The Experts below are selected from a list of 135 Experts worldwide ranked by ideXlab platform
Frederic M Quitkin - One of the best experts on this subject based on the ideXlab platform.
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Prophylactic efficacy of phenelzine and Imipramine in chronic atypical depression: likelihood of recurrence on discontinuation after 6 months' remission.
The American journal of psychiatry, 1997Co-Authors: Jonathan W. Stewart, Patrick J Mcgrath, E Tricamo, Frederic M QuitkinAbstract:Objective: Demonstration of antidepressant efficacy beyond 6 months has infrequently been addressed, and no long-term efficacy data exist for patients with chronic atypical depression. Method: Sixty patients with atypical depression (according to Columbia University criteria) of at least 2 years’ duration and who had improved with Imipramine or phenelzine were stabilized for 6 months and then randomly continued the same medication or placebo for 6 months. Results: Several baseline differences suggested that patients who entered the discontinuation trial on a regimen of phenelzine were more chronically depressed than the Imipramine-treated patients. Survival analysis showed a marked advantage for phenelzine relative to placebo. In addition, patients switched to placebo from phenelzine experienced a recurrence of depressive symptoms significantly more often than patients switched to placebo from Imipramine. Patients maintained with Imipramine did not have lower relapse rates than those switched from Imipramine to placebo. Recurrence rates were 23% for patients maintained on a regimen of phenelzine, 41% for those maintained on a regimen of Imipramine, 47% for those switched from Imipramine to placebo, and 87% for placebo-treated patients originally treated with phenelzine. Conclusions: Patients with chronic atypical depression are at high risk of recurrence if phenelzine is withdrawn 6 months after initial improvement. Similar findings were not demonstrated for Imipramine; this replicates acute trials demonstrating Imipramine’s relative ineffectiveness in patients with atypical depression. Differences in recurrence rates after the switch to placebo from phenelzine and Imipramine could be due to the two drugs’ different mechanisms of action or to baseline differences in the two populations. (Am J Psychiatry 1997; 154:31‐36)
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Imipramine is effective after unsuccessful cognitive therapy: sequential use of cognitive therapy and Imipramine in depressed outpatients.
Journal of clinical psychopharmacology, 1993Co-Authors: Jonathan W. Stewart, Mary A. Mercier, Vito Agosti, Mary Guardino, Frederic M QuitkinAbstract:As a partial test of whether the same or different patients benefit from cognitive therapy and tricyclic antidepressant agents, depressed outpatients first received cognitive therapy, then nonresponders were treated with either Imipramine or placebo. If the two treatments were effective for the same subgroup of patients, Imipramine should not be more effective than placebo because potential responders should already have been removed by treatment with cognitive therapy. Alternatively, if cognitive therapy and Imipramine are effective for different subtypes of depressive disorder, then Imipramine ought to be more effective than placebo for patients failing to benefit from cognitive therapy because some potential Imipramine failures would already have been removed. Thirty-six depressed outpatients were treated with weekly cognitive therapy for 16 weeks with 17 (47%) responding. Nonresponders were then randomly assigned to Imipramine or placebo for 6 weeks to a maximum dose of 300 mg of Imipramine per day. Of 12 patients completing the double-blind medication trial, all 5 assigned to Imipramine had a clear-cut response, whereas none of the other seven benefited from placebo (chi 2 = 12.00; p = 0.001). Although the numbers are small, these results suggest rejection of the hypothesis that Imipramine is effective for the same subpopulation of depressed patients as is cognitive therapy.
Patrick Schloss - One of the best experts on this subject based on the ideXlab platform.
