The present study was undertaken to investigate the effect of aqueous and ethanolic extracts of T. bellirica on depression in mice using forced swim test (FST) and tail suspension test (TST). The extracts were administered orally for 10 successive days in separate groups of Swiss young male albino mice. Aqueous extract (50, 100 and 200 mg/kg) in a dose-dependent manner and ethanolic extract (100 mg/kg) significantly reduced the immobility time of mice in both FST and TST. The extracts were without any significant effect on locomotor activity of mice. The efficacies of aqueous extract (200 mg/kg) and ethanolic extract (100 mg/kg) were found to be similar to that of imipramine (15 mg/kg, po) and fluoxetine (20 mg/kg, po) administered for 10 successive days. Both extracts reversed reserpine-induced extension of immobility period of mice in FST and TST. Prazosin (62.5 microg/kg, ip; an alpha1-adrenoceptor antagonist), sulpiride (50 mg/kg, ip; a selective D2 receptor antagonist) and p-chlorophenylalanine (100 mg/kg, ip; an inhibitor of serotonin synthesis) significantly attenuated the aqueous and ethanolic extract-induced antidepressant-like effect in TST. Thus, both the aqueous and ethanolic extracts of T. bellirica elicited a significant antidepressant-like effect in mice by interaction with adrenergic, dopaminergic and serotonergic systems.
Subtoxic doses of physostigmine have been found to potentiate the convulsive toxicity and lethality of amitriptyline and imipramine in CD1 and B6A mice. Neostigmine failed to potentiate the toxicity and lethality of imipramine. Physostigmine tended to protect mice against atropine-induced lethality. These data suggest the site of toxicity of this drug-drug interaction between the tricyclic antidepressants and physostigmine may be occurring in the CNS through a mechanism distinct from the anticholinergic actions of the antidepressants.
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Presynaptic inhibition of the extensor (quadriceps, QUAD) monosynaptic reflex (MSR) in unanaesthetized decerebrate cats was antagonized by imipramine hydrochloride (2-5 mg/kg), 5-hydroxytryptophan (75 mg/kg) and a specific 5-hydroxytryptamine (5-HT) neuronal uptake blocker, fluoxetine hydrochloride (Lilly 110140, 0.25-6 mg/kg). These effects of imipramine and fluoxetine were partially reversed by the 5-HT antagonist, cyproheptadine hydrochloride (5 mg/kg), and completely reversed by the application of a thoracic cold block which prevents supraspinal inputs to the caudal spinal cord. Imipramine, however, failed to antagonize this inhibition in animals pretreated with either DL-p-chlorophenylalanine (p-CPA, 300 mg/kg i.p. for 2 consecutive days) or DL-a-methyl-p-tyrosine methyl ester hydrochloride (a-MPt, 125 mg/kg i.p. 16 and 4 h prior to the experiment). Cyproheptadine (2.5--5 mg/kg); phenoxybenzamine hydrochloride (2.5-5 mg/kg) and a cold block enhanced the inhibition of this extensor MSR but a cold block failed to alter the inhibition in animals pretreated with p-CPA or a-MPT. Presynaptic inhibition of the flexor (posterior biceps-semitendinosus, PBST) MSR was however not blocked by imipramine, fluoxetine or a cold block nor enhanced by cyproheptadine or phenoxybenzamine. The effects of the drugs tested and a cold block on the excitability of the QUAD group Ia afferents were reciprocal to those on the MSR during presynaptic inhibition. The results of this study indicate that descending tonically active systems (1) involving 5-HT and noradrenaline, antagonize presynaptic inhibition of the QUAD but not the PBST-MSR, (2) decrease the excitability of the QUAD Ia afferents and (3) increase the excitability of QUAD motoneurones.
