Serotonin paroxetine

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. 

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. 

Antidepressants Trazodone, mirtazapine, paroxetine, other selective serotonin reuptake inhibitors venlafaxine... 

The enantiomerically pure 3-arylglutaric ester are precursors for the synthesis of (—)-paroxetine [10], a selective serotonin reuptake inhibitor used in the treatment of depression, obsessive compulsive disorder, and panic, and (i )-Baclofen [11], a GABAb receptor agonist, which is used cHnically in the treatment of spasticity (Chart 5.1). 

Corby CL> Dunne G (1997). Paroxetine a review./ Serotonin ResA 47—64. 

Dr. Gibb s hypothesis regarding dopamine involvement, we thought that perhaps MBDB would not be neurotoxic because of a lack of effect on dopamine. But, in fact, it is neurotoxic as well, measured by whole-brain serotonin 5-HIAA and tritiated paroxetine binding sites. It is perhaps two-thirds the toxicity, on a molecular weight basis, of MDMA, but it is toxic. 

TABLE 2. Effects of repeated systemic administration of MDMA on the regional decreases in [ H]paroxetine-labeled serotonin uptake sites... 

H]MDMA interacted with multiple sites in rat brain. A low affinity pH]MDA binding site (apparent Kd>1.0 mM) was found to be resistant to boiling of the synaptosomal preparation for 15 minutes. This site was saturable, as indicated by a 30 pereent inhibition of [ H]MDA binding to boiled synaptosomes by 1.0 mM MDA and a 56 pereent inhibition of the binding by 0.1 mM of the serotonin uptake bloeker paroxetine. The indication of a saturable, nonspecific binding site for [ H]MDA in boiled membranes necessitated that we use boiled tissue to assess nonspecific binding in all subsequent experiments. 

Battaglia, G. Yeh, S.Y. O Heam, E. Molliver. M.E. Kuhar, M.J. and De Souza, E.B. 3,4-Methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxyamphetamine (MDA) preferentially destroy serotonin terminals in rat brain Quantification of neurodegeneration by measurement of H-paroxetine-labeled serotonin uptake sites. 

The selective serotonin reuptake inhibitors (SSRIs) paroxetine, fluoxetine, and sertraline are potentially useful due to... 

The first-line therapeutic options for PMDD include the selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, fluvoxamine, sertraline, paroxetine, and citalopram. These agents can be given either continuously or only during the luteal phase of the menstrual cycle, i.e., initiated at the time of ovulation and discontinued on the first day of menses. 

SSRIs are theorized to reduce the frequency of hot flashes by increasing serotonin in the central nervous system and by decreasing LH. Of the SSRIs, citalopram, paroxetine, and sertraline all have been studied and have demonstrated a reduction in hot flashes while treating other symptomatic complaints such as depression and anxiety.33 Venlafaxine, which blocks the reuptake of serotonin and norepinephrine, has demonstrated a reduction in hot flashes primarily in the oncology population.34 Overall, these antidepressant medications offer a reasonable option for women who are unwilling or cannot take hormonal therapies, particularly those who suffer from depression or anxiety. These agents should be prescribed at the lowest effective dose to treat symptoms and may be titrated based on individual response. 

Pollock, B. G., Ferrell, R. E. et al. (2000). Allelic variation in the serotonin transporter promoter affects onset of paroxetine treatment response in late-life depression. Neuropsychopharmacology, 23(5), 587-90. 

Zanardi, R. et al. (2000). Efficacy of paroxetine in depression is influenced by a functional polymorphism within the promoter of the serotonin transporter gene. /. Clin. Psychopharmacol., 20(1), 105-7. 

Selective serotonin reuptake inhibitor (SSRI) Currently, the most widely used antidepressants (e.g., fluoxetine and paroxetine). 

Since the introduction of fluoxetine (3) in 1987, a series of selective serotonin reuptake inhibitors (SSRIs) have been discovered that have seen broad application in many facets of mood disorders. These compounds include fluvoxamine (4) which contains a trifluoromethyl group and paroxetine (5) and citalopram (6) which contain 4-fluorophenyl groups [5,6]. 

Inhibitors of serotonin (5-HT) uptake such as paroxetine interact significantly with which of the following drugs ... 

Treatment with a selective serotonin reuptake inhibitor is usually initiated in depressed patients with AD. Paroxetine causes more anticholinergic side effects than the other selective serotonin reuptake inhibitors. Ven-lafaxine may also be used. 

Venlafaxine extended release, duloxetine, paroxetine, and escitalopram are FDA approved for treatment of GAD. Sertraline is also effective. Acute response and remission rates are approximately 65% and 30%, respectively. Imipramine may be used when patients fail to respond to selective serotonin reuptake inhibitors (SSRIs). In one trial, diazepam, trazodone, and imipramine had greater anxiolytic activity than placebo. 

Tricyclic drugs have, as the name implies, a three-ring structure, and interfere with reuptake of norepinephrine and/or serotonin into axon terminals. Tricyclic drugs include imipramine (Tofranil), amitriptyline (Elavil), clomipramine (Anafranil), and nortriptyline (Pamelor, Aventil). Tricyclics have the occasional but unfortunate cardiovascular side effects of arrhythmia and postural hypotension. Newer, nontricyclic antidepressants have been developed that are collectively referred to as SSRIs. These have a potent and selective action on serotonin, and lack the cardiovascular side effects of the tricyclics. These include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), and fluvoxamine (Luvox). A fifth SSRI, citalopram (Celexa) has been used in Europe and has recently been approved in the United States. Venlafaxine (Effexor) blocks reuptake of norepinephrine and serotonin, while bupropion (Wellbutrin) acts on both dopamine and norepinephrine. 

A breakthrough in the treatment of major depression was the discovery of fluoxetine, marketed as Prozac. Fluoxetine has a mechanism of action similar to that of imipramine with an important exception. It is a selective serotonin reuptake inhibitor, an SSRI. This strongly suggests that, in some sense, the symptoms of major depression result from a deficit in serotonin specifically. By inhibiting its reuptake from the synapse, the activity of serotonin is enhanced. Two other important drugs for major depression, sertraline (Zoloft) and paroxetine (Paxil), among several others,... 

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