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Talk:Sertraline

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Serotonin syndrome and/or a prolonged heart QT interval can occur with using SSRIs (such as citalopram, paroxetine, or sertraline) with SNRIs, SRAs (such as MDMA), DXM, serotonergic stimulants (such as cocaine), MAOIs, and RIMAs.

It is strongly discouraged to consume moderate to heavy dosages of these substances together.

Structure of sertraline.

Sertraline (also known as Zoloft) is a widely-known SSRI substance and pharmaceutical of the substituted tametraline chemical class that produces anxiolytic and antidepressive effects when administered. Sertraline is primarily prescribed for major depressive disorder in adult outpatients as well as obsessive–compulsive disorder, panic disorder, and social anxiety disorder, in both adults and children.

Chemistry

Sertraline is a substituted tametraline.

Pharmacology

Sertraline is a selective reuptake inhibitor of serotonin; this allows sertraline to increase levels of extracellular serotonin, meaning that more serotonin comes into the brain. Sertraline is used for depression because it is hypothesized that people with depression have low serotonin levels.

Sertraline promotes neurogenesis (the growth of neurons). This is a useful property in neurodegenerative diseases, such as Huntington's disease.[1][2][3]

Sertraline is somewhat unique among SSRIs for containing no fluorine atoms. Some pharmaceuticals contaning flourine can be metabolized into the fluoride (F-) anion,[4][5][6] which may cause harm to the human body in excess, such as leaving mineral deposits on the pineal gland and bones.[7][8] On a related note, it is not certain of whether fluorine-containing antidepressants, such as citalopram and fluoxetine, can be metabolized into fluoride.

Its metabolite, norsertraline, also inhibits reuptake of serotonin. [9]

Subjective effects

Physical effects

Cognitive effects

See also

References

  1. Anacker, C., Zunszain, P. A., Cattaneo, A., Carvalho, L. A., Garabedian, M. J., Thuret, S., ... & Pariante, C. M. (2011). Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor. Molecular psychiatry, 16(7), 738.
  2. Peng, Q., Masuda, N., Jiang, M., Li, Q., Zhao, M., Ross, C. A., & Duan, W. (2008). The antidepressant sertraline improves the phenotype, promotes neurogenesis and increases BDNF levels in the R6/2 Huntington's disease mouse model. Experimental neurology, 210(1), 154-163.
  3. Duan, W., Peng, Q., Masuda, N., Ford, E., Tryggestad, E., Ladenheim, B., ... & Ross, C. A. (2008). Sertraline slows disease progression and increases neurogenesis in N171-82Q mouse model of Huntington's disease. Neurobiology of disease, 30(3), 312-322.
  4. Wermers, R. A., Cooper, K., Razonable, R. R., Deziel, P. J., Whitford, G. M., Kremers, W. K., & Moyer, T. P. (2011). Fluoride excess and periostitis in transplant patients receiving long-term voriconazole therapy. Clinical Infectious Diseases, 52(5), 604-611.
  5. Meunier, P. J., Courpron, P., Smoller, J. S., & Briancon, D. (1980). Niflumic Acid-Induced Skeletal Fluorosis: Iatrogenic Disease or Therapeutic Perspective for Osteoporosis?. Clinical orthopaedics and related research, 148, 304-309.
  6. Rimoli, C., Carducci, C. N., Dabas, C., Vescina, C., Quindimil, M. E., & Mascaro, A. (1991). Relationship between serum concentrations of flecainide and fluoride in humans. Bollettino chimico farmaceutico, 130(7), 279-282.
  7. Luke, J. (2001). Fluoride deposition in the aged human pineal gland. Caries Research, 35(2), 125-128.
  8. Meunier, P. J., Courpron, P., Smoller, J. S., & Briancon, D. (1980). Niflumic Acid-Induced Skeletal Fluorosis: Iatrogenic Disease or Therapeutic Perspective for Osteoporosis?. Clinical orthopaedics and related research, 148, 304-309.
  9. Koe, B. K., Weissman, A. L. B. E. R. T., Welch, W. M., & Browne, R. G. (1983). Sertraline, 1S, 4S-N-methyl-4-(3, 4-dichlorophenyl)-1, 2, 3, 4-tetrahydro-1-naphthylamine, a new uptake inhibitor with selectivity for serotonin. Journal of Pharmacology and Experimental Therapeutics, 226(3), 686-700.