Prof. Enrico Smeraldi - Official site

PSYCHOPHARMACOLOGY

2C: Delusional depression

Double-blind controlled trial of sertraline versus paroxetine in the treatment of delusional depression.
Zanardi R, Franchini L, Gasperini M, Perez J, Smeraldi E.
1996. Am. J. Psychiat. 153, 1631.

OBJECTIVE:
In this study the authors evaluated the efficacy and the tolerability of sertraline and paroxetine in the treatment of delusional depression. METHOD: Under double-blind conditions, 46 hospitalized patients who met the DSM-III-R criteria for major depression with psychotic features were treated with sertraline or paroxetine for 6 weeks. RESULTS: The response rates were 75% and 46% for sertraline and paroxetine, respectively. The dropout rate was substantial (41%) in the paroxetine group and was attributable to side effects. CONCLUSIONS: Selective serotonin reuptake inhibitors administered alone are useful in the treatment of delusional depression.

Quoted in:

Muller, W.E., Eckert, A., 1997. The pharmacological basis of the clinical use of the selective serotonin reuptake inhibitors. Psychopharmakotherapie 4, 2.
Nelson, E.B., McElroy, S.L., 1997. Psychotic depression - A guide to drug choice. CNS Drugs 8, 457.
Pies, R.W., 1997. Must we now consider SRIs neuroleptics? J. Clin. Psychopharmacol. 17, 443.
Reiff, J., Laux, G., Muller, W.E., Moller, H.J., 1997. Sertraline in the treatment of depressive disorders. Psychopharmakotherapie 4, 18.
Reiff, J., Laux, G., Muller, W.E., Moller, H.J., 1997. Tolerability and side-effect profile of sertraline. Psychopharmakotherapie 4, 26.
Wolfersdorf, M., Konig, F., Barg, T., 1997. Monotherapy of delusional depression with zotepine - results of a 28-day-monotherapy. Psychopharmakotherapie 4, 149.
Amsterdam, J.D., 1998. Selective serotonin reuptake inhibitor efficacy in severe and melancholic depression. J. Psychopharmacol. 12, S99.
Flint, A.J., Rifat, S.L., 1998. Two-year outcome of psychotic depression in late life. Am. J. Psychiat. 155, 178.
Goldstein, B.J., Goodnick, P.J., 1998. Selective serotonin reuptake inhibitors in the treatment of affective disorders - III. Tolerability, safety and pharmacoeconomics. J. Psychopharmacol. 12, S55.
Goodnick, P.J., Goldstein, B.J., 1998. Selective serotonin reuptake inhibitors in affective disorders - I. Basic pharmacology. J. Psychopharmacol. 12, S5.
Goodnick, P.J., Goldstein, B.J., 1998. Selective serotonin reuptake inhibitors in affective disorders - II. Efficacy and quality of life. J. Psychopharmacol. 12, S21.
Gunasekara, N.S., Noble, S., Benfield, P., 1998. Paroxetine - An update of its pharmacology and therapeutic use in depression and a review of its use in other disorders. Drugs 55, 85.
Lane, R.M., 1998. SSRI-induced extrapyramidal side-effects and akathisia: implications for treatment. J. Psychopharmacol. 12, 192.
Licht, R.W., Kassow, P., 1998. Venlafaxin for the treatment of psychotic depression. Eur. Psychiat. 13, 276.
Moller, H.J., Gallinat, J., Hegerl, U., Arato, M., Janka, Z., Pflug, B., Bauer, H., 1998. Double-blind, multicenter comparative study of sertraline and amitriptyline in hospitalized patients with major depression. Pharmacopsychiatry 31, 170.
Mulsant, B.H., Pollock, B.G., 1998. Treatment-resistant depression in late life. J. Geriatr. Psychiatry Neurol. 11, 186.