Platelet 3H-imipramine binding and serotonin uptake were studied simultaneously in normal subjects and in depressed, parkinsonian and Alzheimer's disease patients to investigate the usefulness of these variables in the diagnosis of depression in the elderly. Whereas Vmax of platelet serotonin uptake was significantly reduced in all patient groups compared to age matched normal subjects, the density of 3H-imipramine binding was reduced in depressed patients only. The lower Bmax values in depressed patients was independent of patient age. These data suggest that platelet 3H-imipramine binding may be a useful laboratory index which discriminates depression from dementia in the elderly.
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This study investigated the effect of tricyclic and atypical antidepressants on adenosine triphosphate (ATP) dependent calcium uptake by the endoplasmic reticulum of lysed synaptosomes from rat brain cortex. Tricyclic antidepressants (imipramine, desipramine, clomipramine, amitriptyline) exhibited no effect in the lower range (0.06 to 2 microM) of drug concentrations, and a concentration-dependent inhibition of calcium uptake in the upper range (6 to 200 microM). A concentration-dependent inhibition was observed for atypical antidepressants (mianserin, desmethylmianserin, venlafaxine, desmethylvenlafaxine, fluoxetine) in both the lower and the upper range of drug concentrations. Since no stimulation of calcium uptake was observed in either concentration range, it appears that the tricyclic and atypical antidepressants tested are not capable of normalizing, through their effect on the endoplasmic reticulum, an overactive calcium signal. which is possibly implicated in the etiology of affective disorders. Also, although only marginal inhibition of calcium uptake is expected at brain concentrations of tricyclics and mianserin-desmethylmianserin that are likely to be encountered during clinical use, a more substantial inhibition could occur with fluoxetine.
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Venlafaxine and imipramine were associated with small, but statistically significant, increases in SDBP during acute phase therapy. When compared with imipramine and placebo, venlafaxine was also associated with a greater proportion of persistent elevations of SDBP during continuation therapy. The effect of venlafaxine was highly dose dependent, and the incidence of elevated SDBP was statistically and clinically significant only at dosages above 300 mg/day. Venlafaxine did not adversely affect the control of blood pressure for patients with preexisting high blood pressure or elevated baseline values.
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The aim of the present study was to confirm the efficacy of antidepressants in post-stroke depression and to identify the factors related to outcome. Subjects consisted of 20 inpatients suffering from post-stroke in a rehabilitation hospital. The subjects were treated with various antidepressants, mainly imipramine, amitriptyline, and amoxapine. After 4 weeks of treatment, 13 showed some improvement; significant improvement in 5, moderate improvement in 5, mild improvement in 3 by a clinical global impression. Whereas all the patients aged less than 65 yr were responders, only 3 of the 10 patients over 65 yr were responders. All of the male patients, but only half of the female patients, were responders. With regards to the presence of a spouse, 13 of the 16 patients with a spouse, but none of 4 patients without, showed a response. No significant correlation was found between the occurrence of each depressive symptom and outcome. Thus, the responders were younger and had better social support in comparison with the non-responders. This result implies that antidepressants are effective for post-stroke depression.
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We compared 19 OCD patients before and after 8 weeks of SRI treatment with 19 sex-matched and age-matched controls. We assessed clinical improvement and whole-blood serotonin (5-HT) concentration, platelet 5-HT transporter (5-HTT) and 5-HT2A receptor binding characteristics and platelet IP3 content.
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A solid basis for the M4-approach has been developed over the past 10 years. Recent examples of the production of difficult-to-synthesize mammalian metabolites through microbial transformations attest to the utility of the methodology. There is, however, much more to be done. Model studies should be conducted to test parallels between microbial and mammalian S- and N-oxidations, O-glucuronidations, and ester and amide hydrolyses. Subsequently, even greater applications of M4- work can be envisioned. We have been pleased to see our colleagues in industry and academia adopt the M4- approach to solve difficult pharmacological and toxicological problems. In large measure, this has been our greatest reward for efforts initially presented before the membership of the American Society of Pharmacognosy in 1973.
