Affective Disorders and Antidepressant Drugs

Marc Fakhoury

Department of Neuroscience, Faculty of Medicine, University of Montreal, Montreal, Canada.

DOI: 10.4236/oalib.1100597                

Abstract

Affective disorders are a group of psychiatric diseases that can affect an individual at any given age. Also called mood disorders, they can be distinguished into two different types: major depressive disorder, also called major depression, and bipolar disorder, which is known as manic depression. People affected by major depression most often have a low mood, and are consistently in a state of unhappiness. Although it was shown that genetics play a role in the predisposition of depression, this disease most often occurs in response to a variety of external factors such as a stressful life event, the loss of a loved one, and following drug or substance abuse. A variety of antidepressant drugs, such as the monoamine oxidase inhibitors (MAOIs), the tricyclic antidepressants (TCAs), and the second-generation antidepressants are able to provide significant relief for people suffering from affective disorders like depression. However, several of these pharmaceutical agents can cause serious side effects to the patients. Therefore, there is a need to identify novel antidepressant therapies that are more efficient and that present minimal side effects. A better understanding of the neurobiology of depression will definitively help scientists develop new therapeutic ideas. This paper will first discuss the clinical profile of depression and explain the physiological mechanisms and the neurochemistry involved in this disease. It will then give you an overview of the effectiveness of the most common antidepressants used, with a description of their mode of action and most notable side effects.

