کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10299082 | 539684 | 2014 | 37 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Immediate ketamine treatment does not prevent posttraumatic stress responses in an animal model for PTSD
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
روانپزشکی بیولوژیکی
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چکیده انگلیسی
Clinical studies suggest that administration of ketamine hydrochloride-an antagonist at the N-methyl-d-aspartate ionophore-provides short-term amelioration for depressive symptoms. The effects of a brief course of ketamine given immediately following exposure to psychogenic stress on the behavioral stress responses were assessed in an animal model of posttraumatic stress disorder. Animals exposed to stress were treated 1Â h later with ketamine (0.5, 5, and 15Â mg/kg) or vehicle for three days (N=107). Outcome measures included behavior in the elevated plus maze (EPM) and acoustic startle response (ASR) tests 30 days after initial exposure and freezing behavior upon exposure to a trauma-cue on day 31. Pre-set cut-off behavioral criteria classified exposed animals according to their EPM and ASR response-patterns into “extreme,” “minimal,” or “partial” behavioral response for analysis of prevalence rates of “PTSD-like behavior.” Circulating corticosterone levels were assessed 20Â min after injection of ketamine in exposed and unexposed animals (N=62). The dexamethasone suppression test was used to assess negative feedback inhibition of the HPA axis. Prevalence rates of extremely-, partially-, or minimally-disrupted behavior demonstrated that ketamine administered immediately following stress exposure was ineffective in alleviating “PTSD-like behavior” at day 30 after exposure. Administration of ketamine was associated with increase in freezing behavior after exposure to a trauma-cue on day 31. Corticosterone levels were significantly suppressed by ketamine only in the exposed animals. Administration of ketamine immediately following trauma-exposure may not only be ineffective but actually detrimental in the long term. A disruption of the post-stress HPA-response has been raised as a contributing factor.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Neuropsychopharmacology - Volume 24, Issue 3, March 2014, Pages 469-479
Journal: European Neuropsychopharmacology - Volume 24, Issue 3, March 2014, Pages 469-479
نویسندگان
Alzbeta Juven-Wetzler, Hagit Cohen, Zeev Kaplan, Avi Kohen, Oren Porat, Joseph Zohar,