Nucleus Raphe Obscurus Participates in Regulation of Gallbladder Motility through Vagus and Sympathetic Nerves in Rabbits

The aim of the present study is to investigate if the nucleus raphe obscurus (NRO) participate in regulating the gallbladder motility in rabbits. Rabbits were fasted for about 20-24 hours. After anesthetization with urethane, an incision was made at the middle of the abdomen and the gallbladder was exposed. A frog bladder connected with force transducer was inserted into the gallbladder through a small incision at the funds to record gallbladder motility (tonic contraction and phasic contraction). Glutamate and other chemicals were microinjected into NRO through a vitreous tube attached to a microsyringe. We found both the tonic contraction and phasic contraction of the gallbladder were enhanced after the glutamate was injected into NRO. GABA inhibited gallbladder motility if administrated in the same way. Microinjection of ketamine, NMDA (N-methyl-D-aspartate) receptor antagonist, into NRO inhibited the phasic contraction of gallbladder. Administration of CNQX (6-cyano-7nitroquinoxaline-2, 3-dione), a non-NMDA receptor antagonist, enhanced the gallbladder tonic contraction. Pretreatment of ketamine into NRO attenuated the effect of glutamate, while pretreatment of CQNX had no effect on it. Intravenous injection of atropine or vagotomy completely abolished the effect of glutamate on gallbladder phasic contraction, while intravenous injection of phentolamine or transecting the spinal cord at T3~4 inhibited that on tonic contraction. Intravenous injection of propranolol did not influence the glutamate effect. These results suggested that glutamate in NRO participates in regulating the motility of the gallbladder through NMDA receptor. When excited, the NMDA receptors in NRO enhance the phasic contraction of the gallbladder through vagus nerve and peripheral M-receptors, and enhance the tonic contraction of the gallbladder through sympathetic nerve and peripheral α -receptors. GABA in NRO is also involved in the regulation of gallbladder motility.