| First Author | Azzena GB | Year | 1999 |
| Journal | Neurosci Lett | Volume | 261 |
| Issue | 1-2 | Pages | 9-12 |
| PubMed ID | 10081914 | Mgi Jnum | J:107984 |
| Mgi Id | MGI:3622619 | Doi | 10.1016/s0304-3940(98)00993-8 |
| Citation | Azzena GB, et al. (1999) Nitric oxide regenerates the normal colonic peristaltic activity in mdx dystrophic mouse. Neurosci Lett 261(1-2):9-12 |
| abstractText | We demonstrated in vitro that the colonic peristaltic activity is modified in dystrophin-deficient mdx mouse indicating a defect in the enteric nervous system (ENS). Since nitric oxide (NO) has been proposed as a putative inhibitory mediator of ENS, here we have examined the effects of both L-Arginine (L-Arg) and Nomega-nitro-L-arginine methyl ester (L-NAME) on the peristaltic activity of mdx mouse distal colon. The motor pattern of colonic segment showed irregular peristaltic waves. L-Arg (10(-7) - 10(-5) M) induced the peristaltic activity to slow down. At a concentration of 10(-5) M, L-Arg produced hypomotility, characterised by a decrease in amplitude, frequency and ejected fluid volume. Conversely, L-NAME elicited hypermotility, this effect being reversed once again by the subsequent addition of L-Arg. Interestingly the addition of 10(-5) M L-Arg to the organ bath led to the normal progression, in an oral to aboral direction, of 90% of the peristaltic waves. This last result strongly suggests that exogenous application of L-Arg restores the integrative circuits of the ENS responsible for programming and co-ordinating peristaltic activity in the distal colon of mdx mouse. |