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We have previously found that tricyclic antidepressants (TCAs) induce apoptosis in quiescent human lymphocytes. The aim of the present study was to evaluate if TCAs induce apoptosis in proliferating human lymphocytes and in established blastoid lymphocytes also. The development of conA-induced lymphoblast populations was followed by measuring the CD25 membrane expression. Three TCA compounds were run with the following concentrations: imipramine (10, 20, 30, 40, 60 microM), clomipramine (1, 10, 20, 30, 40 microM) and citalopram (40, 60, 80, 100, 180 microM). They all induced a dose-dependent apoptosis both in continuously transformed, as well as in established lymphoblasts. Preincubation of the TCA up to 48 h did not significantly increase induction of apoptosis. The three drugs tested were found to be potent inducers of apoptosis in proliferating lymphocytes. Furthermore, we found that the apoptotic populations in proliferating and in established blastoid lymphocytes were of fairly the same magnitude than in the corresponding population in TCA-incubated resting lymphocytes. In conclusion, we demonstrate that TCAs induce apoptosis in proliferating lymphocytes, as they do in quiescent lymphocytes. Furthermore, the extent of apoptosis was even more pronounced in TCA-incubated lymphoblasts compared to TCA-treated resting lymphocytes.
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Acid sphingomyelinase (A-SMase) and its reaction product ceramide may play a role in the pathophysiology of depressive disorders and in the therapeutic action of antidepressive drugs. In a prospective case-control study, A-SMase activity was measured in peripheral blood mononuclear cells of 17 patients with a major depressive episode who were free of antidepressant drug therapy for at least 10 days and 8 healthy volunteers. In the patient group, A-SMase activity was correlated to the score (n=17, r=0.64, P=0.005). The patient group exhibited higher A-SMase activity compared to healthy volunteers (T=2.09, df=21.33, P<0.05). In addition, we demonstrate that the antidepressants imipramine and amitriptyline induce a long-term reduction of the activity of A-SMase in cultured cells.
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Eighteen patients were included. The reduction of wet nights was much better with either reboxetine in monotherapy or in combination with desmopressin than during the placebo period (p = 0.002) (Figure). However, only one patient achieved complete dryness, this during monotherapy. There were three intermediate responders to monotherapy and five to combination treatment. With reboxetine in monotherapy, six children experienced negative side effects compared with three with combination therapy, and two with placebo. All of these side effects were mild and reversible. Only one patient chose to cease treatment because of side effects. No prognostic factors were found in either the case history or in voiding chart data.
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The adherence rate was 66% (1,407/2,137); the rate of non-informed prescribers was 3% (1,547/55,296) among the general population, and 52% (1,547/2,954) when only TCA users were considered. While adherence was higher among older and female subjects, the number of other medications did not affect adherence rate.
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Five groups of albino mice (20-25 g) were selected for the study, with five animals in each group. Group A served as the naïve control and Group B served as the stressed control. Groups C and D received EETA (100 mg/kg and 200 mg/kg b.w.). Group E received imipramine (20 mg/kg b.w.). Except for Group A, mice in each group were forced to swim 6 min each for 7 days to induce a state of chronic fatigue. Duration of immobility was measured on every alternate day. After 7 days, various behavioral tests (mirror chamber and elevated plus maize test for anxiety, open field test for locomotor activity) and biochemical estimations (malondialdehyde [MDA] and catalase activity) in mice brain were performed.
3H-imipramine binding was studied in the blood platelets of 80 normal controls and 50 depressed (psychotic and nonpsychotic) patients. Protein concentration in the incubation mixture, and Kd and Bmax values were correlated in normal controls and depressed patients. A small but significant correlation between protein in the incubation mixture and Bmax was observed in normal controls and depressed patients. There was also a significant correlation between protein and Kd of imipramine binding in the blood platelets of unipolar psychotic depressed patients. However, analysis of covariance to remove the effect of protein on Kd and Bmax did not change the basic finding of decreased Bmax in the blood platelets of psychotic depressed patients.
