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Citalopram

SSRIs are widely used for treatment of depression, as well as, for example, panic disorders and obsessive—compulsive disorder. These dmgs are well recognized as clinically effective antidepressants having an improved side-effect profile as compared to the TCAs and irreversible MAO inhibitors. Indeed, these dmgs lack the anticholinergic, cardiovascular, and sedative effects characteristic of TCAs. Their main adverse effects include nervousness /anxiety, nausea, diarrhea or constipation, insomnia, tremor, dizziness, headache, and sexual dysfunction. The most commonly prescribed SSRIs for depression are fluoxetine (31), fluvoxamine (32), sertraline (52), citalopram (53), and paroxetine (54). SSRIs together represent about one-fifth of total worldwide antidepressant unit sales. [Pg.232]

Two recently introduced antidepressants are notable m that they are selective serotonin uptake inhibitors Citalopram (19) is reported to be as effective as amitriptyline m the treatment of endogenous depression [75, 16] Fluoxetine (20) as the hydrochlonde is approved for major depressive disorders mcludmg those with concomitant anxiety Interestmgly, it also appears useful m the treatment of obesity [17]... [Pg.1121]

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. [Pg.77]

Selective serotonine reuptake inhibitor (SSRI) is an abbreviation for the class of antidepressants known as the Selective Serotonin Reuptake Inhibitors. Examples of SSRIs include fluoxetine, paroxetine, citalopram, and sertraline. These drugs selectively inhibit the serotonin transporter thus prolonging the synaptic lifespan of the neurotransmitter serotonin. [Pg.1113]

Indeed, 5-HT is also a substrate for the 5-HT transporter, itself an important player in the treatment of depression, and more recently for the whole range of anxiety disorders spectrum (GAD, OCD, social and other phobias, panic and post-traumatic stress disorders). It is the target for SSRIs (selective serotonin reuptake inhibitors) such as fluoxetine, paroxetine, fluvoxamine, and citalopram or the more recent dual reuptake inhibitors (for 5-HT and noradrenaline, also known as SNRIs) such as venlafaxine. Currently, there are efforts to develop triple uptake inhibitors (5-HT, NE, and DA). Further combinations are possible, e.g. SB-649915, a combined 5-HTia, 5-HT1b, 5-HT1d inhibitor/selective serotonin reuptake inhibitor (SSRI), is investigated for the treatment of major depressive disorder. [Pg.1124]

CCuN 544-92-3) see Cinoxacin Citalopram Lamotrigine Mabuterol Methallenestril Trimetrexate glucuronate Corey lactone... [Pg.2338]

C5H12CIN 109-54-6) see Acepromazine Bencyclane Benzydamine Chlorpromazine Citalopram Clomipramine Dimetacrine Imipramine Promazine Prothipendyl Triflupromazine... [Pg.2362]

Amit Z, Brown Z, Sutherland A, et al Reduction in alcohol intake in humans as a function of treatment with zimelidine implications for rrearment, in Research Advances in New Psychopharmacological Treatments for Alcoholism. Edired by Naranjo CA, Sellers EM. Amsrerdam, Elsevier, 1985 Angelone SM, Bellini L, Di Bella D, er al Effects of fluvoxamine and citalopram in maintaining abstinence in a sample of Italian detoxified alcoholics. Alcohol Alcohol 33 151-156, 1998... [Pg.41]

Balldin J, Berggren U, Engel J, et al Effect of citalopram on alcohol intake in heavy drinkers. Alcohol Clin Exp Res 18 1133-1136, 1994... [Pg.42]

Naranjo CA, Sellers EM, Chater K, et al Non-pharmacological interventions in acute alcohol withdrawal. Clin Pharmacol Ther 34 214—219, 1983 Naranjo CA, Sellers EM, Roach CA, et al Zimelidine-induced variations in alcohol intake hy nondeptessed heavy drinkers. Clin Pharmacol Ther 35 374-381, 1984 Naranjo CA, Sellers EM, Sullivan ]T, et al The serotonin uptake inhibitor citalopram attenuates ethanol intake. Clin Pharmacol Ther 41 266-274, 1987 Naranjo CA, Sullivan ]T, Kadlec KE, et al Differential effects of viqualine on alcohol intake and other consummatory behaviors. Clin Pharmacol Ther 46 301 -309,1989 Naranjo CA, Kadlec KE, Sanhueza P, et al Fluoxetine differentially alters alcohol intake and other consummatory behaviors in problem drinkers. Clin Pharmacol Ther 47 490 98, 1990... [Pg.50]

