Dopamine- induced hypophagia is mediated via NMDA and mGlu1 receptors in chicken

Document Type : Physiology

Authors

1 Department of Physiology, Faculty of Veterinary Medicine, University of Tehran, 14155-6453, Tehran, Iran

2 Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran

Abstract

Background: Feeding behavior is regulated by a complex network which interacts via diverse signals from central and peripheral tissues. It is known dopaminergic and glutamatergic systems have crucial role on food intake regulation but scarce reports exist on their interaction in appetite regulation in broilers. OBJECTIVES: The present study was designed to examine the role of glutamatergic system on dopamine-induced hypophagia in neonatal meat-type chicken. METHODS: In experiment 1, chicks received ICV injection of control solution, dopamine (40 nmol), MK-801 (NMDA glutamate receptors antagonist, 15 nmol) and co-injection of dopamine + MK-801. In experiment 2, birds were ICV injected with saline, dopamine (40 nmol), CNQX (AMPA glutamate receptors antagonist, 390 nmol) and co-injection of dopamine + CNQX. In experiment 3, chicks received ICV injection of control solution, dopamine (40 nmol), AIDA (mGLUR1 glutamate receptors antagonist, 2 nmol), dopamine + AIDA. Experiments 4 and 5 were similar to experiment 3, except birds were injected with LY341495 (mGLUR2 glutamate receptors antagonist, 150 nmol) and UBP1112 (mGLUR3 glutamate receptors antagonist, 2 nmol) instead of AIDA. Then the cumulative food intake was measured until 120 min post injection. RESULTS: According to the results, ICV injection of dopamine significantly decreased food intake (p<0.001). Co-injection of dopamine and MK-801 decreased dopamine induced hypophagia (p<0.001). Moreover, the food intake of chicks was significantly increased by co-injection of AIDA and dopamine (p<0.001). CONCLUSIONS: These results suggest dopamine-induced hypophagia is mediated via NMDA and mGlu1 receptors in chicken.
 

Keywords

Article Title [Persian]

میانجیگری گیرند ههای NMDA و متابوتروپیک نوع 1 گلوتامات ب ر ک ا ه ش اخذ غذای القا شده با دوپامین در جوجه

Authors [Persian]

  • محمدرضا طاهریان 1
  • علی باغبانزاده 1
  • مرتضی زنده دل 2
1 گروه علوم پایه، دانشکده دامپزشکی دانشگاه تهران، تهران، ایران
2 گروه علوم پایه، دانشکده دامپزشکی دانشگاه تهران، تهران، ایران
Abstract [Persian]

زمینه مطالعه:  رفتار تغذیه‌ای از  راه مسیرهای پیچیده بواسطه سیگنال‌های مرکزی و اندام‌های محیطی تنظیم می‌شود. مشخص شده است که سیستم دوپامینرژیک و گلوتاماترژیک نقش مهمی در تنظیم مصرف خوراک دارند اما گزارشات کمی در مورد تقابل عمل آنها در پرندگان وجود دارد. هدف: این مطالعه به‌منظور بررسی نقش سیستم گلوتاماترژیک بر کاهش اشتهای ناشی از دوپامین در جوجه‌های گوشتی یک روزه طراحی شد. روش کار: در آزمایش اول جوجه‌ها تزریق داخل بطنی مغزی محلول کنترل، دوپامین (4nmol)، رMK-801 (آنتاگونیست گیرنده NMDA گلوتاماتی، nmol‌15) و تزریق توام دوپامین + MK-801 را دریافت کردند. در آزمایش دوم جوجه‌ها با محلول کنترل، دوپامین (4nmol)،ر CNQX (آنتاگونیست گیرنده AMPA گلوتاماتی، nmol‌390) و استفاده توام دوپامین + AMPA تزریق داخل بطنی مغزی شدند. در آزمایش سوم جوجه‌ها تزریق داخل بطنی مغزی محلول کنترل، دوپامین (4nmol)،رAIDA (آنتاگونیست گیرنده mGLUR1 گلوتاماتی، nmol‌2) و دوپامین + AIDA را دریافت کردند. آزمایش 4 و 5 مشابه آزمایش 3 بود بطوری‌که جوجه‌ها LY341495 (آنتاگونیست گیرنده mGLUR2 گلوتاماتی، nmol‌150) و UBP1112 (آنتاگونیست گیرنده mGLUR3 گلوتاماتی، nmol‌2) را بجای AIDA دریافت کردند. سپس مصرف تجمعی خوراک تا 120 دقیقه پس از تزریق اندازه‌گیری شد. نتایج: با توجه به نتایج بدست آمده تزریق داخل بطنی مغزی دوپامین بطور معنی‌داری موجب کاهش اخذ غذا شد (001/0>p). تزریق توام دوپامین و MK-801 موجب کاهش اثرات ضد اشتهایی دوپامین شد (001/0>p). مصرف خوراک در جوجه‌ها بواسطه تزریق توام دوپامین و AIDA  افزایش یافت (001/0>p). نتیجه‌گیری نهایی: نتایج نشان‌دهنده این بود که کاهش اشتهای ناشی از دوپامین از طریق گیرنده‌های NMDA و mGLUR1 گلوتاماترژیک در جوجه‌های گوشتی میانجی‌گری می‌شود.

Keywords [Persian]

  • دوپامین
  • گلوتامات
  • مصرف غذا
  • جوجه‌های گوشتی یک روزه

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Iranian Journal of Veterinary Medicine
Volume 10, Issue 3
September 2016
Pages 191-199

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