ABSTRACT
Objective To explore the effects of acupuncture on pruritic behaviors, expression of 5-HT neurons in medulla oblongata and 5-HTR2B on mice with chloroquine-induced pruritus; To discuss the mechanism of action of acupuncture in chloroquine-induced pruritus. Methods A non-histamine-dependent pruritus model was prepared by subcutaneous injection of chloroquine into the back of the neck. Forty C57B/6J mice were randomly divided into model-acupuncture group, model-non-acupuncture group, normal saline group and blank control group, with 10 mice in each group. After modeling, acupuncture was given in Xuehai, Quchi and Hegu on both sides. The plug and twist way was used to stimulate, once a day, three times. Model-non-acupuncture group received no acupuncture. Normal saline group received the neck injection of saline in the back. Blank control group received no treatment. Behavioral changes were observed, and immunofluorescence technique and Western blot were used to test the expression of 5-HT neurons and 5-HTR2B in medulla oblongata neurons. Results The number of scratches in model-acupuncture group and model-non-acupuncture group was obviously more than normal saline group and blank control group (P<0.05). The number of scratches in model-acupuncture group was lower than that of model-non-acupuncture group (P<0.05). The expression of 5-HT in medulla oblongata neurons was unclear in both normal saline group and blank control group. The expression of 5-HT neurons in medulla oblongata significantly increased in model group, which decreased after acupuncture. The expression of 5-HTR2B of model group was significant higher than normal saline group and blank control group (P<0.01). Compared with model-non-acupuncture group, the expression of 5-HTR2B in model-acupuncture group significant decreased (P<0.01). Conclusion Acupuncture can significantly inhibitscratching behaviors in mice induced by chloroquine, and the mechanism may be realized by decreasing the expression of 5-HT neurons and 5-HTR2B in medulla oblongata neurons.
ABSTRACT
The colonic migrating motor complex (CMMC) is a critical neurally mediated rhythmic propulsive contraction observed in the large intestine of many mammals. It seems to be equivalent to the high amplitude propagating contractions (HAPCs) in humans. This review focuses on the probable neural mechanisms involved in producing the CMMC or HAPC, their likely dependence on mucosal and neuronal serotonin and pacemaker insterstitial cells of Cajal networks and how intrinsic neural reflexes affect them. Discussed is the possibility that myenteric 5-hydroxytryptamine (5-HT) neurons are not only involved in tonic inhibition of the colon, but are also involved in generating the CMMC and modulation of the entire enteric nervous system, including coupling motility to secretion and blood flow. Mucosal 5-HT appears to be important for the initiation and effective propagation of CMMCs, although this mechanism is a longstanding controversy since the 1950s, which we will address. We argue that the slow apparent propagation of the CMMC/HAPC down the colon is unlikely to result from a slowly conducting wave front of neural activity, but more likely because of an interaction between ascending excitatory and descending (serotonergic) inhibitory neural pathways interacting both within the myenteric plexus and at the level of the muscle. That is, CMMC/HAPC propagation appears to be similar to esophageal peristalsis. The suppression of inhibitory (neuronal nitric oxide synthase) motor neurons and mucosal 5-HT release by an upregulation of prostaglandins has important implications in a number of gastrointestinal disorders, especially slow transit constipation.