سامانه مدیریت نشریات علمی دانشگاه شاهد

Khalili, Mohsen, Zahedi, Elham, Narenjkar, Jamshid, Sanaie Rad, Ashkan. (1396). Ameliorative activity of co-administration of ketamine and ECT on depression like behaviors in depressed rats. , 6(1), 43-48. doi: 10.22070/jbcp.2018.3005.1091
Mohsen Khalili; Elham Zahedi; Jamshid Narenjkar; Ashkan Sanaie Rad. "Ameliorative activity of co-administration of ketamine and ECT on depression like behaviors in depressed rats". , 6, 1, 1396, 43-48. doi: 10.22070/jbcp.2018.3005.1091
Khalili, Mohsen, Zahedi, Elham, Narenjkar, Jamshid, Sanaie Rad, Ashkan. (1396). 'Ameliorative activity of co-administration of ketamine and ECT on depression like behaviors in depressed rats', , 6(1), pp. 43-48. doi: 10.22070/jbcp.2018.3005.1091
Khalili, Mohsen, Zahedi, Elham, Narenjkar, Jamshid, Sanaie Rad, Ashkan. Ameliorative activity of co-administration of ketamine and ECT on depression like behaviors in depressed rats. , 1396; 6(1): 43-48. doi: 10.22070/jbcp.2018.3005.1091

Ameliorative activity of co-administration of ketamine and ECT on depression like behaviors in depressed rats

