کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2002111 1066094 2006 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
AMPA receptor-induced intracellular calcium response in the paraventricular nucleus is modulated by nitric oxide: Calcium imaging in a hypothalamic organotypic cell culture model
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
AMPA receptor-induced intracellular calcium response in the paraventricular nucleus is modulated by nitric oxide: Calcium imaging in a hypothalamic organotypic cell culture model
چکیده انگلیسی

An organotypic cell culture (OCC) model of the rat hypothalamic paraventricular nucleus (PVN) was established to monitor intracellular calcium levels ([Ca2+]i) of magnocellular neurons in response to glutamate and nitric oxide (NO). The histoarchitectural organization of these cultures was characterized either by immunohistochemical labeling of vasopressin, neuronal nitric oxide synthase (nNOS) and the neuronal marker NeuN or by the enzyme histochemical NADPH-diaphorase staining. A distinct NeuN positive cell population in 14-days old OCC’s was confirmed as being the PVN by its vasopressin- and nNOS-immunostained neurons as well as by its NADPH-diaphorase labeling. Life cell imaging was performed using the [Ca2+]i sensor Fluo-4 to measure [Ca2+]i transients in response to bath applications of glutamate, high potassium (60 mM), and ATP. The glutamate-induced [Ca2+]i response was mimicked by AMPA but not NMDA in the PVN. NMDA, however, elicited a [Ca2+]i transient in a different area of the OCC that corresponds to the suprachiasmatic nucleus indicating the potential effectiveness of the stimulus. The AMPA-receptor blocker NBQX abolished the glutamate-induced response in the PVN. An inhibition of endogenous NO production by the NOS inhibitor L-NAME decreased the amplitude of AMPA- and glutamate-induced [Ca2+]i rises. Taken together, these data suggest that AMPA mediates the glutamate-induced [Ca2+]i rises within the PVN, where endogenous NO is able to modulate such glutamate signaling in OCC.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nitric Oxide - Volume 14, Issue 4, June 2006, Pages 290–299
نویسندگان
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