Neuroleptics, antidepressants and anticholinergics were compared in their action on the hypothermia produced by apomorphine (AP, 5.0 mg/kg i.p.) or piribedil (PRB, 100 mg/kg i.p.) in mice. Anticholinergics atropine, scopolamine and benactizine did not affect either hypothermia in contrast to neuroleptics and imipramine-like antidepressants which antagonized both hypothermias. Among neuroleptics studied the minimal effective doses (MED) antagonizing AP hypothermia (APH) ranged from 0.006 (trifluperidol) to 0.5 mg/kg (chlorpromazine), while MED antagonizing PRB hypothermia (PRBH) ranged from 0.05 (trifluperidol and perphenazine) to 2.0 mg/kg (haloperidol). Amongst antidepressants the MED ranged from 0.2 (desipramine) to 5.0 mg/kg (amitriptyline) in the case of APH, and ranged from 0.025 (desipramine) to 0.5 mg/kg (amitriptyline) in the case of PRBH, the potency correlated directly with the adrenopositive activity. The higher activity of neuroleptics in the case of APH, and the discrepancy between the order of their effectiveness in tests of APH and PRBH are discussed. The data confirm that the stimulation of the dopamine receptors results in hypothermia and are in accord with the postulated importance of the adrenergic link in the hypothermia produced by dopaminomimetics.
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Treatment-related decreases in Dysfunctional Attitudes Scale (DAS; Weissman & Beck, 1978) scores have been interpreted as evidence that dysfunctional attitudes are state-dependent concomitants of depression. Data from the National Institute of Mental Health Treatment of Depression Collaborative Research Program were used to reexamine the stability of dysfunctional attitudes. Mean scores for Perfectionism, Need for Approval, and total DAS decreased after 16 weeks of treatment. However, test-retest correlations showed that the DAS variables displayed considerable relative stability. Structural equation models demonstrated that dysfunctional attitudes after treatment were significantly predicted by initial level of dysfunctional attitudes as well as by posttreatment depression. The relative stability of dysfunctional attitudes was even higher during the 18-month follow-up period. The results were consistent with Beck's (1967) and Blatt's (1974) theories of vulnerability.
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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.
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Upon activation of specific cell signaling, hepatocytes rapidly accumulate or release an amount of Mg(2+) equivalent to 10% of their total Mg(2+) content. Although it is widely accepted that Mg(2+) efflux is Na(+)-dependent, little is known about transporter identity and the overall regulation. Even less is known about the mechanism of cellular Mg(2+) uptake. Using sealed and right-sided rat liver plasma membrane vesicles representing either the basolateral (bLPM) or apical (aLPM) domain, it was possible to dissect three different Mg(2+) transport mechanisms based upon specific inhibition, localization within the plasma membrane, and directionality. The bLPM possesses only one Mg(2+) transporter, which is strictly Na(+)-dependent, bi-directional, and not inhibited by amiloride. The aLPM possesses two separate Mg(2+) transporters. One, similar to that in the bLPM because it strictly depends on Na(+) transport, and it can be differentiated from that of the bLPM because it is unidirectional and fully inhibited by amiloride. The second is a novel Ca(2+)/Mg(2+) exchanger that is unidirectional and inhibited by amiloride and imipramine. Hence, the bLPM transporter may be responsible for the exchange of Mg(2+) between hepatocytes and plasma, and vice versa, shown in livers upon specific metabolic stimulation, whereas the aLPM transporters can only extrude Mg(2+) into the biliary tract. The dissection of these three distinct pathways and, therefore, the opportunity to study each individually will greatly facilitate further characterization of these transporters and a better understanding of Mg(2+) homeostasis.
