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PubMed1980

Effect of neuroleptics and tricyclic antidepressants upon d-amphetamine discrimination.

After rats were trained to differentiate between the effects of intraperitqoneal administration of 0.6 mg/kg d-amphetamine and saline, pretreatment with various neuroleptic drugs was observed to significantly inhibit d-amphetamine discrimination. Thus, trifluoperazine, haloperidol, fluphenazine, chlorpromazine and thioridazine, but not clozapine, decreased d-amphetamine-induced control of discriminative performance. The ED50s of the effective neuroleptics for this inhibition were similar to those reported for antagonism of amphetamine-induced stereotypic behavior in the rat and the slopes of the dose-response curves were parallel indicating a common site and mechanism of action, presumably blockade of postsynaptic dopaminergic receptors. In contrast, pretreatment with the tricyclic antidepressant agents, imipramine, nortryptiline and desipramine had no significant effect on the discrimination of a dose of d-amphetamine which produced a low degree of discriminative control. The results are viewed in relation to the "dopamine hypothesis" of schizophrenia and affective disorders and the use of this animal behavioral method for determining brain dopamine interactions is discussed.

Animals↗

PubMed2004

Brain plasticity and antidepressant treatments: new cells, new connections.

It is now a decade since we first wrote about the impact of antidepressant agents on plastic processes in the hippocampus (Stewart and Reid, 1993). Since then, the roles of various forms of brain plasticity have moved centre stage in efforts to understand the pathophysiology of depressive disorder. Here, we review the background to current views relating cytoarchitectural and synaptic changes to the aetiology and treatment of affective disease.

Animals↗

PubMed2005

Pharmacological therapy of atypical facial pain: actuality and perspective.

Atypical facial pain is a condition, which creates a difficult challenge for every physician, either for diagnosis or for choice of treatment. There are very few controlled studies and evidence-based data about what constitutes the gold standard treatment. Most physicians treat this condition with antidepressant agents, thinking that the psychiatric aspects, often present in these patients, play a fundamental role in the pathogenesis of the condition. However, antidepressant drugs are effective also in non-psychiatric patients, and new compounds, with no effect on psychological aspects, have recently seemed to show good activity in controlling pain in this disorder. We review the different possibilities available for treating this frustrating condition.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1992

Efficacy and tolerability of moclobemide compared with fluvoxamine in depressive disorder (DSM III). A French/Swiss double-blind trial.

The efficacy and tolerability of moclobemide and fluvoxamine, two new types of antidepressant agents, were compared in a multicentre, double-blind prospective study of patients with a diagnosis of major depressive episode (DSM III). Patients were randomized to receive either moclobemide (150 mg) or fluvoxamine (50 mg) twice daily for 7 days, immediately following a washout period of at least 1 week. Dosages were increased where necessary on day 8, to a maximum of moclobemide 450 mg or fluvoxamine 200 mg and in most cases were maintained at these levels for the remainder of the study period (4-6 weeks). Both treatment groups showed a marked antidepressant effect. While both treatments were well tolerated, moclobemide showed a more favourable side-effect profile than fluvoxamine. Of the 126 patients eligible for evaluation, 34 withdrew from therapy, 22% in the moclobemide group and 30% in the fluvoxamine group. Adverse events were reported in 41.8% of patients treated with moclobemide compared to 60.3% of patients in the fluvoxamine group. Reports of dry mouth and other anticholinergic effects were more frequent among those treated with fluvoxamine. A greater number of gastrointestinal complaints, especially nausea, also occurred in the fluvoxamine-treated patients.

Adult↗

PubMedDate not supplied

Two fatal cases of venlafaxine poisoning.

Venlafaxine is a phenethylamine derivative that has recently been approved for use in the treatment of depression. It is chemically unrelated to tricyclic, tetracyclic, or other available antidepressant agents. Anticholinergic, hypotensive, hypertensive, and cardiotoxic side effects are rare. Two fatal cases encountered at separate laboratories are discussed, both involve high levels of venlafaxine. Concentrations of the drug in peripheral blood, heart blood, urine, vitreous humor, and liver are reported. Descriptions of extraction and gas chromatographic methods for confirmation and quantitation are included.

Antidepressive Agents, Second-Generation↗

PubMed1982

Human brain receptor alterations in suicide victims.

