Hrabovszky Z, Hutson J M
F. Douglas Stephens Surgical Research Laboratory, Royal Children's Hospital Research Institute, Melbourne, Australia.
J Pediatr Surg. 1999 Dec;34(12):1769-72. doi: 10.1016/s0022-3468(99)90309-3.
BACKGROUND/PURPOSE: Calcitonin gene-related peptide (CGRP) may stimulate gubernacular migration during testicular descent by release from the genitofemoral nerve (GFN). The origin of CGRP within the nerve, however, is controversial. This study examines whether sensory nerve destruction alters gubernacular contractility in vitro in Sprague-Dawley (SD) and congenitally cryptochid (TS) rats.
Part 1: Twenty-four SD and 16 TS rats (day 0) had either both GFNs transected or sham operation. Gubernacula were removed on day 2 and cultured with or without CGRP (714 nmol/L). Contractility was recorded by video. Part 2: Twenty-two SD and 17 TS rats (day 0) were injected with either capsaicin or vehicle. Gubernacula were removed (day 2) and cultured as above.
Part 1: In sham-operated SD rats gubernacular contracility increased from 8% to 83% with added CGRP. After GFN transection contractility was not affected by CGRP (21% without and 86% with CGRP; not significant). TS rat gubernacula had no endogenous contractions, but after GFN transection, the contractile response to CGRP increased from 6% to 44% (P = .04). Part 2: In vehicle-treated SD rats, rhythmic contractions increased from 10% to 86% with CGRP, which was unchanged by capsaicin treatment (82%; not significant). In vehicle-treated TS rats, gubernacular contractions were 6% after CGRP. After capsaicin pretreatment, contractions increased to 59% with CGRP (P = .002).
Results of this study show that chemical destruction of sensory nerves restores gubernacular contractility in mutant cryptorchid TS rats. Release of CGRP appears to occur through sensory nerves.