Expression of the non-neuronal cholinergic system in rat liver.

摘要: Insulin secretion is, in part, regulated by acetylcholine (ACh), as released from postganglionic, vagal neurons with intra-islet terminals, and binding to muscarinic receptors of the M3 type plasma membrane β-cells (Gilon Henquin, 2001). Additionally, non-neuronal cellsmay produce AChwhich could affect cell functions an autocrine/paracrine fashion e.g. modulate inflammation (Wessler Kirkpatrick, 2008). Rodriguez-Diaz et al. (2011) reported that human (but notmurine) islets, glucagon secreting α-cells ACh which serves a non-neuronal, paracrine mediator release insulin β-cells. Markers cholinergic phenotype are: choline acetyltransferase (ChAT; synthesizes acetyl coenzyme A), acetylcholinesterase (AChE; main degrading enzyme), highaffinity transporter (CHT-1), vesicular (VAChT) (Kawashima Fujii, 2008; Wessler In current report, protein expression these markers also α7 subunit nicotinic receptors, latter being particular importance modulation (Wang al., 2003), is suggested rat pancreatic Sprague–Dawley rats either sex (Scanbur AB, Sollentuna, Sweden; n=5) were killed exsanguination under pentobarbital anesthesia. Pancreatic specimens fixed formalin, embedded paraffin, arranged for immunohistochemistry using following antibodies:mousemonoclonal anti-ChAT (Chemicon Int., supplied byMillipore, Chandlers Ford, UK; optimal dilution 1:100), rabbit polyclonal (Abcam, Cambridge, 1:800), anti-