Pharmacotherapy of depressive disorders

Authors

Keywords:

depression, noradrenergic neurons, serotonergic neuron, antidepressants, NMDA receptor

Abstract

Depression is currently the most frequently occurring affective disorder. According to World Health Organization (WHO) data, depression is one of the four major global health problems. The growing spread of affective disorders and harmful aftermaths of this fact bring about a rising interest in these illnesses either in the medical or social context. This situation may contribute to a greater awareness of the society and successful prospecting for new antidepressant drugs. The mechanism of depressive disorders formation is most probably connected with the diminished activity of noradrenergic and serotonergic neurons (5-HT) in CNS. Pharmacotherapy of depressive disorders includes the usage of medications from different chemical groups and of different action mechanisms. A common feature of pharmacotherapy is the activation of noradrenergic and serotonergic transmission in CNS. The efficacy of contemporary antidepressant drugs is estimated at 70%. These medicines evoke a great number of adverse reactions and a therapeutic effect appears after several weeks of use. Therefore, some other, safer and more effective antidepressant drugs are still sought. A number of research studies carried out in the recent years has shown that the glutaminergic system also plays an important role in pathophysiology of depressive disorders.

References

1. Altamura C.A. et al.: Plasma and platelet excitatory amino acids in psychiatry disorders. Am. J. Psychiatry., 150, 1731, 1993.

2. Altamura C.A. et al.: Plasma concentrations of excitatory amino acids, serine, glycine, taurine and histidine in major depression. Eur. J. Neuropsychopharmacol. Suppl. 71, 1995.

3. Bonanno G. et al.: Chronic antidepressants reduce depolarization-evoked glutamate release and protein interactions favoring formation of SNARE complex in hippocampus. J. Neurosci., 25, 3270, 2005.

4. Carson R.C., Butcher J.N., Mineka, S. Abnormal Psychology. 2005.

5. Cichy A. et al.: Zinc-induced adaptive changes in NMDA/glutamatergic and serotonergic receptors. Pharmacol. Rep., 61, 1184, 2009.

6. Czernikiewicz A.: Are dual action antidepressants superior to selective antidepressants? Psychiatria w Praktyce Ogólnolekarskiej, tom 7, 2, 2007.

7. Dybała M. et al.: Medium supplementation with zinc enables detection of imipramine-induced adaptation in glycine/NMDA receptors labeled with [3H]L-689, 560. Pharmacol. Rep., 58, 753, 2006.

8. Dybała M. et al.: Lack of NMDA-AMPA interaction in antidepressant-like effect of CGP 37849, an antagonist of NMDA receptor, in the forced swim test. J. Neural. Transm. 115, 1519, 2008.

9. Gałecki P. et al.: Calcium ions, glutaminate acid, hypothalamic- pituitary- adrenal axis, calcium dependent ATP-ase as causes of oxidative damage in depression patients – Part I. Pol. Merk. Lek. XXIII, 2007.

10. Gawlik O., Nowak J.Z.: Biological rhythm disturbances in depression: in search of new therapeutic strategies. Postępy Psychiatrii i Neurologii, 15, 171, 2006.

11. Gelwan E. Tricyclic Antidepressants. Internet article 2000.

12. Godlewska B.R.: Genetics and psychiatry in general medical practice Psychiatria w Praktyce Ogólnolekarskiej, 2, 297, 2007.

13. Gołembiowska K., Dziubina A.: Effect of acute and chronic administration of citalopram on glutamate and aspartate release in the rat prefrontal cortex. Pol. J. Pharmacology, 52, 441, 2000.

14. Heresco-Levry U. et al.: Controlled trial of D-cycloserine adjuvant therapy for treatment-resistant major depressive disorder. J. Affective. Disord., 93, 239, 2006.

15. Kendall D.A. et al.: Activation of CB1 and CB2 receptors attenuates the induction and maintenance of inflammatory pain in the rat. Pain, 118, 327, 2005.

16. Kessler R.C. et al.: The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). 2003.

17. Kostowski W.: Novel studies on stress and depression and their influence on opinions about mechanism of action of antidepressants. Psychiatria. Via Medica tom 1, 2, 63, 2004.

18. Kostowski W., Herman Z.S., editors (2007). Pharmacology. Foundations of pharmacotherapy.

19. Lopez J.F.: The Neurobiology of Depression. 2000.

20. Lotufo-Neto F., Trivedi M., Thase M.E.: Meta-Analysis of the Reversible Inhibitors of Monoamine Oxidase Type A Moclobemide and Brofaromine for the Treatment of Depression. Neuropsychopharmacol., 20, 226, 1999.

21. Łabuda A.: Depresja jej rodzaje, objawy i przyczyny. (Depression - its types, symptoms and causes) 2006.

22. MacQueen G., Born L., Steiner M.: Sertralina – The selective serotonin reuptake inhibitor sertraline: its profile and use in psychiatric disorders. Przewodnik Lekarski, 6, 3, 53, 2003.

