Functional And Mechanism Study Of Tacr2 On Stomach Motility

Functional dyspepsia is a common clinical constellation defined as presence of symptoms thought to originate from the upper abdominal region.Now functional dyspepsia is poorly elucidated in etiology and pathophysiology.Gastrointestinal motility disorder is the most primary pathophysiological mechanism underlying in specific symptom patterns.Tachykinin Receptor 2(Tacr2),also known as NK2 r,is present in the smooth muscle cells and neurons of the gastric tracks,and co-localized with PGP9.5.Now Tacr2 is known that its ligand is neurokinin A,and classically couples to Gq protein-mediated inositol 1,4,5-trisphosphate(IP3)synthesis and liberation of intracellular Ca2+,which initiates SMC contraction.But its function which regulates the liberation of neurotransmitters is incompletely understood.We generated stomach samples of Tacr2 knockout mice,and compared with wile type mice in synthesis of neurotransmitters using Real-Time PCR and Western Blot.And for evaluation,we use transferred Tacr2-EGFP vector into neuro-2a cell exposed to different concentration of NKA.Tacr2 knockout mice showed inhibited gastric emptying,and higher expression of nNOS and VIP,so as cGMP,the downstream of Nitric Oxide in stomach of Tacr2 knockout mice.Tacr2 up-regulates gastric emptying by inhibiting the expression of nNOS and VIP.