Edwards, J.G., Anderson, I., 1999. Systematic review and guide to selection of selective serotonin reuptake inhibitors. Drugs 57, 507.
Flament, M.F., Lane, R.M., Zhu, R., Ying, Z., 1999. Predictors of an acute antidepressant response to fluoxetine and sertraline. Int. Clin. Psychopharmacol. 14, 259.
Louiz, H., Ben Nasr, S., Salhi, J.E., Ghaoui, S., Ali, B.B., 1999. The cultural aspect of delusions and hallucinations in a context of depression. Enceph.-Rev. Psychiatr. Clin. Biol. Ther. 25, 22.
Rothschild, A.J., Phillips, K.A., 1999. Selective serotonin reuptake inhibitors and delusional depression. Am. J. Psychiat. 156, 977.
Schatzberg, A.F., 1999. Antidepressant effectiveness in severe depression and melancholia. J. Clin. Psychiatry 60, 14.
Carpenter, L.L., Price, L.H., 2000. Psychotic depression: What is it and how should we treat it? Harv. Rev. Psychiatr. 8, 40.
Duval, F., Mokrani, M.C., Crocq, M.A., Bailey, P.E., Diep, T.S., Correa, H., Macher, J.P., 2000. Dopaminergic function and the cortisol response to dexamethasone in psychotic depression. Prog. Neuro-Psychopharmacol. Biol. Psychiatry 24, 207.
Hawley, C.J., Loughlin, P.J., Quick, S.J., Gale, T.M., Sivakumaran, T., Hayes, J., McPhee, S., 2000. Efficacy, safety and tolerability of combined administration of lithium and selective serotonin reuptake inhibitors: a review of the current evidence. Int. Clin. Psychopharmacol. 15, 197.
Lepine, J.P., Goger, J., Blashko, C., Probst, C., Moles, M.F., Kosolowski, J., Scharfetter, B., Lane, R.M., 2000. A double-blind study of the efficacy and safety of sertraline and clomipramine in outpatients with severe major depression. Int. Clin. Psychopharmacol. 15, 263.
Schuld, A., Archelos, J.J., Friess, E., 2000. Visual hallucinations and psychotic symptoms during treatment with selective serotonin reuptake inhibitors: Is the sigma receptor involved? J. Clin. Psychopharmacol. 20, 579.
Thase, M.E., 2000. Treatment of severe depression. J. Clin. Psychiatry 61, 17.
Vega, J.A.W., Mortimer, A.M., Tyson, P.J., 2000. Somatic treatment of psychotic depression: Review and recommendations for practice. J. Clin. Psychopharmacol. 20, 504.
Bourin, M., Chue, P., Guillon, Y., 2001. Paroxetine: A review. CNS Drug Rev. 7, 25.
Kennedy, S.H., Lam, R.W., Cohen, N.L., Ravindran, A.V., 2001. Clinical guidelines for the treatment of depressive disorders IV. Medications and other biological treatments. Can. J. Psychiat.-Rev. Can. Psychiat. 46, 38S.
Konig, F., von Hippel, C., Petersdorff, T., Neuhoffer-Weiss, M., Wolfersdorf, M., Kaschka, W.P., 2001. First experiences in combination therapy using olanzapine with SSRIs (Citalopram, paroxetine) in delusional depression. Neuropsychobiology 43, 170.
Kropp, S., Schneider, U., 2001. Psychotic depression, subcortical arteriosclerotic encephalopathy and holocaust-conditioned posttraumatic stress disorder. Aust. N. Z. J. Psych. 35, 129.
MacQueen, G., Born, L., Steiner, M., 2001. The selective serotonin reuptake inhibitor sertraline: Its profile and use in psychiatric disorders. CNS Drug Rev. 7, 1.
Solai, L.K.K., Mulsant, B.H., Pollock, B.G., 2001. Selective serotonin reuptake inhibitors for late-life depression - A comparative review. Drugs Aging 18, 355.