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SK channels are small conductance, Ca(2+)-activated K(+) channels that underlie neuronal slow afterhyperpolarization and mediate spike frequency adaptation. Using the patch clamp technique, we tested the effects of eight clinically relevant psychoactive compounds structurally related to the tricyclic antidepressants, on SK2 subtype channels cloned from rat brain and functionally expressed in the human embryonic kidney cell line, HEK293. Amitriptyline, carbamazepine, chlorpromazine, cyproheptadine, imipramine, tacrine and trifluperazine blocked SK2 channel currents with micromolar affinity. The block was reversible and concentration-dependent. The potency differed according to chemical structure. In contrast, the cognitive enhancer linopirdine was ineffective at blocking these channels. Our results point to a distinct pharmacological profile for SK channels.
This study investigated the involvement of NMDA receptors and the L-arginine-nitric oxide (NO) pathway in the antidepressant-like effects of zinc in the forced swimming test (FST). The immobility times in the FST and in the tail suspension test (TST) were reduced by zinc chloride (ZnCl(2), 30 and 10-30 mg/kg intraperitoneal (i.p.), respectively). The doses active in the FST and TST reduced locomotor activity in an open-field. The antidepressant-like effect of ZnCl(2) in the FST was prevented by pre-treatment of animals with guanosine 5'-monophosphate (GMP), ascorbic acid, L-arginine, or S-nitroso-N-acetyl-penicillamine (SNAP), but not with D-arginine, administered at doses that per se produced no anti-immobility effect. The immobility time of mice treated with ZnCl(2)+MK-801 was not different from the result obtained with ZnCl(2) or MK-801 alone, but ZnCl(2)+imipramine had a greater effect in the FST than administration of either drug alone. Pre-treatment of animals with a sub-threshold dose of ZnCl(2) prevented the anti-immobility effect of MK-801, ketamine, GMP, L-arginine or N(G)-nitro-L-arginine (L-NNA), but did not alter the effect of imipramine or fluoxetine. Taken together, the results demonstrate that zinc produced an antidepressant-like effect that seems to be mediated through its interaction with NMDA receptors and the L-arginine-NO pathway.
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The biological basis for the therapeutic mechanisms of depression are still unknown. While performing EST (expressed sequence tag) analysis to identify some molecular machinery responsible for the antidepressant effect, we determined the full-length nucleotide sequence of rat frizzled-3 protein (Frz3) cDNA. Interestingly, Northern blot analysis demonstrated that elevated levels of Frz3 were expressed continually from embryonic day 20.5 to postnatal 4 weeks in developing rat brain. In adult rat brain, Frz3 mRNA was expressed predominantly in the cerebral cortex and hypothalamus and moderately in the hippocampus. Using real-time quantitative PCR, we demonstrated that chronic treatment with two different classes of antidepressants, imipramine and sertraline, reduced Frz3 mRNA expression significantly in rat frontal cortex. Electroconvulsive treatment (ECT) also reduced Frz3 expression. In contrast, antidepressants and ECT failed to reduce Frz2 expression. Additionally, chronic treatment with the antipsychotic drug haloperidol did not affect Frz3 expression. Recently, the Frz/Wingless protein pathway has been proposed to direct a complex behavioral phenomenon. In conclusion, the Frz3-mediated signaling cascade may be a component of the molecular machinery targeted by therapeutics commonly used to treat depression.
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The psychotropic activity of a series of new aminouracil derivatives was studied on the widely applied models of pharmacological screening in rats. The most expressed antidepressant effect at the stage of primary pharmacological screening was been revealed for compound PIR-03-52 in a dose of 10 mg/kg. A profound study of the antidepressant activity on models of pathological states, PIR-03-52 exhibited a pronounced antidepressant effect that was comparable with that of a reference drug (imipramine). The given effect is related to the positive influence of PIR-03-52 on the serotoninergic and dopaminergic systems.
To study the transport system of propranolol (PL), a basic drug, in the blood-brain barrier, the uptake of PL into isolated bovine brain microvessels was investigated. The uptake of PL was a concentrative one via saturable process (Km = 42.5 microM) that was decreased by hypothermia (Q10 = 2.2), but not by metabolic inhibitors (2,4-dinitrophenol, KCN, ouabain). Although basic drugs such as quinidine and imipramine decreased both the initial rate of uptake and the steady-state cell-to-medium concentration ratio (C/M) of PL, acidic drugs (phenobarbital, salicylic acid) did not affect them. These results suggest that PL is taken up by the endothelial cells of the isolated brain microvessels by facilitated diffusion which is specific for basic drugs and then binds to certain binding sites in the cells.