Naranjo CA, Poulos CX, Bremner KE, et al Citalopram decreases desirability, liking, and consumption of alcohol in alcohol-dependent drinkers. Clin Pharmacol Ther 31 729-739, 1992... [Pg.50]

Naranjo CA, Bremner KE, Lanctot KL Effects of citalopram and a brief psychosocial intervention on alcohol intake, dependence, and problems. Addiction 90 87-99, 1995... [Pg.50]

Angelone SM, Bellini L, DiBella D, et al Effects of fluvoxamine and citalopram in maintaining abstinence in a sample of Italian detoxified alcoholics. Alcohol Alcoholism 33 151-156, 1998... [Pg.356]

Nuitjen MJC, Hardens M, Souetre E (1995). A Markov Process Analysis comparing the cost effectiveness of maintenance therapy with citalopram versus standard therapy in major depression. Pharmacoeconomics, 159-68. [Pg.54]

SSRF Inhibition of 5-HT reuptake Citalopram Fluoxetine Various... [Pg.434]

Paroxetine is the most potent inhibitor of 5-HT reuptake but, in terms of distinguishing one compound from another, their preferential selectivity for inhibition of 5-HT rather than noradrenaline reuptake is the key criterion. Citalopram is by far the most selective in vitro (1500-3000-fold) and fluoxetine, the most frequently prescribed SSRI in the UK, is the least selective of all these agents (see Stanford 1999). In fact, it is worth questioning whether fluoxetine is a true SSRI at all. [Pg.440]

It is perhaps not surprising that, even after taking into account pharmacokinetic differences between these drugs, the therapeutic doses of the SSRIs do not parallel their Ki for inhibition of 5-HT reuptake. For instance, citalopram is about a thousand times more selective than fluoxetine for inhibition of 5-HT uptake, and yet their clinically effective doses are similar. In short, not only is their selectivity for the 5-HT transporter in vitro a poor predictor of their efficacy in vivo but it has to be questioned whether any of these compounds actually work by blocking 5-HT uptake alone. [Pg.441]

Because the SSRIs are derived from different chemical groups, their receptor interactions vary from compound to compound but, apart from paroxetine, none of them shows any appreciable binding to muscarinic receptors, a prime objective of their development. However, compared with other SSRIs, fluoxetine binds with moderately high affinity to human 5-HT2A (.K) 280 nM) and 5-HT2C receptors (Aij 55 nM) sertraline is a relatively potent ligand for ai-adrenoceptors, 2-adrenoceptors and Dj receptors and citalopram shows appreciable binding to 5-HTia, oc]-adrenoceptors and Hi receptors (Table 20.6 Stanford 1996). The extent to which any of these receptor interactions affects the efficacy of these compounds is not known. [Pg.441]

The above conclusion is supported by the results shown in figure 4. Just as inhibitors of the 5-HT uptake carrier can antagonize MDMA-induced [ H]5-HT release in vitro, coadministration of MDMA with an uptake inhibitor such as citalopram can completely block the acute depletion of 5-HT. Although citalopram also antagonized the MDMA-induced decrease in TPH activity, there was still a significant loss of enzyme activity when compared to control. This implies that if MDMA requires access to the interior of the nerve terminals to affect TPH activity, it does not require the activity of the uptake carrier to gain entrance. Hence, these results are consistent with the outcome of synaptosomal uptake experiments with [ HJMDMA (Schmidt et al. 1987), which show that MDMA is not actively concentrated by a carrier system. Furthermore, it is apparent that the loss of enzyme activity alone is not sufficient to reduce 5-HT concentrations, but that release via the carrier must occur simultaneously, to deplete the terminal once synthetic capacity is reduced. [Pg.181]

FIGURE 4. Effect of inhibition of the 5-HT uptake carrier by citalopram... [Pg.183]