Long-term treatment of psychotic (delusional) depression with fluvoxamine: an open pilot study.
Zanardi R, Franchini L, Gasperini M, Smeraldi E, Perez J.
1997. Int. Clin. Psychopharmacol. 12, 195.

The aim of this open pilot study was to evaluate the efficacy of fluvoxamine in the continuation as well as in the maintenance therapy of delusional depression. Thirty patients with recurrent, unipolar depression (DSM-IV criteria) were selected who had at least one depressive episode during the 18 months preceding the delusional depressive index episode and were treated with fluvoxamine 300 mg/day. Twenty-five of them had a sustained response to this short-term treatment and agreed to enter into the 30-month follow up study. All participants completed the follow up period. No relapse was observed during the 6 months of continuation therapy. During the further 24 months of maintenance therapy, 80% of the patients remained well, whereas 20% (five out of 25) had a single recurrence. Based on these observations, fluvoxamine might be a promising drug for long-term therapy of delusional depression. Further controlled studies are required to confirm this finding.

Quoted in:

Iwanami, A., Oyamada, S., Shirayama, Y., Kamijima, K., 1999. Algorithms for the pharmacotherapy psychotic depression. Psychiatry Clin. Neurosci. 53, S45.
Gumnick, J.F., Nemeroff, C.B., 2000. Problems with currently available antidepressants. J. Clin. Psychiatry 61, 5.

Venlafaxine versus fluvoxamine in the treatment of delusional depression: a pilot double-blind controlled study.
Zanardi R, Franchini L, Serretti A, Perez J, Smeraldi E.
2000. J. Clin. Psychiatry 61, 26.

BACKGROUND:
Previous studies have reported the efficacy of selective serotonin reuptake inhibitors as monotherapy in the treatment of delusional depression. The clinical efficacy of venlafaxine, a serotonin-norepinephrine reuptake blocker, has been demonstrated in the treatment of patients with moderate-to-severe depression, but, to date, no evidence is available about its use in depressed patients with psychotic features. METHOD: Under double-blind conditions, 28 hospitalized patients who met DSM-IV criteria for major depression, severe with psychotic features, were randomly assigned to receive fluvoxamine or venlafaxine, 300 mg/day, for 6 weeks. Severity was evaluated using the Hamilton Rating Scale for Depression (HAM-D) and the Dimensions of Delusional Experience Rating Scale (DDERS) administered at baseline and every week thereafter. Side effects were also recorded. Clinical response was defined as a reduction of the scores in the 21-item HAM-D to 8 or below and in the DDERS to 0. RESULTS: At study completion, the response rates were 78.6% (N = 11) and 58.3% (N = 7) for fluvoxamine and venlafaxine, respectively. No significant difference was found between drugs (Fisher exact test, p = .40). Analysis of covariance on HAM-D scores did not reveal a significantly different decrease of depressive symptomatology between the 2 treatment groups (p = .14). Treatment response appeared to be unrelated to the demographic and clinical characteristics recorded. The overall safety profile of both fluvoxamine and venlafaxine was favorable. CONCLUSION: The results of this pilot double-blind trial show that fluvoxamine is useful in the treatment of delusional depression and suggest that venlafaxine may also be an effective compound in the treatment of this disorder. The latter finding, although promising, warrants further replication in a larger sample of patients.

Quoted in:

Bech, P., 2001. The significance of delusions in depressive disorders. Curr. Opin. Psychiatr. 14, 47.
Kumar, S., Oakley-Browne, M., 2001. Problems with ensuring a double blind. J. Clin. Psychiatry 62, 295.

2d: Clozapine

Response to clozapine in acute mania is more rapid than that of chlorpromazine.
Barbini B, Scherillo P, Benedetti F, Crespi G, Colombo C, Smeraldi E.
1997. Int. Clin. Psychopharmacol. 12, 109.

The purpose of the present study was to compare the efficacy of clozapine with that of chlorpromazine in an open label manner (both given in association with lithium salts) in the treatment of acute mania. Thirty hospitalized manic patients were entered into the study. All patients met DSM-IV criteria for bipolar disorder, Manic Episode; 27 patients completed the study and three patients dropped for noncompliance. The duration of the study was 3 weeks. Patients were randomly assigned to two treatment groups; group 1 (n = 15) was treated with clozapine at a mean dose of 166 mg/day and group 2 (n = 12) was treated with chlorpromazine at a mean dose of 310 mg/day. Manic symptomatology was rated on Young Rating Scale for Mania (YRSM) each week; side effects were recorded on dosage records and treatment emergent symptoms; extrapyramidal acute side effects were rated on the Simpson-Angus Rating Scale performed at the beginning of the study and after 3 weeks of treatment. A two-way repeated measures analysis of variance on YRMS scores showed a significant time effect (p < 0.0001) and a significant time-group interaction (p < 0.0001). Post-hoc comparison between the two groups showed a significant difference after 2 weeks of treatment (p = 0.0001), with clozapine treated patients showing lower YRSM scores than chlorpromazine treated patients. YRSM scores at the end of the study were not significantly different. Patients treated with clozapine showed a more rapid trend toward amelioration. No clinically relevant side effect was observed during the study.

