Cavernous nerve injury elicits GAP-43 mRNA expression but not regeneration of injured pelvic ganglion neurons.
Recovery of erectile dysfunction after cavernous nerve injury takes a long period. To elucidate this mechanism, unilateral cavernous nerve of male rat was cut, and the expression level of a nerve regeneration marker, the growth associated protein-43 (GAP-43) mRNA was evaluated by in situ hybridization and RT-PCR. While GAP-43 mRNA expression was transiently increased in the injured neurons of the major pelvic ganglion (MPG) at 7 days after nerve injury, continuous increase of GAP-43 mRNA was observed in the contralateral MPG from 7 days to 6 months after the nerve injury. Histochemical double-labeling studies for either neuronal NOS (nNOS) or tyrosine hydroxylase (TH) and the GAP-43 mRNA expression demonstrated that in injured MPG the transient up-regulation of GAP-43 mRNA was mainly seen in nNOS negative and/or TH positive neurons, suggesting non-parasympathetic post-ganglionic neurons, and also demonstrated that in contralateral MPG GAP-43 mRNA positive neurons were gradually increased in nNOS positive but TH negative neurons, suggesting parasympathetic post-ganglionic neurons. When a retrograde tracer Fluorogold (FG) was injected into the penile crus 7 days before histological experiments, FG-positive neurons were, if any, hardly seen in nNOS-positive neurons of the injured MPG for at least 6 months, whereas numerous FG-positive cells were seen in nNOS-positive neurons of the contralateral MPG. These results suggest that post-ganglionic projecting neurons of the intact side, which express increased GAP-43 mRNA, would be most likely to contribute to the recovery of the erectile function after unilateral cavernous nerve injury possibly by a plastic change such as nerve sprouting.
Kato
Ryuichi
R
Department of Anatomy and Neurobiology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan.
Kiryu-Seo
Sumiko
S
Sato
Yoshikazu
Y
Hisasue
Shinichi
S
Tsukamoto
Taiji
T
Kiyama
Hiroshi
H
D000818:Animals; D015415:Biomarkers; D007172:Erectile Dysfunction / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D005456:Fluorescent Dyes; D007839:Functional Laterality / Q000502:physiology; D019922:GAP-43 Protein / Q000235:genetics*; D005725:Ganglia, Autonomic / Q000166:cytology / Q000378:metabolism*; D007001:Hypogastric Plexus / Q000293:injuries* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D010413:Penis / Q000294:innervation*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology; D013266:Stilbamidines; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D015415:Biomarkers; D005456:Fluorescent Dyes; D019922:GAP-43 Protein; D012333:RNA, Messenger; D013266:Stilbamidines; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D014446:Tyrosine 3-Monooxygenase; D009638:Norepinephrine