کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278138 | 1295796 | 2008 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Opioid activation in the lateral parabrachial nucleus induces hypertonic sodium intake
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کلمات کلیدی
SCPCRFCCKLPBNNTSβ-endorphin - β-آندورفینAngiotensin II - آنژیوتانسین دوsuperior cerebellar peduncle - اسب سواری مخچه بزرگsodium appetite - اشتها سدیمFURO - حلقهSatiety - خوشبختیAng II - دومcorticotropin-releasing factor - عامل تخریب کورتیکوتروپینfurosemide - فوروزمایدPVN - مالیات بر ارزش افزودهWater intake - مصرف آبNaloxone - نالوکسانnucleus of the solitary tract - هسته دستگاه انفرادیlateral parabrachial nucleus - هسته پاراباژیال جانبی جانبیmedial parabrachial nucleus - هسته پاراباژیالی MedialParaventricular nucleus of hypothalamus - هسته پروژسترونیک هیپوتالاموسcaptopril - کاپتوپریلCaP - کلاه لبه دارcholecystokinin - کولهسیستوکینین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Opioid mechanisms are involved in the control of water and NaCl intake and opioid receptors are present in the lateral parabrachial nucleus (LPBN), a site of important inhibitory mechanisms related to the control of sodium appetite. Therefore, in the present study we investigated the effects of opioid receptor activation in the LPBN on 0.3 M NaCl and water intake in rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. In normohydrated and satiated rats, bilateral injections of the opioid receptor agonist β-endorphin (2 nmol/0.2 μl) into the LPBN induced 0.3 M NaCl (17.8±5.9 vs. saline: 0.9±0.5 ml/240 min) and water intake (11.4±3.0 vs. saline: 1.0±0.4 ml/240 min) in a two-bottle test. Bilateral injections of the opioid antagonist naloxone (100 nmol/0.2 μl) into the LPBN abolished sodium and water intake induced by β-endorphin into the LPBN and also reduced 0.3 M NaCl intake (12.8±1.5 vs. vehicle: 22.4±3.1 ml/180 min) induced by 24 h of sodium depletion (produced by the treatment with the diuretic furosemide s.c.+sodium deficient food for 24 h). Bilateral injections of β-endorphin into the LPBN in satiated rats produced no effect on water or 2% sucrose intake when water alone or simultaneously with 2% sucrose was offered to the animals. The results show that opioid receptor activation in the LPBN induces hypertonic sodium intake in satiated and normohydrated rats, an effect not due to general ingestive behavior facilitation. In addition, sodium depletion induced 0.3 M NaCl intake also partially depends on opioid receptor activation in the LPBN. The results suggest that deactivation of inhibitory mechanisms by opioid receptor activation in the LPBN releases sodium intake if excitatory signals were activated (sodium depletion) or not.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 155, Issue 2, 13 August 2008, Pages 350-358
Journal: Neuroscience - Volume 155, Issue 2, 13 August 2008, Pages 350-358
نویسندگان
L.B. De Oliveira, L.A. Jr, J.V. Menani,