کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6274279 1614821 2013 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Effects of hypocretin and norepinephrine interaction in bed nucleus of the stria terminalis on arterial pressure
ترجمه فارسی عنوان
اثرات هیپوکورتین و متابولیسم نوراپی نفرین در هسته بستر ترمینال استریال بر فشار شریانی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


- hcrt-1 and NE axons have overlapping distributions in BST.
- Glu stimulation of BST elicits decreases in MAP and HR.
- Injections of hcrt-1/NE in BST attenuate decreases in MAP and HR elicited by Glu.
- α2-AR and GABAA receptor antagonists attenuated the hcrt-1/NE inhibition of Glu responses.
- hcrt-1 involved in the release of NE that acts at α2-AR effecting GABA neurons.

Forebrain neuronal circuits containing hypocretin-1 (hcrt-1) and norepinephrine (NE) are important components of central arousal-related processes. Recently, these two systems have been shown to have an overlapping distribution within the bed nucleus of the stria terminalis (BST), a limbic structure activated by stressful challenges, and which functions to adjust arterial pressure (AP) and heart rate (HR) to the stressor. However, whether hcrt-1 and NE interact in BST to alter cardiovascular function is unknown. Experiments were done in urethane-α-chloralose anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effect of hcrt-1 and NE on the cardiovascular responses elicited by l-glutamate (Glu) stimulation of BST neurons. Microinjections of hcrt-1, NE or tyramine into BST attenuated the decrease in AP and HR to Glu stimulation of BST. Additionally, combined injections of hcrt-1 with NE or tyramine did not elicit a greater attenuation than either compound alone. Furthermore, injections into BST of the α2-adrenergic receptor (α2-AR) antagonist yohimbine, but not the α1-AR antagonist 2-{[β-(4-hydroxyphenyl)ethyl]aminomethyl}-1-tetralone hydrochloride, blocked both the hcrt-1 and NE-induced inhibition of the BST cardiovascular depressors responses. Finally, injections into BST of the GABAA receptor antagonist bicuculline, but not the GABAB receptor antagonist phaclofen, blocked the hcrt-1 and NE attenuation of the BST Glu-induced depressor and bradycardia responses. These data suggest that hcrt-1 effects in BST are mediated by NE neurons, and hcrt-1 likely acts to facilitate the synaptic release of NE. NE neurons, acting through α2-AR may activate Gabaergic neurons in BST, which in turn through the activation of GABAA receptors inhibit a BST sympathoinhibitory pathway. Taken together, these data suggest that hcrt-1 pathways to BST through their interaction with NE and Gabaergic neurons may function in the coordination of cardiovascular responses associated with different behavioral states.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 255, 26 December 2013, Pages 278-291
نویسندگان
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