title: Does the sensory nucleus of the genitofemoral nerve have a role in testicular descent?
abstract: OBJECTIVE
  A role for the genitofemoral nerve (GFN) and its neurotransmitter, CGRP, in testicular descent has been well established. The exact mechanism, however, by which circulating androgens act on the GFN is not yet known. The authors studied the sensory nucleus of the GFN (L1-L2 dorsal root ganglia [DRG]) to determine whether it is sexually dimorphic and able to be influenced by intrauterine antiandrogen treatment.
  
  
  METHODS
  Sprague-Dawley rats were injected daily with 100 mg/kg/d of the antiandrogen flutamide on day 16 to 19 of pregnancy. Control animals were treated with vehicle only. At the age of 2 to 3 days the newborn rats underwent unilateral dissection of the GFN. The proximal end was labelled with fluorescent dye, diamidinophenyl indole. The rats were killed 48 hours later, and the relevant ganglia (L1,L2) were removed. Cryostat frozen serial sections were cut, and retrogradely labelled fluorescent cells were counted under an epifluorescence microscope. In 32 animals, the cells were double fluorescent labelled with antibody to CGRP and FITC.
  
  
  RESULTS
  Of 75 rats evaluated, the mean number of the DAPI-positive, retrogradely labelled cells in the control groups was 266 +/- 55 in the male, and 230 +/- 67 in the female as opposed to 186 +/- 45 and 161 +/- 35 in the flutamide-treated male and female groups, respectively. In 32 animals the DRG sections were double labelled for CGRP. The number of CGRP plus DAPI-positive cells were as follows: control males, 60 +/-12; control females, 50 +/- 9; flutamide males, 36 +/- 8; flutamide females, 40 +/- 10.
  
  
  CONCLUSIONS
  These findings show a sexual dimorphism in the number of GFN cell bodies in the DRG. Flutamide decreases the number of GFN cell bodies in the DRG of both males and females. Our results are consistent with a role for circulating androgens acting on the sensory nucleus of the GFN (DRG) instead of the motor nucleus as previously thought. The release of CGRP from the nerve endings may occur via the sensory branch of the GFN.
authors.affiliation: F. Douglas Stephens Surgical Research Laboratory, Royal Children's Hospital Research Institute, Melbourne, Australia.
authors.forename: Z
authors.initials: Z
authors.lastname: Hrabovszky
authors.forename: P J
authors.initials: PJ
authors.lastname: Farmer
authors.forename: J M
authors.initials: JM
authors.lastname: Hutson
mesh_terms: D000726:Androgen Antagonists / Q000494:pharmacology; D000728:Androgens / Q000502:physiology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism / Q000502:physiology; D003456:Cryptorchidism / Q000503:physiopathology; D005260:Female; D005267:Femoral Nerve / Q000502:physiology*; D005455:Fluorescent Antibody Technique; D005485:Flutamide / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000378:metabolism; D005837:Genitalia, Male / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012727:Sex Characteristics; D013737:Testis / Q000294:innervation / Q000502:physiology*
chemical_list: D000726:Androgen Antagonists; D000728:Androgens; D005485:Flutamide; D015740:Calcitonin Gene-Related Peptide