Keywords

Antidepressant Drugs, Bipolar Depression, Depression, Neurobiology

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	Weissman, M.M. and Boyd, J.D. (1984) The Epidemiology of Affective Disorders. Neurobiology of Mood Disorders. Williams and Wilkins, Baltimore, 60-75.
[2]	Kenneson A, Funderburk JS, Maisto SA (2013) Substance Use Disorders Increase the Odds of Subsequent Mood Disorders. Drug and Alcohol Dependence, 133, 338-343. http://dx.doi.org/10.1016/j.drugalcdep.2013.06.011
[3]	Marchand, R., Dilda, V. and Jensen, C.R. (2005) Neurobiology of Mood Disorders. Hosp Physician, 41, 17-26.
[4]	American Psychiatric Association (2013) Diagnostic and Statistical Manual of Mental Disorders. 5th Edition, American Psychiatric Publishing, Arlington, 302.
[5]	Brotman, A.W., Falk, W.E. and Gelemberg, A.J. (1987) Pharmacological Treatment of Acute Depressive Subtypes. In: Melter, H.Y., Ed., Psychopharmacology: The Third Generation of Progress, 1031-1040.
[6]	Daniel, T.G., Daniel, L.S. and Daniel, M.W., eds. (2011) Psychology. 2nd Edition. Worth Publishers, New York, 564.
[7]	Keller, M.B., Lavori, P.W., Endicott, J., Coryell, W. and Klerman, G.L. (1983) “Double Depression”: Two-Year Follow-Up. American Journal of Psychiatry, 140, 689-694.
[8]	Chanaka, W. and Perminder, S. (2008) Treatment-Resistant Depression: Critique of Current Approaches. The Australian and New Zealand Journal of Psychiatry, 42, 751-762. http://dx.doi.org/10.1080/00048670802277206
[9]	Kern, S., Rohleder, N., Eisenhofer, G., Lange, J. and Ziemssen, T. (2014) Time Matters—Acute Stress Response and Glucocorticoid Sensitivity in Early Multiple Sclerosis. Brain, Behavior, and Immunity.
[10]	Kandel, E.R. (1991) Disorders of Mood: Depression, Mania, and Anxiety Disorders. In: Kandel, et al., Eds., Principles of Neural Science, Elsevier, New York, 869-886.
[11]	Gold, P.W., Goodwin, F.K. and Chrousos, G.P. (1988) Clinical and Biochemical Manifestations of Depression. The New England Journal of Medicine, 319, 413-420. http://dx.doi.org/10.1056/NEJM198808183190706
[12]	Hayes, P.E. and Ettigi, P. (1983) Dexamethasone Suppression Test in Diagnosis of Depressive Illness. Clinical Pharmacology, 2, 538-545.
[13]	Reddy, M.S. and Kuruvilla, K. (1986) Dexamethasone Suppression Test in Depression. Indian Journal of Psychiatry, 28, 195-200.
[14]	Brodie, B.B., Olin, J.S., Kuntzman, R.G. and Shore, P.A. (1957) Possible Interrelationship between Release of Brain Norepinephrine and Serotonin by Reserpine. Science, 125, 1293-1294.
[15]	Lee, M.J. and Wei, J.W. (2013) The Influences of Reserpine and Imipramine on the 5-HT2 Receptor Binding Site and Its Coupled Second Messenger in Rat Cerebral Cortex. The Chinese Journal of Physiology, 56, 199-208. http://dx.doi.org/10.1126/science.125.3261.1293
[16]	Nutt, D.J. (2008) Relationship of Neurotransmitters to the Symptoms of Major Depressive Disorder. Journal of Clinical Psychiatry, 69, 4-7.
[17]	Legoabe, L.J., Petzer, A. and Petzer, J.P. (2014) α-Tetralone Derivatives as Inhibitors of Monoamine Oxidase. Bioorganic Medicinal Chemistry Letters, 24, 2758-2763. http://dx.doi.org/10.1016/j.bmcl.2014.04.021
[18]	Singh, T. and Williams, K. (2006) Atypical Depression. Psychiatry (Edgmont), 3, 33-39.
[19]	López-Muñoz, F. and Alamo, C. (2009) Monoaminergic Neurotransmission: The History of the Discovery of Antidepressants from 1950s until Today. Current Pharmaceutical Design, 15, 1563-1586. http://dx.doi.org/10.2174/138161209788168001
[20]	Moncrieff, J. (2008) The Creation of the Concept of an Antidepressant: An Historical Analysis. Social Science Medicine, 66, 2346-2355. http://dx.doi.org/10.1016/j.socscimed.2008.01.047
[21]	Shulman, K.I., Herrmann, N. and Walker, S.E. (2013) Current Place of Monoamine Oxidase Inhibitors in the Treatment of Depression. CNS Drugs, 27, 789-797. http://dx.doi.org/10.1007/s40263-013-0097-3
[22]	Carson, V.B. (2000) Mental Health Nursing: The Nurse-Patient Journey. W.B. Saunders, Philadelphia, 423.
[23]	Gillman, P.K. (2007) Tricyclic Antidepressant Pharmacology and Therapeutic Drug Interactions Updated. British Journal of Pharmacology, 151, 737-748. http://dx.doi.org/10.1038/sj.bjp.0707253
[24]	Olver, J.S., Burrows, G.D. and Norman, T.R. (2001) Third-Generation Antidepressants: Do They Offer Advantages over the SSRIs? CNS Drugs, 15, 941-954. http://dx.doi.org/10.2165/00023210-200115120-00004
[25]	Feldman, R.S., Meyer, J.S. and Quenzer, L.F. (1997) Principles of Neuropsychopharmacology. Sinauer Associates Inc., Sunderland, Massachusetts, 834.
[26]	Dennehy, E.B., Marangell, L.B., Martinez, J., Balasubramani, G.K. and Wisniewski, S.R. (2014) Clinical and Functional Outcomes of Patients Who Experience Partial Response to Citalopram: Secondary Analysis of STAR*D. Journal of Psychiatric Practice, 20, 178-187. http://dx.doi.org/10.1097/01.pra.0000450317.76117.62
[27]	American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorder (DSM-IV). 4th Edition, APA, Washington DC.
[28]	Barnett, J.H. and Smoller, J.W. (2009) The Genetics of Bipolar Disorder. Neuroscience, 164, 331-343. http://dx.doi.org/10.1016/j.neuroscience.2009.03.080
[29]	Renk, K., White, R., Lauer, B.A., McSwiggan, M., Puff, J. and Lowell, A. (2014) Bipolar Disorder in Children. Psychiatry Journal, 2014, Article ID: 928685.
[30]	Geddes, J.R. and Miklowitz, D.J. (2013) Treatment of Bipolar Disorder. The Lancet, 381, 1672-1682. http://dx.doi.org/10.1016/S0140-6736(13)60857-0
[31]	Brown, K.M. and Tracy, D.K. (2013) Lithium: The Pharmacodynamic Actions of the Amazing Ion. Therapeutic Advances in Psychopharmacology, 3, 163-176. http://dx.doi.org/10.1177/2045125312471963
[32]	Scheuch, K., Höltje, M., Budde, H., Lautenschlager, M., Heinz, A., Ahnert-Hilger, G. and Priller, J. (2010) Lithium Modulates Tryptophan Hydroxylase 2 Gene Expression and Serotonin Release in Primary Cultures of Serotonergic Raphe Neurons. Brain Research, 1307, 14-21. http://dx.doi.org/10.1016/j.brainres.2009.10.027
[33]	Marmol, F. (2008) Lithium: Bipolar Disorder and Neurodegenerative Diseases Possible Cellular Mechanisms of the Therapeutic Effects of Lithium. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 32, 1761-1771. http://dx.doi.org/10.1016/j.pnpbp.2008.08.012
[34]	Kozier, B., Harvey, S. and Morgan-Samuel, H. (2008) Fundamentals of Nursing, Concepts, Process and Practice. Pearson Education, London, 189.
[35]	Rapoport, S.I., Basselin, M., Kim, H.W. and Rao, J.S. (2009) Bipolar Disorder and Mechanisms of Action of Mood Stabilizers. Brain Research Reviews, 61, 185-209. http://dx.doi.org/10.1016/j.brainresrev.2009.06.003
[36]	Bowden, C.L., Brugger, A.M., Swann, A.C., Calabrese, J.R., Janicak, P.G., Petty, F., Dilsaver, S.C., Davis, J.M., Rush, A.J. and Small, J.G. (1994) Efficacy of Divalproex Sodium vs Lithium and Placebo in the Treatment of Mania. Journal of the American Medical Association, 271, 918-924. http://dx.doi.org/10.1001/jama.1994.03510360044034
[37]	Katayama, Y., Terao, T., Kamei, K., Hatano, K., Kohno, K., Makino, M., Mizokami, Y., Kodama, K. and Itoh, H. (2014) Therapeutic Window of Lamotrigine for Mood Disorders: A Naturalistic Retrospective Study. Pharmacopsychiatry, 47, 111-114. http://dx.doi.org/10.1055/s-0034-1375618