Bladder outlet obstruction causes up-regulation of nicotinic acetylcholine receptors in bladder-projecting pelvic ganglion neurons.

Pelvic ganglion (PG) neurons relay sympathetic and parasympathetic signals to the lower urinary tract, comprising the urinary bladder and bladder outlet, and are thus essential for both storage and voiding reflexes. Autonomic transmission is mediated by activation of the nicotinic acetylcholine receptor (nAChR) in PG neurons. Previously, bladder outlet obstruction (BOO), secondary to benign prostatic hyperplasia, was found to increase soma sizes of bladder-projecting PG neurons. To date, however, it remains unknown whether these morphological changes are accompanied by functional plasticity in PG neurons. In the present study, we investigated whether BOO alters acetylcholine receptor (nAChR) transcript expression and current density in bladder PG neurons. Partial ligation of the rat urethra for six weeks induced detrusor overactivity (DO), as observed during cystometrical measurement. In rats exhibiting DO, membrane capacitance of parasympathetic bladder PG neurons was selectively increased. Real-time PCR analysis revealed that BOO enhanced the expression of the transcripts encoding the nAChR α3 and ß4 subunits in PG neurons. Notably, BOO significantly increased ACh-evoked current density in parasympathetic bladder PG neurons, whereas no changes were observed in sympathetic bladder and parasympathetic penile PG neurons. In addition, other ligand-gated ionic currents were immune to BOO in bladder PG neurons. Taken together, these data suggest that BOO causes upregulation of nAChR in parasympathetic bladder PG neurons, which in turn may potentiate ganglionic transmission and contribute to the development of DO.

The nervus intermedius: a review of its anatomy, function, pathology, and role in neurosurgery.

BACKGROUND: Geniculate neuralgia, although uncommon, can be a debilitating pathology. Unfortunately, a thorough review of this pain syndrome and the clinical anatomy, function, and pathology of its most commonly associated nerve, the nervus intermedius, is lacking in the literature. Therefore, the present study aimed to further elucidate the diagnosis of this pain syndrome and its surgical treatment based on a review of the literature. METHODS: Using standard search engines, the literature was evaluated for germane reports regarding the nervus intermedius and associated pathology. A summary of this body of literature is presented. RESULTS: Since 1968, only approximately 50 peer-reviewed reports have been published regarding the nervus intermedius. Most of these are single-case reports and in reference to geniculate neuralgia. No report was a review of the literature. CONCLUSIONS: Neuralgia involving the nervus intermedius is uncommon, but when present, can be life altering. Microvascular decompression may be effective as a treatment. Along its cisternal course, the nerve may be difficult to distinguish from the facial nerve. Based on case reports and small series, long-term pain control can be seen after nerve sectioning or microvascular decompression, but no prospective studies exist. Such studies are now necessary to shed light on the efficacy of surgical treatment of nervus intermedius neuralgia.