Quoted in:

Dunayevich, E., McElroy, S.L., 2000. Atypical antipsychotics in the treatment of bipolar disorder - Pharmacological and clinical effects. CNS Drugs 13, 433.
McElroy, S.L., Keck, P.E., 2000. Pharmacologic agents for the treatment of acute bipolar mania. Biol. Psychiatry 48, 539.
Nemeroff, C.B., 2000. An ever-increasing pharmacopoeia for the management of patients with bipolar disorder. J. Clin. Psychiatry 61, 19.
Soares, J.C., 2000. Recent advances in the treatment of bipolar mania, depression, mixed states, and rapid cycling. Int. Clin. Psychopharmacol. 15, 183.
Tohen, M., Jacobs, T.G., Feldman, P.D., 2000. Onset of action of antipsychotics in the treatment of mania. Bipolar Disord. 2, 261.
Cookson, J., 2001. Use of antipsychotic drugs and lithium in mania. Br. J. Psychiatry 178, S148.
Licht, R.W., Bysted, M., Christensen, H., 2001. Fixed-dosed risperidone in mania: an open experimental trial. Int. Clin. Psychopharmacol. 16, 103.
Tohen, M., Zhang, F., Taylor, C.C., Burns, P., Zarate, C., Sanger, T., Tollefson, G., 2001. A meta-analysis of the use of typical antipsychotic agents in bipolar disorder. J. Affect. Disord. 65, 85.
Licht, R.W., 1998. Drug treatment of mania: a critical review. Acta Psychiatr. Scand. 97, 387.
Grunze, H., Erfurth, A., Schafer, M., Amann, B., Meyendorf, R., 1999. Electroconvulsive therapy in the treatment of severe mania. Case report and state of knowledge. Nervenarzt 70, 662.

The Sequential Treatment Approach to resistant Schizophrenia with Risperidone and clozapine: Results of an Open Study with Follow-Up
Cavallaro R, P. Brambilla and E. Smeraldi
1998. Hum. Psychopharmacol.-Clin. Exp. 13, 91.

In this paper we extend and test with long-term follow-up the results of a previous paper on the usefulness of a sequential treatment protocol with risperidone an clozapine in resistant schizophrenia. Twenty- four patients diagnosed as resistant schizophrenics according to DSM III R and Kane et al.'s (1988) criteria were treated with risperidone for 3 months. Eight patients responded (according to a priori criteria: improvement of basal BPRS, SAPS and SANS total scores over 20 per cent at 3 months observation), while of the remaining 16 patients two dropped out and nine responded to clozapine treatment within the next month. Five patients had partial or no response to clozapine. Follow-up lasting up 37 months (mean 22.4 months for risperidone responders and 18.3 months for clozapine responders) showed good stability of response, no significant differences in relapses and re-hospitalizations between risperidone and clozapine responders and no tardive responses.

Quoted in:

Bradford, D.W., Chakos, M.H., Sheitman, B.B., Lieberman, J.A., 1998. Atypical antipsyshotic drugs in treatment-refractory schizophrenia. Psychiatr. Ann. 28, 618.
Foster, R.H., Goa, K.L., 1998. Risperidone - A pharmacoeconomic review of its use in schizophrenia. Pharmacoeconomics 14, 97.
Bondolfi, G., Baumann, P., 1999. Risperidone and clozapine for treatment-resistant schizophrenia - Drs. Bondolfi and Baumann reply. Am. J. Psychiat. 156, 1127.

Low-dose clozapine in acute and continuation treatment of severe borderline personality disorder.
Benedetti F, Sforzini L, Colombo C, Maffei C, Smeraldi E.
1998. J. Clin. Psychiatry 59, 103.

BACKGROUND:
Psychotic-like symptoms in patients affected by borderline personality disorder (BPD) are usually treated with low-dose neuroleptics, which show controversial acute effects and lead to a worsening of affective-related symptoms and to severe neurologic side effects after prolonged administration. Clozapine lacks the neurologic side effects of traditional neuroleptics and has been shown to successfully treat psychotic-like symptoms in BPD patients at medium dose. We performed an open-label trial of low-dose clozapine in severe BPD patients. METHOD: Twelve BPD inpatients (DSM-IV criteria) with severe psychotic-like symptoms were studied. Exclusion criteria included comorbid Axis I and medical pathologies. All patients had followed a therapeutic program without improvement for at least 4 months before admission. The clozapine dose was titrated upward on an individual basis until the complete disappearance of psychotic-like symptoms was achieved. Clinician-rated scales were completed at the beginning of the study and after 4 and 16 weeks. RESULTS: All patients completed the 16-week study. Individual clozapine doses ranged from 25 to 100 mg/day. Psychotic-like symptoms decreased within the first 3 weeks of treatment, as confirmed by a statistically significant decrease in Brief Psychiatric Rating Scale scores. This amelioration was coupled with an overall improvement, including a reduction in impulsive behaviors and in affective-related symptoms (Hamilton Rating Scale for Depression) and an increase in global functioning (Global Assessment of Functioning). CONCLUSION: Low-dose clozapine for acute and continuation treatment led to improvement in overall symptomatology in a small sample of severe BPD patients.