A comparison was made of human postmortem muscarinic-cholinergic, beta-adrenergic and serotonergic (presynaptic) recognition sites in cortical tissues derived from suicide and homicide (control) victims. An elevation of 47% and 35% in the suicide group compared to controls was observed in receptor ligand binding for 3H-quinuclidinyl benzilate (QNB, muscarinic antagonist) and 3H-imipramine (IMI, a presynaptic serotonin marker), respectively. In contrast, no appreciable differences in 3H-dihydroalprenolol (DHA, beta-adrenergic antagonist) binding were observed between the two groups. Additionally, tissues from both groups of subjects were analyzed for tricyclic antidepressive agent (TAD) content. High performance liquid chromatographic (HPLC) tissue analysis revealed no detectable levels of tricyclic agents with an assay sensitivity of 50 picograms/mg tissue. The results presented herein demonstrate neurotransmitter-receptor alterations in suicide subjects compared to homicide (control) victims. The attendant roles of serotonergic and muscarinic-cholinergic processes in the psychobiology of suicide and depression are addressed.

Antidepressive Agents, Tricyclic↗

PubMed1992

Direct activation of purified Go-type GTP binding protein by tricyclic antidepressants.

A growing body of evidence suggests that tricyclic antidepressant agents (TCAs) interact with GTP binding proteins (G proteins). We have investigated if TCAs directly alter the function of the purified Go protein which is specifically expressed in neuronal tissue. Several TCAs markedly enhanced the GTPase activity of Go protein in a pertussis toxin-susceptible manner, whereas MAO-inhibitor and anxiolytic agent did not. This enhancing effect of TCAs on Go function may be due to an increase in the GDP-GTP exchange reaction occurring on Go. Thus, it is very likely that TCAs can modify various signal transduction by directly interacting with G proteins in brain cells.

Animals↗

PubMed1993

Long-term outcome of treatment-resistant depression in older adults.

Seventeen elderly patients with treatment-resistant depression were reassessed 15 months and 4 years after treatment with an antidepressant agent or ECT. At 15 months 47% (seven of 15) were clinically improved, and at the 4-year follow-up 71% (10 of 14) were improved. These results indicate that treatment-resistant depression may improve over time because of either the natural course of the illness or persistent treatment efforts.

Age Factors↗

PubMed1999

Venlafaxine and bupropion combination therapy in a case of treatment-resistant depression.

OBJECTIVE: To report the therapeutic efficacy of venlafaxine and bupropion in a patient with treatment-refractory major depression. CASE SUMMARY: A 21-year-old white woman with chronic and recurrent major depression presented with lack of response to several antidepressants. On examination, the patient exhibited neurovegetative signs of depression, guilt feelings, and suicidal ideation. The patient was administered venlafaxine 75 mg three times daily. The dose was titrated to 150 mg three times daily over the next month. Later bupropion was instituted up to 100 mg three times daily over a four-month period. The patient responded favorably to combination therapy and has remained free of depression for approximately 23 months. DISCUSSION: Venlafaxine and bupropion are antidepressant agents with unique pharmacologic profiles, each effective in the treatment of depression. Recent data indicate that combinations of selective serotonin-reuptake inhibitors and bupropion can convert partial response to full response in patients with treatment-resistant depression. We considered whether a combination of venlafaxine and bupropion would reduce the depressive symptoms of a patient who was unresponsive to various classes of psychotropic agents. Gradual administration of venlafaxine and bupropion acted synergistically to significantly reduce depressive symptoms (p < 0.002) and significantly increase social function (p < 0.002) over a period of eight months. CONCLUSIONS: To our knowledge this is the first report of successful combination therapy with venlafaxine and bupropion in treatment of chronic recurrent and refractory major depression.

Adult↗

PubMed1988

Prescribing patterns in agoraphobia with panic attacks.

Although medication is used commonly in the treatment of agoraphobia with panic attacks, the actual drug-prescribing patterns of the medical profession have not been well studied in this condition. The present study compares the prescribing patterns of general practitioners and psychiatrists in their treatment of agoraphobia with panic attacks. The medical records of 111 agoraphobic patients with panic attacks were analysed and divided into those who were referred by general practitioners and those who were referred by psychiatrists. Over all, in the treatment of agoraphobia with panic attacks, general practitioners prescribed drugs less often than did psychiatrists. They used fewer combinations of drugs and tended to prescribe tricyclic antidepressant agents in doses which generally are considered to be below the therapeutic range. This finding would suggest that general practitioners are less effective than are psychiatrists in prescribing for this condition as judged by current practice, although they are less likely to prescribe combinations of drugs--a practice which might well be to their credit.

