Noradrenergic neurons of the area postrema mediate amylin's hypophagic action
| Autor: | Victoria F. Turek, Barbara L. Roland, Thomas A. Lutz, Calvin Vu, Thomas Riediger, Catarina Soares Potes, Rebecca L. Cole, Jonathan D. Roth |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Amyloid endocrine system medicine.medical_specialty Time Factors endocrine system diseases Saporin Physiology Injections Subcutaneous Central nervous system Amylin Dopamine beta-Hydroxylase macromolecular substances Rats Sprague-Dawley Lesion Eating Norepinephrine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Physiology (medical) Internal medicine medicine Animals Neurotransmitter 030304 developmental biology 0303 health sciences Behavior Animal biology Appetite Regulation Area postrema Solitary tract Immunohistochemistry Anorexia Islet Amyloid Polypeptide Rats Phenotype Endocrinology medicine.anatomical_structure Area Postrema nervous system chemistry biology.protein Catecholamine medicine.symptom Adrenergic Fibers Proto-Oncogene Proteins c-fos 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 299:R623-R631 |
| ISSN: | 1522-1490 0363-6119 |
| Popis: | Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim of this study was to identify the neurochemical phenotype of the neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression of c-Fos protein was used as a marker for neuronal activation and dopamine-beta-hydroxylase (DBH), the enzyme-catalyzing noradrenaline synthesis, as a marker for noradrenergic neurons. We found that approximately 50% of amylin-activated AP neurons are noradrenergic. To clarify the functional role of these neurons in amylin's effect on eating, noradrenaline-containing neurons in the AP were lesioned using a saporin conjugated to an antibody against DBH. Amylin (5 or 20 microg/kg s.c.)-induced anorexia was observed in sham-lesioned rats with both amylin doses. Rats with a lesion of > 50% of the noradrenaline neurons were unresponsive to the low dose of amylin (5 microg/kg) and only displayed a reduction in food intake 60 min after injection of the high amylin dose (20 microg/kg). In a terminal experiment, the same rats received amylin (20 microg/kg) or saline. The AP and nucleus of the solitary tract (NTS) were stained for DBH to assess noradrenaline lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. In contrast to sham-lesioned animals, noradrenaline-lesioned rats did not show a significant increase in amylin-induced c-Fos expression in the AP and NTS. We conclude that the noradrenergic neurons in the AP mediate at least part of amylin's hypophagic effect. |
| Databáze: | OpenAIRE |
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