Quoted in:

Gabbard, G.O., 1998. Treatment-resistant borderline personality disorder. Psychiatr. Ann. 28, 651.
Battaglia, J., Wolff, T.K., Wagner-Johnson, D.S., Rush, A.J., Carmody, T.J., Basco, M.R., 1999. Structured diagnostic assessment and depot fluphenazine treatment of multiple suicide attempters in the emergency department. Int. Clin. Psychopharmacol. 14, 361.
Chengappa, K.N.R., Ebeling, T., Kang, J.S., Levine, J., Parepally, H., 1999. Clozapine reduces severe self-mutilation and aggression in psychotic patients with borderline personality disorder. J. Clin. Psychiatry 60, 477.
Trestman, R.L., 2000. Behind bars: Personality disorders. J. Am. Acad. Psychiatry Law 28, 232.
Bridler, R., Umbricht, D., Hell, D., 2001. Drug treatment of non-organic psychotic disorders. Schweiz. Rundsch. Med. Prax. 90, 981.
Hough, D.W., 2001. Low-dose olanzapine for self-mutilation behavior in patients with borderline personality disorder. J. Clin. Psychiatry 62, 296.
Zanarini, M.C., Frankenburg, F.R., Khera, G.S., Bleichmar, J., 2001. Treatment histories of borderline inpatients. Compr. Psychiat. 42, 144.

Olanzapine-induced neutropenia after clozapine-induced neutropenia.
Benedetti F, Cavallaro R, Smeraldi E.
1999. Lancet 354, 567.

Olanzapine is a new antipsychotic drug, pharmacodynamically similar to clozapine, but putatively devoid of haematological iatrogenicity. We report a case of relapse of previously clozapine-induced neutropenia after olanzapine treatment.

Quoted in:

Ascari-Raccagni, A., Baldari, U., Rossi, E., Alessandrini, F., 2000. Exacerbation of chronic large plaque psoriasis associated with Olanzepine therapy. J. Eur. Acad. Dermatol. Venereol. 14, 315.
Lambert, M., Moritz, S., Haasen, C., Naber, D., 2000. Conversion from conventional to atypical neuroleptics - recommendations for inpatient and outpatient treatment. Nervenarzt 71, 859.
Liegeois, J.F., Zahid, N., Bruhwyler, J., Uetrecht, J., 2000. Hypochlorous acid, a major oxidant produced by activated neutrophils, has low effect on two pyridobenzazepine derivatives, JL 3 and JL 13. Arch. Pharm. 333, 63.
Schuld, A., Kraus, T., Hinze-Selch, D., Haack, M., Pollmacher, T., 2000. Granulocyte colony-stimulating factor plasma levels during clozapine- and olanzapine-induced granulocytopenia. Acta Psychiatr. Scand. 102, 153.
Solvason, H.B., 2000. Agranulocytosis associated with lamotrigine. Am. J. Psychiat. 157, 1704.
Teter, C.J., Early, J.J., Frachtling, R.J., 2000. Olanzapine-induced neutropenia in patients with history of clozapine treatment: Two case reports from a state psychiatric institution. J. Clin. Psychiatry 61, 872.
Bhana, N., Foster, R.H., Olney, R., Plosker, G.L., 2001. Olanzapine - An updated review of its use in the management of schizophrenia. Drugs 61, 111.
Diaz, P., Hogan, T.P., 2001. Granulocytopenia with clozapine and quetiapine. Am. J. Psychiat. 158, 651.
Vaamonde, J., Gonzalez, J.M., Hernandez, A., Ibanez, R., Gudin, M.A., Francia, M.A.D., 2001. Writer's tramp induced by olanzapine. J. Neurol. 248, 422.

2e:Tecniques of potentiation

How long should pindolol be associated with paroxetine to improve the antidepressant response?
Zanardi R, Artigas F, Franchini L, Sforzini L, Gasperini M, Smeraldi E, Perez J.
1997. J. Clin. Psychopharmacol. 17, 446.

