کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4311994 1612917 2017 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lateral parabrachial nucleus and opioid mechanisms of the central nucleus of the amygdala in the control of sodium intake
ترجمه فارسی عنوان
parabrachial هسته جانبی و مواد مخدر مکانیزم از هسته مرکزی آمیگدال در کنترل مصرف سدیم
کلمات کلیدی
ANG دوم، آنژیوتانسین II؛ CAP، کاپتوپریل؛ CEA، هسته مرکزی آمیگدال؛ FURO، فوروزماید؛ LPBN، هسته parabrachial جانبی، NTS، هسته از دستگاه انفرادی، s.c.، اشتها subcutaneouslySodium؛ گیرنده های مواد مخدر؛ کم شدن آب بدن. تشنگی؛ گابا. Adrenergi
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب رفتاری
چکیده انگلیسی


• CeA facilitatory and LPBN inhibitory mechanisms interact to control NaCl intake.
• Naloxone in the CeA blocks NaCl intake by euhydrated rats with muscimol into the LPBN.
• Naloxone in the CeA blocks NaCl intake by hyperosmotic rats with LPBN moxonidine.
• Opioids in the CeA are important for sodium intake induced by LPBN deactivation.
• Connection between LPBN and CeA mechanisms may depend on opioids action in the CeA.

Facilitatory and inhibitory mechanisms in the central nucleus of the amygdala (CeA) and the lateral parabrachial nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3 M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n = 4–8/group) with stainless steel cannulas implanted bilaterally in the CeA and in the LPBN were used. The ingestion of 0.3 M NaCl and water by euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN (29.4 ± 2.7 and 15.0 ± 2.4 ml/4 h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40 μg/0.2 μl) into the CeA (0.7 ± 0.3 and 0.3 ± 0.1 ml/4 h, respectively). The ingestion of 0.3 M NaCl by rats treated with intragastric 2 M NaCl (2 ml/rat) combined with moxonidine (0.5 nmol/0.2 μl) into the LPBN (17.0 ± 3.8 ml/2 h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2 ± 2.5 ml/2 h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Behavioural Brain Research SreeTestContent1 - Volume 316, 1 January 2017, Pages 11–17
نویسندگان
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