Since the neurotoxic effects of drugs such as parachloroamphetamine on serotonin neurons can be prevented by serotonin uptake blockers (Ross 1976 Sanders-Bush and Steranka 1978). the possibility that serotonin uptake carrier protein was likewise involved in the neurotoxic effects of MDMA was investigated. As shown in figure 4, pretreatment of rats with the seleetive serotonin uptake blocker citalopram (10 ml/kg), prior to each injection of 10 mg/kg MDMA, resulted in nearly complete protection against the neurotoxic effects of MDMA. Citalopram-pretreated rats exhibited only a 15 pereent decrease in serotonin uptake sites. No significant alterations in the eontent of serotonin and 5-HIAA were observed following MDMA treatment, in eomparison with 60 to 80 percent reductions in the serotonergie parameters observed in rats treated with an identical dose of MDMA alone. [Pg.203]

The data deseribed above demonstrate that destruction of serotonin axons by MDMA involves the serotonin aetive uptake carrier and that administration of citalopram, a selective serotonin uptake blocker, prior to administration of MDMA, ean prevent the decreases in serotonin markers elicited by MDMA alone. These data are eonsistent with previous reports for other potent serotonin neurotoxins, demonstrating that pretreatment with serotonin uptake blockers can prevent the neurotoxic effects of parachloroamphetamine (Ross 1976 Sanders-Bush and Steranka 1978). Furthermore, it has been shown that MDMA-induced neurotoxicity can be prevented or reversed if a serotonin uptake blocker such as fluoxetine is administered no later than 12 hours after MDMA treatment (Schmidt 1986). [Pg.203]

MDMA, MDMA plus 10 mg/kg citalopram, and MDMA plus 25 mg/kg SKF 525A on the density of serotonin (5-HT) uptake sites in homogenates of rat frontal cerebral cortex... [Pg.204]


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Acenocoumarol Citalopram

Alprazolam Citalopram

Amitriptyline Citalopram

Antidepressants citalopram

Antidepressants fluoxetine/citalopram/fluvoxamine

Benzodiazepines 4- Citalopram

Buspirone Citalopram

Carbamazepine Citalopram

Celexa - Citalopram hydrobromide

Chlorpromazine Citalopram

Ciclosporin Citalopram

Cimetidine Citalopram

Cipramil - Citalopram hydrobromide

Citalopram , dosing

Citalopram 4- Propafenone

Citalopram 4- Rifampin

Citalopram 4- Sibutramine

Citalopram 4- Theophylline

Citalopram 4- Thioridazine

Citalopram 4- Tramadol

Citalopram 4- Trazodone

Citalopram 4- Warfarin

Citalopram 4- Zolmitriptan

Citalopram Alcohol

Citalopram CYP2C19 substrate

Citalopram Cipramil

Citalopram Clomipramine

Citalopram Cocaine

Citalopram Desipramine

Citalopram Dexamfetamine

Citalopram Dextromethorphan

Citalopram Digoxin

Citalopram Ecstasy

Citalopram Fluvoxamine

Citalopram Haloperidol

Citalopram Imipramine

Citalopram Ketoconazole

Citalopram Levomepromazine

Citalopram Linezolid

Citalopram MAOIs

Citalopram MDMA

Citalopram Maprotiline

Citalopram Metoprolol

Citalopram Monoamine oxidase inhibitors

Citalopram Olanzapine

Citalopram Perphenazine

Citalopram Selegiline

Citalopram Triazolam

Citalopram action

Citalopram adverse effects

Citalopram and escitalopram

Citalopram and metabolites

Citalopram arrhythmia with

Citalopram characteristics

Citalopram chemical structure

Citalopram clozapine

Citalopram conditioning

Citalopram cytochrome P450 inhibition

Citalopram dosage

Citalopram drug interactions

Citalopram enantiomers

Citalopram hydrobromide

Citalopram in Alzheimer’s disease

Citalopram in depression

Citalopram in panic disorder

Citalopram in posttraumatic stress disorder

Citalopram in social anxiety disorder

Citalopram indications

Citalopram interaction with other drugs

Citalopram moclobemide

Citalopram pharmacokinetics

Citalopram side effects

Citalopram side effects profile

Citalopram transporters

Depressants) Citalopram

Depression citalopram

Obsessive-compulsive disorder citalopram

Panic disorder citalopram

Risperidone citalopram

Seizures citalopram

Selective serotonin reuptake inhibitors Citalopram Fluoxetine

Selective serotonin reuptake inhibitors citalopram

Social anxiety disorder citalopram

Withdrawal from citalopram

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