| First Author | Girard BM | Year | 2013 |
| Journal | Am J Physiol Renal Physiol | Volume | 305 |
| Issue | 10 | Pages | F1504-12 |
| PubMed ID | 24049141 | Mgi Jnum | J:202952 |
| Mgi Id | MGI:5523408 | Doi | 10.1152/ajprenal.00343.2013 |
| Citation | Girard BM, et al. (2013) Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture. Am J Physiol Renal Physiol 305(10):F1504-12 |
| abstractText | Quantitative real-time PCR was used to test whether cavernous nerve injury leads to a decrease in major pelvic ganglia (MPG) neuronal nicotinic ACh receptor (nAChR) subunit and postsynaptic density (PSD)-93 transcript levels. Subunits alpha3, beta4, and alpha7, commonly expressed in the MPG, were selected for analysis. After 72 h in explant culture, MPG transcript levels for alpha3, beta4, alpha7, and PSD-93 were significantly depressed. Three days after cavernous nerve axotomy or crush in vivo, transcript levels for alpha3, beta4, and PSD-93, but not for alpha7, were significantly depressed. Three days after dissection of the cavernous nerve free of underlying tissue and application of a 5-mm lateral stretch (manipulation), transcript levels for alpha3 and PSD-93 were also significantly decreased. Seven days after all three surgical procedures, alpha3 transcript levels remained depressed, but PSD-93 transcript levels were still decreased only after axotomy or nerve crush. At 30 days postsurgery, transcript levels for the nAChR subunits and PSD-93 had recovered. ACh-induced currents were significantly smaller in MPG neurons dissociated from 3-day explant cultured ganglia than from those recorded in neurons dissociated from acutely isolated ganglia; this observation provides direct evidence showing that a decrease in nAChR function was coincident with a decrease in nAChR subunit transcript levels. We conclude that a downregulation of nAChR subunit and PSD-93 expression after cavernous nerve injury, or even manipulation, could interrupt synaptic transmission within the MPG and thus contribute to the loss of neural control of urogenital organs after pelvic surgeries. |