Adult↗

PubMedDate not supplied

Interaction between tacrolimus and nefazodone in a stable renal transplant recipient.

Tacrolimus (FK-506) is an important immunosuppressive agent most often given for maintenance immunosuppression to prevent acute cellular organ rejection. A 57-year-old woman with end-stage renal disease presumed secondary to chronic glomerulonephritis underwent a living related renal allograft transplantation. She tolerated the surgery well and was discharged on postoperative day 5. She was stabilized with prednisone, azathioprine, and tacrolimus. Two years after transplantation, nefazodone 50 mg twice/day orally was prescribed due to depression. After 1 week of nefazodone therapy the patient experienced headache, confusion, and "gray areas" in her vision, without abnormal ophthalmologic findings. Her serum creatinine was elevated to 2.2 mg/dl (baseline 1.5 mg/dl), and trough tacrolimus level was markedly elevated (> 30 ng/ml). Both tacrolimus and nefazodone are metabolized by the cytochrome P450 (CYP) 3A4 system. We suspect that nefazodone inhibits metabolism of tacrolimus. Coadministration of antidepressant agents such as nefazodone, or any other drug that inhibits the CYP3A4 isoenzyme subfamily, should be anticipated to interfere with tacrolimus metabolism. Monitoring blood concentrations of tacrolimus is vital, and appropriate dosage adjustments are required when the two drugs are administered concurrently to avoid serious interactions such as nephrotoxicity and neurotoxicity.

Antidepressive Agents, Second-Generation↗

PubMed1999

Changes in the generation of reactive oxygen species and in mitochondrial membrane potential during apoptosis induced by the antidepressants imipramine, clomipramine, and citalopram and the effects on these changes by Bcl-2 and Bcl-X(L).

In order to investigate the molecular mechanism of the antineoplastic effects exerted by the antidepressive agents imipramine, clomipramine, and citalopram, we examined the effects of these compounds on cell viability, generation of reactive oxygen species (ROS), and mitochondrial membrane potential (DeltaPsi(m)) in human acute myeloid leukemia HL-60 cells. Our results indicate that exposure to these compounds causes a loss in cell viability by activating the apoptotic process, as identified by electron microscopy, DNA gel electrophoresis, and flow cytometry. The increased generation of ROS induced by these drugs was a relatively early event and preceded the loss of DeltaPsi(m). Overexpression of the antiapoptotic protein Bcl-2 or Bcl-X(L) prevents antidepressant-induced apoptosis, as well as loss of DeltaPsi(m), but does not affect the generation of ROS.

Antidepressive Agents↗

PubMed2001

Neurokinin(1) receptor antagonists as potential antidepressants.

Selective, nonpeptide antagonists for tachykinin receptors first became available ten years ago. Of the three known tachykinin receptors, drug development has focused most intensively on the substance P-preferring receptor, neurokinin(1) (NK(1)). Although originally studied as potential analgesic compounds, recent evidence suggests that NK(1) receptor antagonists may possess antidepressant and anxiolytic properties. If confirmed by further controlled clinical studies, this will represent a mechanism of action distinct from all existing antidepressant agents. As reviewed in this chapter, the existing preclinical and clinical literature is suggestive of, but not conclusive, concerning a role of substance P and NK(1) receptors in the pathophysiology of depression and/or anxiety disorders. The ongoing clinical trials with NK(1) receptor antagonists have served as an impetus for much needed, basic research in this field.

Animals↗

PubMed1998

Dopaminergic agents and stimulants as antidepressant augmentation strategies.

Dopaminergic agents and stimulants have been used to manage depression when conventional antidepressant treatments fail. We reviewed evidence for the role of dopaminergic dysfunction in depression, the use of dopaminergic agents as antidepressants, and the use of dopaminergic agents and stimulants as antidepressant adjuncts. Dopamine may be part of the pathophysiology of depression for a subset of patients. When used with caution and an appreciation of the potential risk of abuse, dopaminergic agents and stimulants may be useful for patients refractory to antidepressants alone.

