کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341618 | 1295841 | 2008 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Relationship between neuronal vulnerability and potassium-chloride cotransporter 2 immunoreactivity in hippocampus following transient forebrain ischemia
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کلمات کلیدی
DABCA1TBSKCC2NKCC14VO3,3′-diaminobenzidine - 3،3'-diaminobenzidineBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز four-vessel occlusion - انسداد چهار رگTransient forebrain ischemia - ایسکمی پیشانی مزمنphosphate buffer - بافر فسفاتTris-buffered saline - تریس بافر شورBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزHippocampus - هیپوکامپ GABA - گابا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Relationship between neuronal vulnerability and potassium-chloride cotransporter 2 immunoreactivity in hippocampus following transient forebrain ischemia Relationship between neuronal vulnerability and potassium-chloride cotransporter 2 immunoreactivity in hippocampus following transient forebrain ischemia](/preview/png/4341618.png)
چکیده انگلیسی
Cation chloride cotransporters have been reported to be expressed in neurons in the hippocampus and to regulate intracellular Clâ concentration. The neuron-specific K-Cl cotransporter 2 (KCC2) is necessary for maintaining the low intracellular chloride concentration required for the hyperpolarizing actions of GABA. In this study we examined the vulnerability of KCC2-containing neurons as well as the changes in the pattern of KCC2 distribution in the rat hippocampus following 15 min ischemia induced by four-vessel occlusion. Immunostaining for the 72 kDa heat shock protein (HSP-72) was used to investigate the extent of damage in neuronal populations previously shown to be vulnerable to ischemia. At 6-24 h after ischemia, when the pyramidal cells in the CA1 (subfield of cornu Ammonis) region showed no morphological signs of damage, a small rise of KCC2 immunoreactivity was already observed. After 2 days, when the CA1 pyramidal cells started to degenerate, a progressive downregulation of the KCC2 protein was visible. Interestingly, in the same areas, the parvalbumin containing interneurons showed no signs of ischemic damage, and KCC2 immunoreactivity was retained on their membrane surface. In CA1 pyramidal cells, the reduction in KCC2 expression may lead to an elevation of intracellular Clâ concentration, which causes a shift in equilibrium potential toward more positive levels. Consequently, the reduction of the inhibitory action of GABA through downregulation of KCC2 function may be involved in the pathomechanisms of delayed neuronal death in the CA1 subfield.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 154, Issue 2, 23 June 2008, Pages 677-689
Journal: Neuroscience - Volume 154, Issue 2, 23 June 2008, Pages 677-689
نویسندگان
E. Papp, C. Rivera, K. Kaila, T.F. Freund,