کد مقاله کد نشریه سال انتشار مقاله انگلیسی ترجمه فارسی نسخه تمام متن
8840519 1614689 2018 12 صفحه PDF سفارش دهید دانلود رایگان
عنوان انگلیسی مقاله ISI
Chemogenetic Manipulation of Dorsal Hippocampal Astrocytes Protects Against the Development of Stress-enhanced Fear Learning
ترجمه فارسی عنوان
دستکاری چگونگی آستروسیت های هیپوکامپ پشتی محافظت در برابر ترس از تمایل به افزایش فشار است
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موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی
Maladaptive behavioral outcomes following stress have been associated with immune dysregulation. For example, we have previously reported that stress-induced dorsal hippocampal interleukin-1β signaling is critical to the development of stress-enhanced fear learning (SEFL). In parallel, astroglial signaling has been linked to the development of post-traumatic stress disorder (PTSD)-like phenotypes and our most recent studies have revealed astrocytes as the predominant cellular source of stress-induced IL-1β. Here, we used chemogenetic technology and morphological analyses to further explore dorsal hippocampal astrocyte function in the context of SEFL. Using a glial-expressing DREADD construct (AAV8-GFAP-hM4Di(Gi)-mCherry), we show that dorsal hippocampal astroglial Gi activation is sufficient to attenuate SEFL. Furthermore, our data provide the first initial evidence to support the function of the glial-DREADD construct employed. Specifically, we find that CNO (clozapine-n-oxide) significantly attenuated colocalization of the Gi-coupled DREADD receptor and cyclic adenosine monophosphate (cAMP), indicating functional inhibition of cAMP production. Subsequent experiments examined dorsal hippocampal astrocyte volume, surface area, and synaptic contacts (colocalization with postsynaptic density 95 (PSD95)) following exposure to severe stress (capable of inducing SEFL). While severe stress did not alter dorsal hippocampal astrocyte volume or surface area, the severe stressor exposure reduced dorsal hippocampal PSD95 immunoreactivity and the colocalization analysis showed reduced PSD95 colocalized with astrocytes. Collectively, these data provide evidence to support the functional efficacy of the glial-expressing DREADD employed, and suggest that an astrocyte-specific manipulation, activation of astroglial Gi signaling, is sufficient to protect against the development of SEFL, a PTSD-like behavior.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 388, 15 September 2018, Pages 45-56
نویسندگان
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