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distinct effects of Imipramine on 5 hydroxytryptamine uptake mediated by the recombinant rat serotonin transporter sert1
Journal of Neurochemistry, 2002Co-Authors: Heinrich Betz, Patrick SchlossAbstract:Abstract: Tricyclic and nontricyclic serotonin [5-hydroxytryptamine (5-HT)] uptake inhibitors are widely used for the treatment of depression. Here, we show that both the tricyclic antidepressant Imipramine and the nontricyclic antidepressant citalopram competitively inhibit 5-HT transport mediated by the recombinant rat 5-HT transporter SERT1. For citalopram, the concentration producing half-maximal transport inhibition was in the same order of magnitude as its KD value determined by equilibrium binding. In contrast, the inhibitory potency of Imipramine was more than one order of magnitude lower than its KD value. Our data are consistent with low-affinity Imipramine binding occurring at or close to the substrate recognition site, which also binds citalopram. Occupation of the high-affinity Imipramine binding site on SERT1 did not affect 5-HT transport but allosterically displaced citalopram from the substrate recognition site. Consequently, low concentrations of Imipramine partially protected 5-HT transport from citalopram inhibition. This protection was only observed in the presence of Na+ because high-affinity Imipramine binding is strictly sodium-dependent. Thus, depending on which of its binding sites on SERT1 is occupied, Imipramine may exert distinct effects on 5-HT uptake mediated by the recombinant rat 5-HT transporter.
Jonathan W. Stewart - One of the best experts on this subject based on the ideXlab platform.
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Prophylactic efficacy of phenelzine and Imipramine in chronic atypical depression: likelihood of recurrence on discontinuation after 6 months' remission.
The American journal of psychiatry, 1997Co-Authors: Jonathan W. Stewart, Patrick J Mcgrath, E Tricamo, Frederic M QuitkinAbstract:Objective: Demonstration of antidepressant efficacy beyond 6 months has infrequently been addressed, and no long-term efficacy data exist for patients with chronic atypical depression. Method: Sixty patients with atypical depression (according to Columbia University criteria) of at least 2 years’ duration and who had improved with Imipramine or phenelzine were stabilized for 6 months and then randomly continued the same medication or placebo for 6 months. Results: Several baseline differences suggested that patients who entered the discontinuation trial on a regimen of phenelzine were more chronically depressed than the Imipramine-treated patients. Survival analysis showed a marked advantage for phenelzine relative to placebo. In addition, patients switched to placebo from phenelzine experienced a recurrence of depressive symptoms significantly more often than patients switched to placebo from Imipramine. Patients maintained with Imipramine did not have lower relapse rates than those switched from Imipramine to placebo. Recurrence rates were 23% for patients maintained on a regimen of phenelzine, 41% for those maintained on a regimen of Imipramine, 47% for those switched from Imipramine to placebo, and 87% for placebo-treated patients originally treated with phenelzine. Conclusions: Patients with chronic atypical depression are at high risk of recurrence if phenelzine is withdrawn 6 months after initial improvement. Similar findings were not demonstrated for Imipramine; this replicates acute trials demonstrating Imipramine’s relative ineffectiveness in patients with atypical depression. Differences in recurrence rates after the switch to placebo from phenelzine and Imipramine could be due to the two drugs’ different mechanisms of action or to baseline differences in the two populations. (Am J Psychiatry 1997; 154:31‐36)
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Imipramine is effective after unsuccessful cognitive therapy: sequential use of cognitive therapy and Imipramine in depressed outpatients.
Journal of clinical psychopharmacology, 1993Co-Authors: Jonathan W. Stewart, Mary A. Mercier, Vito Agosti, Mary Guardino, Frederic M QuitkinAbstract:As a partial test of whether the same or different patients benefit from cognitive therapy and tricyclic antidepressant agents, depressed outpatients first received cognitive therapy, then nonresponders were treated with either Imipramine or placebo. If the two treatments were effective for the same subgroup of patients, Imipramine should not be more effective than placebo because potential responders should already have been removed by treatment with cognitive therapy. Alternatively, if cognitive therapy and Imipramine are effective for different subtypes of depressive disorder, then Imipramine ought to be more effective than placebo for patients failing to benefit from cognitive therapy because some potential Imipramine failures would already have been removed. Thirty-six depressed outpatients were treated with weekly cognitive therapy for 16 weeks with 17 (47%) responding. Nonresponders were then randomly assigned to Imipramine or placebo for 6 weeks to a maximum dose of 300 mg of Imipramine per day. Of 12 patients completing the double-blind medication trial, all 5 assigned to Imipramine had a clear-cut response, whereas none of the other seven benefited from placebo (chi 2 = 12.00; p = 0.001). Although the numbers are small, these results suggest rejection of the hypothesis that Imipramine is effective for the same subpopulation of depressed patients as is cognitive therapy.
