|
citalopram escitalopram Lexapro The use of citalopram in an integrated approach to the treatment of eating disorders: an open study.
Calandra C, Gulino V, Inserra L, Giuffrida A.
Service for the Therapy of Eating Disorders, University Hospital of Catania, Italy.
This study investigated the efficacy and safety of citalopram in the treatment of eating disorders. Eighteen female patients gave their informed consent to enrollment in the trial: twelve with bulimia nervosa, six with anorexia nervosa according to the DSM IV criteria. They received individual systemic psychotherapy and took 20 mg/day citalopram for 8 weeks. At the beginning and end of the trial, their BMI, body fat and lean mass were checked and they completed the Eating Disorder Inventory and Binge Scale. The results showed that citalopram is effective and safe in the treatment of eating disorders: binge eating episodes and mean scores in three EDI subscales (bulimia, ineffectiveness and interoceptive awareness) significantly decreased in the bulimic patients, and mean scores in the EDI body dissatisfaction subscale significantly decreased in the anorexic patients.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10728184&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro The effect of citalopram treatment on platelet serotonin function in panic disorders.
Neuger J, Wistedt B, Sinner B, Aberg-Wistedt A, Stain-Malmgren R.
Karolinska Institute, Institution of Clinical Neuroscience, Department of Psychiatry, St Goran's Hospital, Stockholm, Sweden. Jolanta.Neuger cspo.sll.se
We investigated the effect of the selective serotonin reuptake inhibitor (SSRI) citalopram after 6-8 weeks and 6 months of treatment on clinical and peripheral indexes for central serotonergic function: platelet [14C]serotonin uptake and [3H]paroxetine- and [3H]LSD-binding to platelets membranes in 33 patients with panic disorder. Basal data from patients were compared with data from a control material consisting of 33 healthy volunteers. Bmax for platelet [3H]paroxetine binding was significantly lower in patients than in controls. There were no differences in serotonin uptake or [3H]LSD-binding between patients and controls. The degree of anxiety and depression was assessed using the Beck Anxiety Inventory (BAI) and Beck Depression Inventory self-assessment scales, and the Clinical Anxiety Scale and the Montgomery Asberg Depression Rating Scale for clinical evaluation. Complete remission was found in one third of the patients after 6-8 weeks and in two-thirds after 6 months of treatment. The reduction in assessment scores was parallelled with similar reductions in platelet 5-HT2-receptor density, [3H]LSD affinity variable (Kd) and Vmax for platelet [14C]5-HT uptake. Citalopram treatment did not alter Bmax and Kd for platelet [3H]paroxetine-binding. A positive correlation was found between Vmax for the platelet [14C]5-HT uptake and BAI after 6 months citalopram treatment. The present study shows that citalopram has a therapeutic effect in panic disorders. A prerequisite of responding to treatment might be plasticity in the serotonergic system.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10759339&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro Mirtazapine enhances frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission by blockade of alpha2-adrenergic and serotonin2C receptors: a comparison with citalopram.
Millan MJ, Gobert A, Rivet JM, Adhumeau-Auclair A, Cussac D, Newman-Tancredi A, Dekeyne A, Nicolas JP, Lejeune F.
Psychopharmacology Department, Institut de Recherches Servier, Centre de Recherches de Croissy, 125, Chemin de Ronde, 78290, Croissy-sur-Seine, Paris, France.
Mirtazapine displayed marked affinity for cloned, human alpha2A-adrenergic (AR) receptors at which it blocked noradrenaline (NA)-induced stimulation of guanosine-5'-O-(3-[35S]thio)-triphosphate ([35S]-GTPgammaS) binding. Similarly, mirtazapine showed high affinity for cloned, human serotonin (5-HT)2C receptors at which it abolished 5-HT-induced phosphoinositide generation. Alpha2-AR antagonist properties were revealed in vivo by blockade of UK-14,304-induced antinociception, while antagonist actions at 5-HT2C receptors were demonstrated by blockade of Ro 60 0175-induced penile erections and discriminative stimulus properties. Mirtazapine showed negligible affinity for 5-HT reuptake sites, in contrast to the selective 5-HT reuptake inhibitor, citalopram. In freely moving rats, in the dorsal hippocampus, frontal cortex (FCX), nucleus accumbens and striatum, citalopram increased dialysate levels of 5-HT, but not dopamine (DA) and NA. On the contrary, mirtazapine markedly elevated dialysate levels of NA and, in FCX, DA, whereas 5-HT was not affected. Citalopram inhibited the firing rate of serotonergic neurons in dorsal raphe nucleus, but not of dopaminergic neurons in the ventral tegmental area, nor adrenergic neurons in the locus coeruleus. Mirtazapine, in contrast, enhanced the firing rate of dopaminergic and adrenergic, but not serotonergic, neurons. Following 2 weeks administration, the facilitatory influence of mirtazapine upon dialysate levels of DA and NA versus 5-HT in FCX was maintained, and the influence of citalopram upon FCX levels of 5-HT versus DA and NA was also unchanged. Moreover, citalopram still inhibited, and mirtazapine still failed to influence, dorsal raphe serotonergic neurons. In conclusion, in contrast to citalopram, mirtazapine reinforces frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission. These actions reflect antagonist properties at alpha2A-AR and 5-HT2C receptors.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10762339&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro Effect of acute treatment with YM992 on extracellular serotonin levels in the rat frontal cortex.