Antidepressive Agents↗

PubMed2000

Hypersensitivity syndrome caused by amitriptyline administration.

Adverse cutaneous manifestations are among the most common side effects associated with psychotropic drugs. Skin reactions due to amitriptyline (a tricyclic antidepressant agent) include rashes and hypersensitivity reactions (for example, urticaria and photosensitivity) as well as hyperpigmentation. Hypersensitivity syndrome is a specific severe idiosyncratic reaction causing skin, liver, joint, and haematological abnormalities, which usually resolve after the discontinuation of the implicated drug. A case of a 24 year old woman who experienced hypersensitivity syndrome three weeks after the initiation of amitriptyline is reported.

Adult↗

PubMed2002

Treatment of depressive disorders with and without medication - a naturalistic study.

OBJECTIVE: Although randomized clinical trials are the standard method for comparing the efficacy of various depression treatments, the external validity and generalizability of findings obtained by this approach can be questioned for several reasons. In this naturalistic study, we compared the effectiveness of treatments conducted by psychiatrists and clinical psychologists without prescription of drugs to treatments by psychiatrists and physicians using antidepressant agents in patients with depressive disorders in a representative sample of the normal population. Our assumption was that this sample is more representative for subjects treated for depressive disorders than subjects included in controlled trials. METHODS: In a post hoc analysis, the health status of depressed patients under treatment for major, minor or recurrent brief depression with medication (20 patients) and without medication (30 patients), and untreated depressed subjects were compared over a one-year period using SCL-90-R depression scale scores. RESULTS: At baseline, the two treatment groups were comparable in terms of diagnosis and severity of symptoms. Treatment effects were relatively small; patients treated with antidepressants tended to improve, whereas patients treated without drugs deteriorated slightly over one year. Seven years later, treated and untreated subjects no longer differed. CONCLUSION: The results are consistent with previous studies on usual care of depressed patients showing low response rates for non-standardized treatments outside of research settings. Despite a number of methodological shortcomings (small sample size, heterogeneity of subjects and treatments, unusual rating instruments), the results presented here are unique, and provide relevant insight into usual care of depressed patients. This study underlines the importance of standardized psychotherapy and pharmacotherapy in routine practice, of studies investigating the transferability of results of outcome studies across clinical populations, and of quality assurance in primary care psychiatry.

Adult↗

PubMed1984

Attenuation of the post-decapitation convulsions after repeated treatment of rats with desipramine, imipramine and maprotiline.

The effects of repeated treatment of rats with the antidepressant or potential antidepressant agents alaproclate, citalopram, clomipramine, desipramine, imipramine, maprotiline, mianserin and zimeldine on the convulsions released by decapitation were examined. The noradrenaline uptake inhibitors desipramine, imipramine and maprotiline increased significantly the latency of onset of the post-decapitation convulsions (PDC's) after repeated administration of 10 mumol/kg orally twice daily, or 66 mumol/kg orally once daily (desipramine), for 15 days. The duration of the PDC's was slightly prolonged by these agents. A single acute dose of desipramine (20 mg/kg) administered at various time intervals before decapitation (1 to 24 hours) had no effect on the PDC's nor did repeated treatment with the other compounds examined, alaproclate, citalopram, clomipramine, mianserin and zimeldine, have any effect upon the PDC latency. The results are interpreted as evidence for noradrenaline receptor subsensitivity following chronic treatment.

Alanine↗

PubMed2006

[Maintenance treatment and relapse prophylaxis of depressive disorders].

After the remission of a depressive episode, the antidepressant should be continued at the same dose level for at least six months to prevent a relapse. Following severe, therapy-refractive depression, or if the course of the disease reveals an increased tendency to relapse, a phase-prophylactic long-term treatment is recommended. In the treatment of unipolar depressive disorders, lithium and antidepressant agents applied at the dosage effective for acute treatment are equally effective. The more severe the successfully treated depression, or the greater the risk of a relapse, the longer the prophylactic treatment should be. Current data show that interpersonal psychotherapy and cognitive-behavioral therapy are also of value in preventing a relapse. An independent suicide-preventing effect is to be seen with lithium, and presumably also with clozapine.

Antidepressive Agents↗