Rapid-onset antidepressant efficacy of glutamatergic system modulators: The neural plasticity hypothesis of depression
详细信息 查看全文
- 作者：Jing Wang ; Liang Jing ; Juan-Carlos Toledo-Salas ; Lin Xu
- 关键词：depression ; stress ; neural plasticity ; glutamatergic transmission ; monoamine ; based antidepressant ; ketamine
- 刊名：Neuroscience Bulletin
- 出版年：2015
- 出版时间：February 2015
- 年：2015
- 卷：31
- 期：1
- 页码：75-86
- 全文大小：304 KB
- 参考文献：1. Kessler RC, Bromet EJ. The epidemiology of depression across cultures. Annu Rev Public Health 2013, 34: 119-38. CrossRef
2. Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, / et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA 2003, 289: 3095-105. CrossRef
3. Manji HK, Drevets WC, Charney DS. The cellular neurobiology of depression. Nat Med 2001, 7: 541-47. CrossRef
4. Belmaker RH, Agam G. Major depressive disorder. N Engl J Med 2008, 358: 55-8. CrossRef
5. Rush AJ, Trivedi MH, Wisniewski SR, Nierenberg AA, Stewart JW, Warden D, / et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR* D report. Am J Psychiatry 2006, 163: 1905-917. CrossRef
6. Berton O, Nestler EJ. New approaches to antidepressant drug discovery: beyond monoamines. Nat Rev Neurosci 2006, 7: 137-51. CrossRef
7. Zarate CA Jr, Brutsche NE, Ibrahim L, Franco-Chaves J, Diazgranados N, Cravchik A, / et al. Replication of ketamine’s antidepressant efficacy in bipolar depression: a randomized controlled add-on trial. Biol Psychiatry 2012, 71: 939-46. CrossRef
8. Berman R M, Cappiello A, Anand A, Oren DA, Heninger GR, Charney DS, / et al. Anti-depressant effects of ketamine in depressed patients. Biol Psychiatry 2000, 47: 351-54. CrossRef
9. Hirschfeld RM. History and evolution of the monoamine hypothesis of depression. J Clin Psychiatry 2000, 61Suppl 6: 4-.
10. Hanson ND, Owens MJ, Nemeroff CB. Depression, antidepressants, and neurogenesis: a critical reappraisal. Neuropsychopharmacology 2011, 36: 2589-602. CrossRef
11. Shakesby AC, Anwyl R, Rowan MJ. Overcoming the effects of stress on synaptic plasticity in the intact hippocampus: rapid actions of serotonergic and antidepressant agents. J Neurosci 2002, 22: 3638-644.
12. LeGates TA, Altimus CM, Wang H, Lee HK, Yang S, Zhao H, / et al. Aberrant light directly impairs mood and learning through melanopsin-expressing neurons. Nature 2012, 491: 594-98. CrossRef
13. Aan Het Rot M, Zarate CA Jr, Charney DS, Mathew SJ. Ketamine for depression: where do we go from here? Biol Psychiatry 2012, 72: 537-47. CrossRef
14. Zarate CA Jr, Singh JB, Carlson PJ, Brutsche NE, Ameli R, Luckenbaugh DA, / et al. A randomized trial of an N-methyl-Daspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry 2006, 63: 856-64. CrossRef
15. Huttenlocher PR. Neural plasticity. Harvard University Press, 2009.
16. Lenn NJ. Neuro plasticity: The basis for brain development, learning, and recovery from injury. Infants Young Child 1991, 3: 39-8. CrossRef
17. McGaugh JL. Memory—a century of consolidation. Science 2000, 287: 248-51. CrossRef
18. Zhang M. Autism Disease: Neural network going awry and therapeutic Sstrategy underlying neural plasticity. N A J Med Sci 2011, 4: 139. CrossRef
19. Pittenger C, Duman RS. Stress, depression, and neuroplasticity: a convergence of mechanisms. Neuropsychopharmacology 2008, 33: 88-09.
文摘
Depression is a devastating psychiatric disorder widely attributed to deficient monoaminergic signaling in the central nervous system. However, most clinical antidepressants enhance monoaminergic neurotransmission with little delay but require 4- weeks to reach therapeutic efficacy, a paradox suggesting that the monoaminergic hypothesis of depression is an oversimplification. In contrast to the antidepressants targeting the monoaminergic system, a single dose of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine produces rapid (within 2 h) and sustained (over 7 days) antidepressant efficacy in treatment-resistant patients. Glutamatergic transmission mediated by NMDARs is critical for experience-dependent synaptic plasticity and learning, processes that can be modified indirectly by the monoaminergic system. To better understand the mechanisms of action of the new antidepressants like ketamine, we review and compare the monoaminergic and glutamatergic antidepressants, with emphasis on neural plasticity. The pathogenesis of depression may involve maladaptive neural plasticity in glutamatergic circuits that may serve as a new class of targets to produce rapid antidepressant effects.