Hatanaka K, Yatsugi S, Yamaguchi T.
Neuroscience Research, Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co., Ltd., 21 Miyukigaoka, Tsukuba, Japan. hatanaka yamanouchi.co.jp
(S)-2-[[(7-fluoroindan-4-yl)oxy]methyl]morpholine monohydrochloride (YM992) is a novel putative antidepressant exhibiting both selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibition and 5-HT(2A) receptor antagonism. In vivo microdialysis revealed that a single treatment with YM992 (3, 10, 30 mg/kg i.p.) dose-dependently increased extracellular 5-HT levels in the rat frontal cortex. Fluoxetine, citalopram and venlafaxine also produced significant increases in 5-HT levels at doses of 10-30 mg/kg. However, the increase in 5-HT levels induced by YM992 was significantly larger than increases elicited by these three compounds at 30 mg/kg. The combined administration of R-(+)-alpha-(2, 3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-piperidine-methanol (MDL100,907) (a selective 5-HT(2A) receptor antagonist) and citalopram produced no additional increase in 5-HT levels compared with citalopram treatment alone. YM992 moderately enhanced [3H]5-HT release from rat cerebral cortex synaptosomes using different mechanisms than p-chloroamphetamine. In comparison, 10-microM fluoxetine markedly induced 5-HT release in vitro, while citalopram and venlafaxine had no noticeable effect on release. YM992 produces a more robust increase of 5-HT levels acutely than other antidepressants in vivo and the effect may be due to 5-HT releasing properties of the drug.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10781669&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro Effect of acute treatment with YM992 on extracellular norepinephrine levels in the rat frontal cortex.
Hatanaka K, Yatsugi S, Yamaguchi T.
Neuroscience Research, Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co. Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki, Japan. hatanaka yamanouchi.co.jp
The effects of acute treatment with (S)-2-[[(7-fluoroindan-4-yl)oxy]methyl]morpholine monohydrochloride (YM992), venlafaxine, fluoxetine and citalopram on extracellular norepinephrine levels were examined in the rat frontal cortex by in vivo microdialysis. YM992 (3, 10, 30 mg/kg, i.p.) dose-dependently increased extracellular norepinephrine levels (3-fold at 10 mg/kg, 5. 5-fold at 30 mg/kg). While venlafaxine and 30 mg/kg fluoxetine also produced significant increases in norepinephrine levels, 30 mg/kg citalopram had no effect. The combined administration of MDL100,907 (a selective 5-HT(2A) receptor antagonist) and citalopram did significantly increase norepinephrine levels compared with either saline or citalopram treatment. Therefore, a synergistic effect due to 5-HT reuptake inhibition and 5-HT(2A) receptor antagonism of YM992 may partly contribute to the increase of extracellular norepinephrine levels. YM992 enhances the neurotransmission of not only 5-HT system but also norepinephrine, and as such may have a preclinical profile different from that of a selective serotonin reuptake inhibitor.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10781670&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro Effects of chronic citalopram treatment on central and peripheral spontaneous open-field behaviours in rats.
Kugelberg FC, Apelqvist G, Bengtsson F.
Division of Clinical Pharmacology, Department of Medicine and Care, Faculty of Health Sciences, Linkoping University, Sweden.