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Chronic depressions are common, disabling, and undertreated, and prior chronicity predicts future chronicity. However, few studies directly inform the acute or maintenance phase treatments of chronic depressions and even less is known about the effects of treatment on psychosocial functioning.
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In tests with cats and rabbits sydnocarb in doses of 3,4-8.5-17 mg/kg (per os or intraperitoneally) produces a more lasting reticulo-cortical activation than does amphetamine used in respectively equimolecular amounts. According to the EEG finding there is also observed a substantial difference in the nature of interaction of these stimulants with chlorpromazine, reserpine and imipramine.
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It has been shown that cytotoxic action of neuropharmacological drugs (transmitter antagonists) on early urchin embryos is reduced or abolished by cyclic nucleotides and sodium fluoride. Such a protective action differs in cAMP and dibutyryl analogs of cyclic nucleotides, depending on the chemical structure of an embryotoxic substance. It is suggested that, endogenous intracellular "prenervous" transmitters and cyclic nucleotides are interrelated in the regulation of cell division in urchin embryos.
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We conclude that stabilization of exogenous surfactant by adding imipramine to create a "fortified surfactant preparation" improves lung function in a clinically relevant piglet model, and that this effect can be attributed to the inhibition of a-SMase as evidenced in the mouse model.
Fluvoxamine facilitates serotoninergic neurotransmission via potent and selective inhibition of serotonin (5-hydroxytryptamine; 5-HT) reuptake into presynaptic neurones. The overall antidepressant efficacy of fluvoxamine 100 to 300 mg/day for 4 to 6 weeks in once daily or divided dosage regimens appears to be at least comparable to that of imipramine and similar to that of clomipramine, dothiepin, desipramine, amitriptyline, lofepramine, maprotiline, mianserin and moclobemide. The efficacy of fluvoxamine has been maintained for up to 1 year, but long term data are limited, and there are no comparative studies of fluvoxamine with other selective serotonin reuptake inhibitors. In some studies, fluvoxamine appeared to have an earlier beneficial effect on suicidal ideation and/or anxiety or somatic complaints compared with imipramine, dothiepin and maprotiline. Gastrointestinal adverse effects, especially nausea, are commonly reported with fluvoxamine but are generally mild to moderate in severity. The tolerability profile of fluvoxamine appears to be more favourable than that of tricyclic antidepressants in terms of cardiotoxic and anticholinergic adverse effects, sedation, weight gain and death from overdosage. Thus, fluvoxamine is an effective and well tolerated antidepressant agent that is becoming established as an alternative to older agents in patients with mild, moderate or severe depression. Fluvoxamine may be particularly beneficial in potentially suicidal patients with severe depression, in those with an underlying compulsive personality or cardiovascular disorder, in patients with coexistent anxiety or agitation, and in the elderly.
TCA treatment in children and adolescents, like that in adults, is associated with cardiovascular changes of uncertain, but probably minor, clinical significance. More information is needed on the contribution of other physiological conditions on the cardiovascular system during exposure to TCAs. Guidelines for using TCAs in children and adolescents are presented.
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In this paper from the Collaborative Depression Study (CDS)--Biological, a set of data analyses are presented which indicate that depressed states and perhaps depressed mood are associated with a greater activation of the adrenomedullary system than the sympathetic nervous system [as measured by norepinephrine (NE) and normetanephrine excretion]. For the most part this finding of predominant activation of the adrenomedullary system is seen in unipolar and not bipolar patients.
