicate that down-regulation of beta-AR may be involved in mediating the therapeutic effects of antidepressants, and this effect can be rapidly achieved by intravenous infusion of drugs.

Amitriptyline↗
PubMed1991

Effect of subchronic antidepressants administration on serotonin-stimulated phosphoinositide hydrolysis in para-chlorophenylalanine-treated rat hippocampal slices.

1. This study examines the effect of subchronic parachlorophenylalanine (PCPA) treatment upon serotonin (5-HT)-stimulated inositol monophosphate (IP-1) accumulation in rat hippocampal slices and also the effect of antidepressants upon this 5-HT response in the hippocampus from rats treated with or without concurrent administration of PCPA. 2. For high dose PCPA treatment, animals were injected intraperitoneally with 300 mg/kg daily for the first 5 days and then 100 mg/kg for 5 days, while for low dose PCPA treatment animals were injected for 10 days at a dose of 100 mg/kg. Imipramine or iprindole (15 mg/kg i.p.) was given once daily for 10 consecutive days. 3. 10-Day treatment with high dose of PCPA resulted in a significant increase in 5-HT-stimulated IP-1 accumulation, whereas low dose of PCPA had no significant effect upon the 5-HT response as compared to vehicle. 5-HT-stimulated IP-1 accumulation in rat hippocampus was not affected by subchronic treatment with imipramine or iprindole. The enhancement of the 5-HT response induced by high dose of PCPA was not attenuated by repeated antidepressants treatment.

Animals↗
PubMed1996

d-Amphetamine interaction with glutathione in freshly isolated rat hepatocytes.

Hepatocellular damage has been reported as a consequence of amphetamine intake for which little is known about the respective biological mechanisms involved. To give a better insight of cellular d-amphetamine effects, the present study was performed to evaluate d-amphetamine effects on glutathione homeostasis, in vitro, using freshly isolated rat hepatocytes. Cell viability and lipid peroxidation were also evaluated. Incubation of freshly isolated rat hepatocytes with d-amphetamine (0.08, 0.20, 0.40, and 2.00 mM) induced a concentration dependent glutathione depletion which was observed at all times (1, 2, and 3 h of incubation). After 3 h of incubation, cellular GSH decreased to 85%, 78%, 71% and 47% of control levels for the referred concentrations, respectively. At the third hour of incubation, GSSG levels were only slightly increased for the three higher concentrations of d-amphetamine. The mass spectral study of the methanolic supernatants obtained from hepatocytes incubated with all d-amphetamine concentrations revealed the presence of the p-hydroxyamphetamine glutathione adduct (glutathion-S-yl)-p-hydroxyamphetamine. Pretreatment of hepatocytes with the P450 inhibitors metyrapone (1 mM) and iprindole (10 microM) significantly prevented the glutathione depletion induced by d-amphetamine. This inhibition was more effective for iprindole than for metyrapone. Incubation of isolated hepatocytes with p-hydroxyamphetamine (0.10 mM) for 3 h did not result in any modification of cell viability or GSH or GSSG levels. Also, in the mass spectrum study performed on these samples, the characteristic adduct obtained for d-amphetamine incubations was not detected. The above data suggest that the observed glutathione depletion induced by d-amphetamine is at least in part due to the conversion of d-amphetamine into (glutathion-S-yl)-p-hydroxyamphetamine and that P450 2D seems to have an important role in this metabolism. In spite of the results obtained, showing glutathione homeostasis alterations, incubation of freshly isolated rat hepatocytes with d-amphetamine did not result in any modification of cell viability or lipid redox status.

Animals↗