The spontaneous open-field behavioural effects of 10 days of chronic treatment with two clinical doses (10 and 20 mg/kg daily) and one high/toxic dose (100 mg/kg daily) of the selective serotonin reuptake inhibitor citalopram (delivered subcutaneously by implanted osmotic pumps) were examined in rats. Central and peripheral arena locomotor and rearing activities were recorded simultaneously, and the data were assessed during the first hour as well as during the following 24 hr (the latter for effects on the diurnal rhythm). Rats treated with 100 mg/kg daily exhibited lower peripheral locomotor and rearing activities than the other groups during the first test hour. The ratio between central and peripheral activity increased in a dose-dependent non-proportional manner during the first test hour, indicating a general increase in the central arena activity exerted by the rats when treated with citalopram. No major differences were observed between any of the four groups in overall behavioural activities over the 24-hr period. This study indicated that the open-field locomotor and rearing behaviours in normal rats were affected by increasing doses of racemic citalopram, particularly during the first hour of adaptation.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12403051&dopt=Abstract citalopram escitalopram Lexapro
citalopram escitalopram Lexapro Cardiac electrophysiological effects of citalopram in guinea pig papillary muscle comparison with clomipramine.
Pacher P, Bagi Z, Lako-Futo Z, Ungvari Z, Nanasi PP, Kecskemeti V.
Department of Pharmacology and Pharmacotherapy, Semmelweis University of Medicine, H-l445, Budapest, Hungary.
The effect of citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant, was studied on cardiac action potential configuration and compared with that of the tricyclic antidepressant (TCA) clomipramine. Conventional microelectrode techniques were used in right ventricular papillary muscle preparations of the guinea pig. Citalopram caused a concentration-dependent (10-100 microM) shortening of action potential duration (APD), depression of plateau and overshoot potential, and reduction of maximum velocity of depolarization (V(max)). No significant changes in resting membrane potential were observed. Similar results were obtained with clomipramine; however, reduction of V(max) and overshoot was more pronounced with clomipramine, whereas citalopram caused relatively greater shortening of APD. Effects of both drugs were partly reversible. The results indicate that the SSRI antidepressant citalopram, similarly to TCA compounds, alters cardiac action potential configuration in guinea pig ventricular muscle, probably owing to inhibition of cardiac Na(+) and Ca(2+) channels. Differences in cardiac side effects of the two drugs may be related to their different actions on cardiac action potential configuration.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10793264&dopt=Abstract citalopram escitalopram Lexapro
Lexapro (escitalopram) References
Lexapro or escitalopram 1 |
Lexapro or escitalopram 2 |
Lexapro or escitalopram 3 |
Lexapro or escitalopram 4 |
Lexapro or escitalopram 5 |
Lexapro or escitalopram 6 |
Lexapro or escitalopram 7 |
Lexapro or escitalopram 8 |
Lexapro or escitalopram 9 |
Lexapro or escitalopram 10 |
Lexapro or escitalopram 11 |
Lexapro or escitalopram 12 |
Lexapro or escitalopram 13 |
Lexapro or escitalopram 14 |
Lexapro or escitalopram 15 |
Lexapro or escitalopram 16 |
Lexapro or escitalopram 17 |
Lexapro or escitalopram 18 |
Lexapro or escitalopram 19 |
Lexapro or escitalopram 20 |
Lexapro or escitalopram 21 |
Lexapro or escitalopram 22 |
Lexapro or escitalopram 23 |
Lexapro or escitalopram 24 |
Lexapro or escitalopram 25 |
Lexapro or escitalopram 26 |
Lexapro or escitalopram 27 |
Lexapro or escitalopram 28 |
Lexapro or escitalopram 29 |
Lexapro or escitalopram 30 |
Lexapro or escitalopram 31 |
Lexapro or escitalopram 32 |
Lexapro or escitalopram 33 |
Lexapro or escitalopram 34 |
Lexapro or escitalopram 35 |
Lexapro or escitalopram 36 |
Lexapro or escitalopram 37 |
Lexapro or escitalopram 38 |
Lexapro or escitalopram 39 |
Lexapro or escitalopram 40 |
Lexapro or escitalopram 41 |
Lexapro or escitalopram 42 |
Lexapro or escitalopram 43 |
Lexapro or escitalopram 44 |
Lexapro or escitalopram 45 |
Lexapro or escitalopram 46 |
Lexapro or escitalopram 47 |
Lexapro or escitalopram 48 |
Lexapro or escitalopram 49 |
Lexapro or escitalopram 50 |
Lexapro or escitalopram 51 |
Lexapro or escitalopram 52 |
Lexapro or escitalopram 53 |
Lexapro or escitalopram 54 |
Lexapro or escitalopram 55 |
Lexapro or escitalopram 56 |
Lexapro or escitalopram 57 |
Lexapro or escitalopram 58
| |