کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425463 | 1295874 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Glucocorticoid receptor activation selectively hampers N-methyl-d-aspartate receptor dependent hippocampal synaptic plasticity in vitro
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کلمات کلیدی
RU 38486VDCCMifepristonefEPSPaCSFAPVN-methyl-d-aspartateNMDADMSO - DMSOStress - استرس یا فشار روانیlong term potentiation - تقویت طولانی مدتLTP - تقویت طولانی مدت یا LTP Dimethyl sulfoxide - دیمتیل سولفواکسیدartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیHippocampus - هیپوکامپ voltage dependent calcium channel - ولتاژ کانال کلسیم وابسته استField excitatory postsynaptic potential - پتانسیل پستنیپتیک مزمن تحریک پذیرCorticosterone - کورتیکوسترونMineralocorticoid receptor - گیرنده مینرالوکورتیکوئید glucocorticoid receptor - گیرنده گلوکوکورتیکوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Glucocorticoid receptor activation selectively hampers N-methyl-d-aspartate receptor dependent hippocampal synaptic plasticity in vitro Glucocorticoid receptor activation selectively hampers N-methyl-d-aspartate receptor dependent hippocampal synaptic plasticity in vitro](/preview/png/9425463.png)
چکیده انگلیسی
Corticosterone and exposure to stressful experiences have been reported to decrease hippocampal synaptic plasticity, in particular when relatively mild stimulation paradigms-presumably activating predominantly N-methyl-d-aspartate receptors-are being used. Using various stimulation paradigms and pharmacological approaches we tested therefore the hypothesis that elevated corticosterone levels, by activating glucocorticoid receptors, predominantly hamper N-methyl-d-aspartate receptor dependent synaptic plasticity in vitro. To address this, mouse hippocampal slices were treated for 20 min with corticosterone (100nM) or vehicle and synaptic efficacy was examined 1-6 h later. First, we found that primed burst potentiation and synaptic potentiation after 10Hz stimulation are predominantly N-methyl-d-aspartate receptor dependent, and are significantly suppressed after corticosterone treatment. Second, these latter effects were prevented by treating slices with the glucocorticoid receptor antagonist mifepristone prior to and during corticosterone administration. Third, theta burst potentiation, which was shown to involve activation of both N-methyl-d-aspartate receptors, voltage-dependent calcium channels and possibly other mechanisms, was not affected by corticosterone. However, theta-burst potentiation in the presence of nifedipine-singling out primarily the N-methyl-d-aspartate receptor dependent component-was reduced by corticosterone. These results indicate that corticosterone, via glucocorticoid receptor activation, selectively hampers N-methyl-d-aspartate receptor dependent synaptic plasticity in vitro and leaves more complex forms of long term potentiation unaffected. We speculate that these effects are involved in the impairment of cognitive performance by corticosteroid hormones after exposure to stressful and traumatic experiences.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 135, Issue 2, 2005, Pages 403-411
Journal: Neuroscience - Volume 135, Issue 2, 2005, Pages 403-411
نویسندگان
O. Wiegert, Z. Pu, S. Shor, M. Joëls, H. Krugers,