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It was shown by the analysis of the in situ data in the pH 6.5-8.5 interval for the lipophilic bases that the average vascular flow F(pf) = 0.036 mL∙g(-1)∙s(-1), centered in a "flow-limit window" (FLW) bounded by P (e) (min) = 170 and P (e) (max) = 776 (10(-6) cm∙s(-1) units). It was shown that the traditional CRE is expected not to work for half of the molecules in the FLW and is expected to underestimate (up to 64-fold) the other half of the molecules.
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In the present study the influence of imipramine, a tricyclic antidepressant, on the expression and function of tyrosine hydroxylase (TH) in dopaminergic rat brain regions was examined. Chronic administration of imipramine (18 days) decreased levels of TH enzyme activity in ventral tegmental area (VTA) and substantia nigra (SN), dopaminergic cell body regions, as well as in caudate-putamen (CP), nucleus accumbens (ACB), prefrontal cortex (PFC), and olfactory tubercle (OT), dopaminergic terminal fields. These effects were dependent on chronic drug treatment, as imipramine administration for 1 or 7 days did not significantly influence levels of TH activity in either SN or VTA. In contrast to drug regulation of enzyme activity, chronic imipramine treatment did not decrease levels of TH immunoreactivity in any of the dopaminergic cell body or terminal field regions studied, although levels of TH immunoreactivity were decreased in locus coeruleus (LC) as previously reported. However, imipramine treatment increased levels of TH back phosphorylation in VTA, suggesting that the antidepressant-induced decrease in levels of TH activity is a result of decreased phosphorylation of the enzyme. These results demonstrate that imipramine treatment regulates levels of TH enzyme activity in dopaminergic brain regions, and may account for some of the previously observed effects of these drugs on dopaminergic function. Finally, imipramine regulation of TH enzyme activity in VTA and immunoreactivity in LC was observed in Sprague Dawley, but not Wistar rats, demonstrating that different rat strains exhibit different biochemical responses to antidepressant treatment.
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The objective of this study is to investigate antidepressant activity of various extracts and fractions of C. indica aerial parts, and to estimate content of quercetin in the plant using TLC densitometry.
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To compare the efficacy of imipramine and fluvoxamine in depressed inpatients who subsequently received lithium supplement in case of poor response.
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Platelet MAO activity decreased by 40% (p less than .001) in a group of 11 male patients with primary depression after 3 weeks of treatment with either amitriptyline or imipramine. This finding, together with data from previous in vitro studies demonstrating tricyclic-induced inhibition of mitochondrial MAO, suggests that inhibition of MAO plays a role in the clinical action of tricyclic antidepressant drugs.
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When chlorpromazine was introduced into psychiatric therapy in 1952 and thus the modern psychopharmacological era was started, the situation in psychiatry was deplorable. The psychiatric hospitals were overcrowded and obsolete, complementary institutions were widely missing. In Germany, even after introducing the neuroleptic era and the beginning of the thymoleptic epoch in 1957, no decisive improvement took place at first. As late as in the 70s successes of psychiatric reform efforts in the sense of humanization became visible, along with modern psychopharmacotherapy making an important contribution to these improvements. With the social attitude towards the mentally ill changing, this contribution became effective. In 1954 the antipsychotic efficacy of Rauwolfia alkaloids was described; in 1958 the butyrophenones, especially haloperidol, were introduced. In 1957 the antidepressive efficacy of imipramine was discovered, in the same year the psychiatric importance of monoaminoxidase inhibitors was defined. In 1949 Cade published his findings on the antimanic effect of lithium salts. As tranquilizers meprobamate (1955) and chlordiazepoxide (1960) were made available. In 1966 clozapine was introduced. Objections to psychopharmacotherapy, which were not always objective, were often raised. The biochemical research in cooperation with psychopharmacology has made progress, yet the target of clarification of the pathophysiology of the main psychoses has not been reached as yet. At present there is considerable resistance towards a further expansion of psychopharmacology, research being hampered by legal reglementation and bureaucracy. This development must be faced. Psychopharmacotherapy is not yet sufficiently effective and safe; it must be improved.