- Peptide (C)RAESDEARR(S)YNDP, corresponding to amino acid residues 200-214 of rat ADRB1 (Accession P18090). 2nd extracellular loop.
- Mouse brain sections (1:60).
- Expression of β1-Adrenoceptor in mouse cerebellumImmunohistochemical staining of mouse cerebellum using Anti-β1-Adrenergic Receptor (extracellular)-ATTO-488 Antibody (#AAR-023-AG), (1:60). β1-adrenoceptor staining (green) appears in granule cells and in the Purkinje cell layer. B. Nuclei staining using DAPI as the counterstain. C. Merged image of panels A and B.
β-Adrenergic receptors control key physiological functions through signals encoded by catecholamine hormones and neurotransmitters to activate intracellular signaling pathways. These receptors belong to the amine receptor cluster of rhodopsin-like family of G-protein coupled receptors (GPCRs).
The β1 adrenergic receptor (β1AR) is comprised of an extracellular N-terminus, seven membrane spanning loops (TM1-7) and an intracellular C-terminus1.
β1AR couples to the stimulatory G protein Gs and thereby activates adenylyl cyclase. β1AR also couples to the inhibitory G protein Gi and can induce G protein independent signaling. Differential activation of these pathways can be modulated by different ligands2.
β1AR is widely expressed in cardiac myocytes and is regulated by the microRNA (miRNA) let-7e. Following acute myocardial infraction (AMI) in rats, expression of β1AR is significantly up-regulated while the expression of miRNA let-7a (as well as miRNAs c, d, e and i) is notably down-regulated 6 and 24 hours post myocardial infarction. Blocking the up-regulation of β1AR can serve as a novel therapeutic approach for the treatment of AMI-induced arrhythmia3.
β1AR is also implicated in the pathophysiology of Alzheimer’s disease (AD). Administration of a partial β1AR agonist, behavioral deficits in a mouse model of AD are restored and amyloid beta and tau levels decrease as measured by regional immunohistochemistry4.