Chiaki Kamei - One of the best experts on this subject based on the ideXlab platform.
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Mechanism of Imipramine-induced seizures in amygdala-kindled rats.
Epilepsy research, 2006Co-Authors: Jun Ago, Takashi Ishikawa, Naotaka Matsumoto, Ashequr Rahman, Chiaki KameiAbstract:The present study was undertaken to get insight in the possible mechanisms of Imipramine-induced seizures in amygdala-kindled rats. The intraperitoneal (i.p.) injection of Imipramine produced potent behavioral and electroencephalogram (EEG) seizures in amygdala-kindled rats. Histidine (1500 mg/kg, i.p.) and histamine (10 and 20 microg, i.c.v.) significantly attenuated the seizures induced by Imipramine (50 mg/kg, i.p.) in kindled rats. In addition, the inhibition of Imipramine-induced seizures by histamine (20 microg, i.c.v.) was antagonized by an H1 antagonist, pyrilamine. An H3 antagonist, thioperamide (50 microg, i.c.v.), also significantly attenuated the Imipramine-induced seizures in kindled rats. The i.p. injection of alpha-methyl-p-tyrosine at a dose of 250 mg/kg significantly diminished the seizures induced by Imipramine. However, p-chlorophenylalanine and physostigmine did not affect the Imipramine-induced seizures to any extent. These data give strong hints that the H1 receptor antagonistic properties and the brain noradrenaline activating effects of Imipramine are centrally involved in Imipramine-induced seizures, and central serotonergic and cholinergic neurotransmissions are not involved in the seizures induced by Imipramine in amygdala-kindled rats.
John F. Sheridan - One of the best experts on this subject based on the ideXlab platform.
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Antidepressant Imipramine diminishes stress-induced inflammation in the periphery and central nervous system and related anxiety- and depressive- like behaviors.
Brain behavior and immunity, 2016Co-Authors: Karol Ramirez, John F. SheridanAbstract:In order to relieve anxiety and depression accompanying stress, physicians resort to tricyclic antidepressants, such as Imipramine. We had previously shown that Imipramine reversed stress-induced social avoidance behavior, and down-regulated microglial activation 24days after stress cessation. To further characterize the effects of Imipramine on stress induced neuroimmune dysregulation and associated changes in behavior, the aims of this study were to determine if Imipramine 1) ameliorated stress-induced inflammation in the periphery and central nervous system, and 2) prevented stress related anxiety- and depressive-like behaviors. C57BL/6 mice were treated with Imipramine (15mg/kg) in their drinking water, and exposed to repeated social defeat (RSD). Imipramine attenuated stress-induced corticosterone and IL-6 responses in plasma. Imipramine decreased the percentage of monocytes and granulocytes in the bone marrow and circulation. However, Imipramine did not prevent splenomegaly, stress-related increased percentage of granulocytes in this organ, and the production of pro-inflammatory cytokines in the spleen, following RSD. Moreover, Imipramine abrogated the accumulation of macrophages in the brain in mice exposed to RSD. Imipramine blocked neuroinflammatory signaling and prevented stress-related anxiety- and depressive-like behaviors. These data support the notion that pharmacomodulation of the monoaminergic system, besides exerting anxiolytic and antidepressant effects, may have therapeutic effects as a neuroimmunomodulator during stress.