A double-blind study was undertaken to investigate the period of treatment with the beta-adrenoreceptor/5-hydroxytryptamine 1A (5-HT1A) antagonist pindolol required to enhance the antidepressant effects of paroxetine. After 1 week of a placebo run-in period, 63 untreated major depressive inpatients were randomly assigned to three different groups. Group 1 received paroxetine (20 mg/day) plus placebo (4 weeks). Group 2 received paroxetine (20 mg/day) plus pindolol (7.5 mg/day) for 1 week and placebo for 3 weeks. Group 3 received both active treatments for the entire duration of the study (4 weeks). Clinical response was defined as a reduction of the score in the Hamilton Rating Scale for Depression (HAM-D) to 8 or below. Also, to preliminarily examine whether beta-adrenoreceptor blockade was involved in the action of pindolol, another group of 10 inpatients was treated in an open-label manner with paroxetine (20 mg/day) plus 50 mg/day of the beta-adrenergic antagonist metoprolol, devoid of significant affinity for 5-HT1A receptors. At endpoint, the incidence of treatment-emergent side effects did not significantly differ among the three groups. After 1 and 2 weeks of treatment, the two groups treated with paroxetine plus pindolol displayed a significantly greater response rate than the group treated with paroxetine plus placebo. At study completion, only the patients treated with pindolol for the entire period showed a significantly greater response rate (p = 0.05). HAM-D score were also significantly lower at endpoint in patients treated with the combination for 4 weeks (p = 0.00003). The group of patients treated with paroxetine and metoprolol exhibited a side-effect profile comparable to that of paroxetine alone. Response rates were also comparable. These findings support the efficacy of pindolol, but not of metoprolol, in accelerating the antidepressant effect of paroxetine and suggest that the administration of pindolol for the entire period of the acute treatment may increase the efficacy of paroxetine.

Quoted in:

