کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2200766 1099970 2013 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Altered Kir and gap junction channels in temporal lobe epilepsy
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Altered Kir and gap junction channels in temporal lobe epilepsy
چکیده انگلیسی

Since astrocytes may sense and respond to neuronal activity these cells are now considered important players in brain signaling. Astrocytes form large gap junction coupled syncytia allowing them to clear the extracellular space from K+ and neurotransmitters accumulating during neuronal activity, and redistribute it to sites of lower extracellular concentrations. Increasing evidence suggests a crucial role for dysfunctional astrocytes in the etiology of epilepsy. Notably, alterations in expression, localization and function of astroglial K+ channels as well as impaired K+ buffering was observed in specimens from patients with pharmacoresistant temporal lobe epilepsy and in chronic epilepsy models. Altered astroglial gap junction coupling has also been reported in epileptic tissue which, however, seems to play a dual role: (i) junctional coupling counteracts hyperactivity by facilitating clearance of elevated extracellular K+ and glutamate while (ii) it also provides a pathway for energetic substrates and fuels neuronal activity. Dysfunctional astrocytes should be considered promising targets for new therapeutic strategies.


► Astrocytes form gap junction coupled networks to regulate brain homeostasis.
► In epilepsy, astroglial K+ channel function is impaired.
► Astroglial gap junction coupling is altered in temporal lobe epilepsy.
► Dysfunctional astrocytes are promising targets for new antiepileptic therapies.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 63, Issue 7, December 2013, Pages 682–687
نویسندگان
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