{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:47:35Z","timestamp":1787017655727,"version":"build-2736575974"},"reference-count":71,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2012,2,1]]},"abstract":"<jats:p>Peripheral amylin inhibits eating via the area postrema (AP). Because amylin activates the extracellular-signal regulated kinase 1\/2 (ERK) pathway in some tissues, and because ERK1\/2 phosphorylation (pERK) leads to acute neuronal responses, we postulated that it may be involved in amylin's eating inhibitory effect. Amylin-induced ERK phosphorylation (pERK) was investigated by immunohistochemistry in brain sections containing the AP. pERK-positive AP neurons were double-stained for the calcitonin 1a\/b receptor, which is part of the functional amylin-receptor. AP sections were also phenotyped using dopamine-\u03b2-hydroxylase (DBH) as a marker of noradrenergic neurons. The effect of fourth ventricular administration of the ERK cascade blocker U0126 on amylin's eating inhibitory action was tested in feeding trials. The number of pERK-positive neurons in the AP was highest \u223c10\u201315 min after amylin treatment; the effect appeared to be dose-dependent (5\u201320 \u03bcg\/kg amylin). A portion of pERK-positive neurons in the AP carried the amylin-receptor and 22% of the pERK-positive neurons were noradrenergic. Pretreatment of rats with U0126 decreased the number of pERK-positive neurons in the AP after amylin injection. U0126 also attenuated the ability of amylin to reduce eating, at least when the animals had been fasted 24 h prior to the feeding trial. Overall, our results suggest that amylin directly stimulates pERK in AP neurons in a time- and dose-dependent manner. Part of the AP neurons displaying pERK were noradrenergic. At least under fasting conditions, pERK was shown to be a necessary part in the signaling cascade mediating amylin's anorectic effect.<\/jats:p>","DOI":"10.1152\/ajpregu.00380.2011","type":"journal-article","created":{"date-parts":[[2011,12,2]],"date-time":"2011-12-02T04:25:40Z","timestamp":1322799940000},"page":"R340-R351","source":"Crossref","is-referenced-by-count":45,"title":["Involvement of the extracellular signal-regulated kinase 1\/2 signaling pathway in amylin's eating inhibitory effect"],"prefix":"10.1152","volume":"302","author":[{"given":"Catarina Soares","family":"Potes","sequence":"first","affiliation":[{"name":"Institute of Veterinary Physiology and Zurich Center for Integrative Human Physiology, Vetsuisse Faculty University of Zurich, Zurich Switzerland; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina Neuner","family":"Boyle","sequence":"additional","affiliation":[{"name":"Institute of Veterinary Physiology and Zurich Center for 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