23. Maletic V. et al.: Neurobiology of depression: an integrated view of key findings. 2007.

24. Muhonen L.H. et al.: Double-blind, randomized comparison of memantine and escitalopram for the treatment of major depressive disorder comorbid with alcohol dependence. J. Clin. Psychiatry, 69, 392, 2008.

25. Nestler E.J. Neurobiology of Depression. 2002.

26. Nowak G. et al.: Ca2+ antagonists effect an antidepressant-like adaptation of the NMDA receptor complex. European Journal of Pharmacology: Mol. Pharmacol., 247, 101, 1993.

27. Nowak G., Li Y., Paul I.A.: Adaptation of cortical but not hippocampal NMDA receptors after chronic citalopram treatment. Eur. J. Pharmacol., 295, 75, 1996.

28. Nowak G et al.: Adaptation of cortical NMDA receptors by chronic treatment with specific serotonin reuptake inhibitors. Eur. J. Pharmacol., 342, 367, 1998.

29. Owens M.J, Nemeroffin ChB: The role of serotonin in the pathophysiology of depression: Focus on the serotonin transporter. Clin. Chem., 40, 288, 1994.

30. Paul L.A. et al.: Adaptation of the NMDA receptor in rat cortex following chronic electroconvulsive shock or imipramine. Eur. J. Pharmacol., 247, 305, 1993.

31. Paul L.A. et al.: Adaptation of the N-methyl-D-aspartate receptor complex following chronic antidepressant treatments. J. Pharmacol. Mol. Pharmacol. Exp. Ther., 269, 95, 1994.

32. Poleszak E. et al.: Activation of the NMDA/glutamate receptor complex antagonizes the NMDA antagonist-induced antidepressant-like effects in the forced swim test. Pharmacol. Rep., 59, 595, 2007.

33. Poleszak E. et al.: D-serine, a selective glicyne/N-methyl-D-aspartate receptor agonist, antagonizes the antidepressant-like effects of magnesium and zinc in mice. Pharmacol. Rep., 60, 996, 2008.

34. Porczyk S. Epidemiologia depresji 2008.

35. Prikhozhan A.V., Kovalev G.I., Raevskii K.S.: Effects of antidepressive agents on glutamatergic autoregulatory presynaptic mechanism in the rat cerebral cortex. Bull. Exp. Biol. Med., 110, 624, 1990.

36. Rajewska-Rager A., Rybakowski J.: The role of stressful live events in the pathogenesis of depression. Neuropsychiatria i Neuropsychologia, 3, 147, 2008.

37. Sanacora G. et al.: Augmentation for Treatment-Resistant Depression. Am. J. Psychiatry., 161, 2132, 2004.

38. Sanacora G. et al.: Subtype-specific alterations of gamma-aminobutyric acid and glutamate in patients with major depression. Arch. Gen. Psychiatry, 61, 705, 2004.

39. Sanacora G. et al.: Specific alterations of gamma-aminobutyric acid and glutamate in patients with major depression. Arch. Gen. Psychiatry, 61, 705, 2004.

40. Sowa-Kućma M. et al.: Antidepressant-like activity of zinc: further behavioral and molecular evidence. J. Neural. Transm., 115, 1621, 2008.

41. Sowa-Kućma M et al.: Chronic treatment with zinc and antidepressants induces enhancement of presynaptic/extracellular zinc concentration in the rat prefrontal cortex. Amino Acids, 40, 249, 2011.

42. Szewczyk B., Kata R., Nowak G.: Rise in zinc affinity for the NMDA receptor evoked by chronic imipramine is speciesspecific. Pol. J. Pharmacol., 53, 641, 2001.

43. Szewczyk G. et al.: Increase in synaptic hippocampal zinc concentration following chronic but not acute zinc treatment in rats. Brain Res., 1090, 69, 2006.

44. Szewczyk B. et al.: Antidepressant activity of zinc and magnesium in view of the current hypotheses of antidepressant action. Pharmacol. Rep., 60, 588, 2008.

45. Szewczyk B. et al.: The involvement of serotonergic system in the antidepressant effect of zinc in the forced swim test. Prog. Neuropsychopharmacol. Biol. Psychiatry., 33, 323, 2009.

46. Szewczyk B. et al.: Involvement of NMDA and AMPA receptors in the antidepressant-like activity of zinc in the forced swim test. Amino Acids, 2010.

47. Yildiz-Yesiloglu A., Ankerst D.P.: Review of 1H magnetic resonance spectroscopy findings in major depressive disorder: A meta-analysis. Psychiatry Res. Neuroimaging., 147, 1, 2006.

48. Zarate C.A. et al.: A randomized trial of N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch. Gen. Psychiatry, 63, 856, 2006.

Downloads

Published

2012-01-09

How to Cite

Szopa, A., Stasiuk, W., & Poleszak, E. (2012). Pharmacotherapy of depressive disorders. Current Issues in Pharmacy and Medical Sciences, 24(2), 65-73. https://czasopisma.umlub.pl/curipms/article/view/3006