Urethral obstruction produces increased voiding frequency (0.7±0.06 to 1.1±0.08 h-') and hypertrophy of the urinary bladder (89±1.7 to 708±40 mg) with profound increments in the dimensions of afferent (4, 6) and efferent neurons (299±4.7 to 573±8.6 gm2) supplying this organ in the rat. We discovered that hypertrophied bladders of rat and human contain significantly more nerve growth factor (NGF) per milligram wet weight, protein, and DNA than normal bladders. The temporal correlation between NGF content, neuronal hypertrophy, and bladder weight was consistent with a role for this growth factor in the neurotrophic effects associated with obstruction. Autoimmunity to NGF abolished the hypertrophy of NGF-sensitive bladder neurons in the pelvic ganglion after obstruction. Relief of urethral obstruction reduced bladder size (349±78 mg), but neuronal hypertrophy (460.2±10.2 Mm2) and elevated NGF levels were only partially reversed. Bladder hypertrophy (133±43 mg) induced by osmotic diuresis slightly increased ganglion cell area (365.2±6.1 gm2) and only doubled NGF content of the bladder. These findings provide important new evidence that parenchymal cells in the hypertrophied bladder can synthesize NGF and possibly other molecular messengers that act to alter the size and function of neurons in adult animals and man. (J.
Retrograde axonal tracing methods using Fluoro-Gold were used to examine the neuronal input to the vas deferens in the adult Wistar rat. The greatest number of labelled efferent neurons were found in the ipsilateral pelvic accessory ganglion (PAG) (68%) and the major pelvic ganglion (MPG) (15%). Fewer than 3% of labelled neurons were localized to the inferior mesenteric and sympathetic chain ganglia. Labelled neurons were also located in the ipsilateral L1, L2, and L6, S1 dorsal root ganglia (DRG), corresponding to afferents that travel in the hypogastric and pelvic nerves, respectively. Contributions from contralateral neurons in the PAG, MPG and L1 DRG were also documented. The role of afferents supplying the vas deferens is not known but they may relay nociceptive or mechanoreceptive input. Efferent input from peripheral ganglia probably contributes to contractility of the vas deferens based on previous investigations.
Electrophysiological analysis of the neural control of the vas deferens was performed in urethan-anesthetized rats. Intraluminal distension (0.2 ml/min) or electrical stimulation of hypogastric (threshold 1-5 V, 20 Hz) and pelvic nerves (2-5 V, 20 Hz) produced contractions of the vas deferens. Distension-evoked contractile activity was not abolished by nicotinic ganglionic blockade or ipsilateral hypogastric and pelvic nerve transection. Contractions following hypogastric nerve stimulation were abolished by prazosin, while pelvic nerve-evoked responses were partially blocked by atropine. Hypogastric nerve, pelvic nerve, and sympathetic chain stimulation evoked volleys with latencies of 10-30 ms in vasal nerves. Crude estimates for conduction velocities for these responses (less than 0.5 m/s) corresponded to activation of unmyelinated C-fibers. Stimulation of the dorsal nerve of the penis (DNP) (10-16 V, 10-40 Hz) or administration of 5-methoxy-N,N-dimethyltryptamine, both of which produce seminal emission, elicited reflex discharges in nerves to the vas deferens. Hypogastric nerve but not pelvic nerve transection abolished both spontaneous and evoked (105- to 380-ms latency) reflex activity. These experiments provide insight into the organization of afferents in the DNP and efferents conveyed by autonomic pathways that regulate male reproduction.
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