Blier, P., Bergeron, R., 1998. The use of pindolol to potentiate antidepressant medication. J. Clin. Psychiatry 59, 16.
Blier, P., de Montigny, C., 1998. Possible serotonergic mechanisms underlying the antidepressant and anti-obsessive-compulsive disorder responses. Biol. Psychiatry 44, 313.
Hervas, I., Artigas, F., 1998. Effect of fluoxetine on extracellular 5-hydroxytryptamine in rat brain. Role of 5-HT autoreceptors. Eur. J. Pharmacol. 358, 9.
Hervas, I., Bel, N., Fernandez, A.G., Palacios, J.M., Artigas, F., 1998. In vivo control of 5-hydroxytryptamine release by terminal autoreceptors in rat brain areas differentially innervated by the dorsal and median raphe nuclei. Naunyn-Schmiedebergs Arch. Pharmacol. 358, 315.
Hughes, Z.A., Sharp, T., 1998. Evidence that pindolol lacks the ability to enhance the effect of SSRIs on presynaptic 5-HT function. Br. J. Pharmacol. 125, 6P.
Maurel, S., Schreiber, R., De Vry, J., 1998. Lack of potentiation of the anti-alcohol effects of fluoxetine by pindolol in alcohol-preferring cAA rats. Prog. Neuro-Psychopharmacol. Biol. Psychiatry 22, 1361.
Nelson, J.C., 1998. Treatment of antidepressant nonresponders: Augmentation or switch? J. Clin. Psychiatry 59, 35.
Nelson, J.C., 1998. Overcoming treatment resistance in depression. J. Clin. Psychiatry 59, 13.
Stockmeier, C.A., Shapiro, L.A., Dilley, G.E., Kolli, T.N., Friedman, L., Rajkowska, G., 1998. Increase in serotonin-1A autoreceptors in the midbrain of suicide victims with major depression - Postmortem evidence for decreased serotonin activity. J. Neurosci. 18, 7394.
Andree, B., Thorberg, S.O., Halldin, C., Farde, L., 1999. Pindolol binding to 5-HT1A receptors in the human brain confirmed with positron emission tomography. Psychopharmacology 144, 303.
Arborelius, L., Wallsten, C., Ahlenius, S., Svensson, T.H., 1999. The 5-HT1A receptor antagonist robalzotan completely reverses citalopram-induced inhibition of serotonergic cell firing. Eur. J. Pharmacol. 382, 133.
Berman, R.M., Anand, A., Cappiello, A., Miller, H.L., Hu, X.S., Oren, D.A., Charney, D.S., 1999. The use of pindolol with fluoxetine in the treatment of major depression: Final results from a double-blind, placebo- controlled trial. Biol. Psychiatry 45, 1170.
Berman, R.M., Charney, D.S., 1999. Models of antidepressant action. J. Clin. Psychiatry 60, 16.
Blier, P., de Montigny, C., 1999. Serotonin and drug-induced therapeutic responses in major depression, obsessive-compulsive and panic disorders. Neuropsychopharmacology 21, S91.
Cryan, J.F., McGrath, C., Leonard, B.E., Norman, T.R., 1999. Onset of the effects of the 5-HT1A antagonist, WAY-100635, alone, and in combination with paroxetine, on olfactory bulbectomy and 8-OH-DPAT-induced changes in the rat. Pharmacol. Biochem. Behav. 63, 333.
Gartside, S.E., Clifford, E.M., Cowen, P.J., Sharp, T., 1999. Effects of (-)-tertatolol, (-)-penbutolol and (+/-)-pindolol in combination with paroxetine on presynaptic 5-HT function: an in vivo microdialysis and electrophysiological study. Br. J. Pharmacol. 127, 145.
Haddjeri, N., de Montigny, C., Blier, P., 1999. Modulation of the firing activity of rat serotonin and noradrenaline neurons by (+/-)pindolol. Biol. Psychiatry 45, 1163.
Hjorth, S., Auerbach, S.B., 1999. Autoreceptors remain functional after prolonged treatment with a serotonin reuptake inhibitor. Brain Res. 835, 224.
Isaac, M., 1999. Where are we going with SSRIs? Eur. Neuropsychopharmacol. 9, S101.
Maes, M., Libbrecht, I., van Hunsel, F., Campens, D., Meltzer, H.Y., 1999. Pindolol and mianserin augment the antidepressant activity of fluoxetine in hospitalized major depressed patients, including those with treatment resistance. J. Clin. Psychopharmacol. 19, 177.
Pineyro, G., Blier, P., 1999. Autoregulation of serotonin neurons: Role in antidepressant drug action. Pharmacol. Rev. 51, 533.
Puzantian, T., Kawase, K., 1999. Does the addition of pindolol accelerate or enhance the response to selective serotonin reuptake inhibitor antidepressants? Pharmacotherapy 19, 205.
Rasanen, P., Hakko, H., Tiihonen, J., 1999. Pindolol and major affective disorders: A three-year follow-up study of 30,485 patients. J. Clin. Psychopharmacol. 19, 297.
Raurich, A., Mengod, G., Artigas, F., Cortes, R., 1999. Displacement of the binding of 5-HT1A receptor ligands to pre- and postsynaptic receptors by (-)pindolol. A comparative study in rodent, primate and human brain. Synapse 34, 68.
Ruedrich, S., Erhardt, L., 1999. Beta-adrenergic blockers in mental retardation and developmental disabilities. Ment. Retard. Dev. Disabil. Res. Rev. 5, 290.
Rueter, L.E., Blier, P., 1999. Electrophysiological examination of the effects of sustained flibanserin administration on serotonin receptors in rat brain. Br. J. Pharmacol. 126, 627.
Scorza, C., Silveira, R., Nichols, D.E., Reyes-Parada, M., 1999. Effects of 5-HT-releasing agents on the extracellullar hippocampal 5-HT of rats. Implications for the development of novel antidepressants with a short onset of action. Neuropharmacology 38, 1055.
Winter, J.C., Fiorella, D.J., Helsley, S.E., Rabin, R.A., 1999. Partial generalization of (-)DOM to fluvoxamine in the rat: implications for SSRI-induced mania and psychosis. Int. J. Neuropsychopharmacol. 2, 165.
Yan, H.M., Lewander, T., 1999. Differential tissue distribution of the enantiomers of racemic pindolol in the rat. Eur. Neuropsychopharmacol. 10, 59.
Andree, B., Halldin, C., Thorberg, S.O., Sandell, J., Farde, L., 2000. Use of PET and the radioligand. Nucl. Med. Biol. 27, 515.
Arborelius, L., Linner, L., Wallsten, C., Ahlenius, S., Svensson, T.H., 2000. Partial 5-HT1A receptor agonist properties of (-)pindolol in combination with citalopram on serotonergic dorsal raphe cell firing in vivo. Psychopharmacology 151, 77.
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