Effect And Mechanisms Of Dopamine In Orbitofrontal Cortex On The Regulation Of Gastric Motility

As the development of technology and increasingly severe competition in society, some illnesses which have numerous interrelate with society psychogenic increased. Digestive system is the most sensitive organs which easy to get some influence about environment and emotion. The variety of diseases and incidence of psychogenic diseases of the digestive system are nearly the most important psychogenic diseases. In 1897, Cannon WB, an American physiologist, his work suggested emotional stimulation can influence the gastric and intestines movement. Mayer EA indicated that key-discriminating items are extra-intestinal features, possibly decreasing disease-related quality of life. Some irritable bowel syndrome patients may reflect neurobiological patterns of dysregulation in central stress systems. The orbitofrontal cortex (OFC) is a heterogeneous prefrontal sector selectively connected with a wide constellation of other prefrontal, limbic, sensory and premotor areas. It is clear from the lesion literature in both animals and humane that the OFC is a functionally complex structure which is implicated in high-level aspects of cognition, as well as mediating aspects of emotional behavior. Some clinic studies showed when give some stimulation on OFC, the gastric movement decrease. But we don't understand the mechanism of them.As an important brain-gut axis neurotransmitter, dopamine have a great effect on regulate gastric movement, gastric secrete, gastric mucosal blood and provide nutrition, and already be recognized an important factor which can be used to protect the gastric mucosal.The effect and mechanisms of dopamine (DA) in orbitfrontal cortex (OFC) on regulation of the gastric motility were studied using microinjected in OFC and recording intragastric pressure (IGP). The result s show that: (1) Dopamine 10μg microinjected in OFC causes a significantly effect on increase in intragastric pressure and enhance gastric motility. (2) SCH (SCH23390, SCH) 2μg makes a significantly effect on decrease in intragastric pressure and reduce gastric motility. SCH 2μg abolishes the gastric excitatory response from DA. Risperidone 2μg can enhance intragastric pressure and gastric motility. Risperidone 2μg could not abolish the gastric excitatory response from DA. (3)When amygdala central nuclear destroyed, intragastric pressure decrease and gastric motility reduce and abolished the gastric excitatory response to DA 10μg. When microinjected sch 2μg in amygdala central nuclear, intragastric pressure decrease and gastric motility reduce and abolished the gastric excitatory response to DA 10μg. It is enhance gastric motility when microinjected DA 10μg in amygdala (4) When cut off vagus, intragastric pressure decrease and gastric motility reduce and abolished the gastric excitatory response to DA 10μg. The frequency of gastric motility does not significantly change in all cases.The results suggest that dopamine in OFC could make an increase in intragastric pressure. This effect is transmitted by amygdala central nuclear and via vagus. SCH as the dopaminergic D1 receptor agonist could abolish the gastric excitatory response from DA. Risperidone as the dopaminergic D2 receptor agonist could not abolish the gastric excitatory response from DA. The increase intragastric pressure caused by DA in OFC is principally mediated by dopaminergic D1 receptor. When dopaminergic neuron in OFC excitatory, they could release DA and combined with dopaminergic D1 receptor and have some excitatory effect on gastric motility.