Adrenergic Agonists Activate Transcriptional Activity in Immortalized Neuronal Cells From the Mouse Suprachiasmatic Nucleus

• Published in: Journal of pineal research 2024-08, Vol.76 (5), p.e12999-n/a
• Main Authors: Langiu, Monica, Dehghani, Faramarz, Hohmann, Urszula, Bechstein, Philipp, Rawashdeh, Oliver, Rami, Abdelhaq, Maronde, Erik
• Format: Article
• Language: English
• Subjects: adrenaline; Adrenergic beta-Agonists - pharmacology; adrenoceptors; Animals; melatonin; Mice; Neurons - drug effects; Neurons - metabolism; SCN; signal transduction; Signal Transduction - drug effects; Suprachiasmatic Nucleus - drug effects; Suprachiasmatic Nucleus - metabolism
• ISSN: 0742-3098; 1600-079X; 1600-079X
• DOI: 10.1111/jpi.12999

ABSTRACT The suprachiasmatic nucleus of the hypothalamus (SCN) houses the central circadian oscillator of mammals. The main neurotransmitters produced in the SCN are γ‐amino‐butyric acid, arginine‐vasopressin (AVP), vasoactive intestinal peptide (VIP), pituitary‐derived adenylate cyclase‐activating peptide (PACAP), prokineticin 2, neuromedin S, and gastrin‐releasing peptide (GRP). Apart from these, catecholamines and their receptors were detected in the SCN as well. In this study, we confirmed the presence of β‐adrenergic receptors in SCN and a mouse SCN‐derived immortalized cell line by immunohistochemical, immuno‐cytochemical, and pharmacological techniques. We then characterized the effects of β‐adrenergic agonists and antagonists on cAMP‐regulated element (CRE) signaling. Moreover, we investigated the interaction of β‐adrenergic signaling with substances influencing parallel signaling pathways. Our findings have potential implications on the role of stress (elevated adrenaline) on the biological clock and may explain some of the side effects of β‐blockers applied as anti‐hypertensive drugs.