Journal of Basic and Clinical Pathophysiology
مقاله 7، دوره 6، شماره 1، اردیبهشت 2018، صفحه 43-48    اصل مقاله (503.85 K)
نوع مقاله: Research Paper
شناسه دیجیتال (DOI): 10.22070/jbcp.2018.3005.1091
نویسندگان
Mohsen Khalili1؛ Elham Zahedi* 2؛ Jamshid Narenjkar3؛ Ashkan Sanaie Rad2
1Neurophysiology Research Center, Shahed University, Tehran, Iran
2Department of Physiology, School of Medicine, Shahed University Tehran, Iran
3Department of Pharmacology, School of Medicine, Shahed University of Medical sciences, Tehran, Iran
چکیده
Background and Objective: Electroconvulsive therapy (ECT) is the end choice treatment for patients with major depressive disorder (MDD). Regarding researches that show NMDA receptor inactivation could yield the same results as anti-depressant drugs, however, the present study examined co-administration of ECT and ketamine (as NMDA antagonist) on depressed rat behaviors.  
Materials and Methods: Fifty healthy adult male Wistar rats were divided into control (normal, no treatment) and CUMS induced depressed rats. The depressed animals were subdivided into 1- ECT, 2-ketamine, and 3- ECT + ketamine and 4- no treatment. We used sucrose preference, forced swimming, open field and elevated plus maze tests for evaluation of depression-related behavioral function.
Results: Data analysis in CUMS depressed rats that treated with ketamine + ECT showed higher sucrose consumption in sucrose preference test, more immobility in forced swimming, and the vast activity in open field and plus maze tests.
Conclusion: The behavioral analysis tests show that combination therapy with ketamine and electroconvulsive could markedly reduce depression and anxiolytic behaviors than ketamine or ECT treatment alone. 
کلیدواژه‌ها
Ketamine؛ Electroconvulsive therapy؛ Depression
مراجع
  1. Greden JF. The burden of recurrent depression: causes, consequences, and future prospects. The Journal of Clinical Psychiatry 2001;62 Suppl 22:5-9.
  2. Lewis L, Hoofnagle L. Treatment-resistant depression: the patient perspective. Biological Psychiatry 2003;53(8):635-9.
  3. Pirnia T, Joshi SH, Leaver AM, Vasavada M, Njau S, Woods RP, et al. Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex 2016;6(6):e832.
  4. Nemeroff CB. Prevalence and management of treatment-resistant depression. The Journal of Clinical Psychiatry 2007;68 Suppl 8:17-25.
  5. Wasserman D. Depression: The Facts: Oxford University Press; 2006.
  6. Baldwin CM, Birtwistle J. An Atlas of Depression: Taylor & Francis; 2002.
  7. Husain SS, Kevan IM, Linnell R, Scott AI. What do psychiatrists mean by medication resistance as an indication for electroconvulsive therapy? The journal of ECT 2005;21(4):211-3.
  8. Braga RJ, Petrides G. [Somatic therapies for treatment-resistant psychiatric disorders]. Revista Brasileira de Psiquiatria (Sao Paulo, Brazil : 1999) 2007;29 Suppl 2:S77-84.
  9. Park M, Niciu MJ, Zarate CA, Jr. Novel Glutamatergic Treatments for Severe Mood Disorders. Current Behavioral Neuroscience Reports 2015;2(4):198-208.
  10. Zorumski CF, Nagele P, Mennerick S, Conway CR. Treatment-Resistant Major Depression: Rationale for NMDA Receptors as Targets and Nitrous Oxide as Therapy. Frontiers in Psychiatry 2015;6:172.
  11. Luo J, Min S, Wei K, Cao J, Wang B, Li P, et al. Propofol prevents electroconvulsive-shock-induced memory impairment through regulation of hippocampal synaptic plasticity in a rat model of depression. Neuropsychiatric Disease and Treatment 2014;10:1847-59.
  12. Luo J, Min S, Wei K, Zhang J, Liu Y. Propofol interacts with stimulus intensities of electroconvulsive shock to regulate behavior and hippocampal BDNF in a rat model of depression. Psychiatry Research 2012;198(2):300-6.
  13. Abdul Shukkoor MS, Baharuldin MT. Antidepressant-Like effect of lipid extract of channa striatus in chronic unpredictable mild stress model of depression in rats 2016:2986090.
  14. Spiacci A, Jr., Kanamaru F, Guimaraes FS, Oliveira RM. Nitric oxide-mediated anxiolytic-like and antidepressant-like effects in animal models of anxiety and depression. Pharmacology, Biochemistry, and Behavior 2008;88(3):247-55.
  15. Sulakhiya K, Patel VK, Saxena R, Dashore J, Srivastava AK, Rathore M. Effect of Beta vulgaris Linn. Leaves extract on anxiety- and depressive-like behavior and oxidative stress in mice after acute restraint stress. Pharmacognosy Research 2016;8(1):1-7.
  16. Doremus-Fitzwater TL, Varlinskaya EI, Spear LP. Social and non-social anxiety in adolescent and adult rats after repeated restraint. Physiology & Behavior 2009;97(3-4):484-94.
  17. Hodge CW, Raber J, McMahon T, Walter H, Sanchez-Perez AM, Olive MF, et al. Decreased anxiety-like behavior, reduced stress hormones, and neurosteroid supersensitivity in mice lacking protein kinase Cepsilon. The Journal of Clinical Investigation 2002;110(7):1003-10.
  18. McCarthy MM, Nielsen DA, Goldman D. Antisense oligonucleotide inhibition of tryptophan hydroxylase activity in mouse brain. Regulatory Peptides 1995;59(2):163-70.
  19. Willner P, Mitchell PJ. The validity of animal models of predisposition to depression. Behavioural Pharmacology 2002;13(3):169-88.
  20. Mohamed BM, Aboul-Fotouh S, Ibrahim EA, Shehata H, Mansour AA, Yassin NA, et al. Effects of pentoxifylline, 7-nitroindazole, and imipramine on tumor necrosis factor-alpha and indoleamine 2,3-dioxygenase enzyme activity in the hippocampus and frontal cortex of chronic mild-stress-exposed rats. Neuropsychiatric Disease and Treatment 2013;9:697-708.
  21. Yang Y, Hu Z, Du X, Davies H, Huo X, Fang M. miR-16 and Fluoxetine Both Reverse Autophagic and Apoptotic Change in Chronic Unpredictable Mild Stress Model Rats. Frontiers in Neuroscience 2017;11:428.
  22. Luo KR, Hong CJ, Liou YJ, Hou SJ, Huang YH, Tsai SJ. Differential regulation of neurotrophin S100B and BDNF in two rat models of depression. Progress in Neuro-Psychopharmacology & Biological Psychiatry 2010;34(8):1433-9.
  23. Qi X, Lin W, Li J, Li H, Wang W, Wang D, et al. Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress Neurobiology of Disease 2008;31(2):278-85.
  24. Yankelevitch-Yahav R, Franko M, Huly A, Doron R. The forced swim test as a model of depressive-like behavior. Journal of Visualized Experiments 2015(97).
  25. Nitsche MA, Boggio PS, Fregni F, Pascual-Leone A. Treatment of depression with transcranial direct current stimulation (tDCS): a review. Experimental Neurology 2009;219(1):14-9.
  26. Duman RS. Pathophysiology of depression and innovative treatments: remodeling glutamatergic synaptic connections. Dialogues in Clinical Neuroscience 2014;16(1):11-27.
آمار
تعداد مشاهده مقاله: 874
تعداد دریافت فایل اصل مقاله: 609