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1.  Effects of acute adult and early-in-life bladder inflammation on bladder neuropeptides in adult female rats 
BMC Urology  2011;11:18.
Background
The purpose of the present study was to determine how acute adult and/or prior early-in life (EIL; P14-P16) exposure to bladder inflammation affects bladder content of calcitonin gene related peptide (CGRP) and substance P (SP). Estrous cycle influences were also studied in the adult-treatment conditions.
Methods
In Experiment 1, intravesical zymosan or isoflurane anesthesia alone was administered to adult female rats. Bladders and serum were collected 24 hours later during each phase of the estrous cycle. In Experiment 2, zymosan or anesthesia alone was administered EIL and as adults, with bladder tissue collection 24 h later.
Results
In general, Experiment 1 showed that bladder content of both CGRP and SP was increased by inflammation. This effect was significant when data were collapsed across all phases of the estrous cycle, but was only significant during proestrus when individual comparisons were made during each phase of estrous. Also, adult bladder inflammation significantly reduced estradiol levels. In Experiment 2, bladder content of CGRP and SP was significantly increased in rats receiving EIL and/or adult inflammation. Bladder weights were also significantly increased by inflammation.
Conclusions
These data indicate that bladder CGRP and SP are maximally increased during the proestrus phase of the estrous cycle in inflamed adult female rats. EIL exposure to bladder inflammation alone can also produce an increase in CGRP and SP lasting into adulthood. Therefore, EIL experience with bladder inflammation may predispose an organism to experience a painful bladder disorder as an adult by increasing primary afferent content of CGRP and/or SP.
doi:10.1186/1471-2490-11-18
PMCID: PMC3171712  PMID: 21843346
2.  Effect of Estrogen on Bladder Nociception in Rats 
The Journal of urology  2010;183(3):1201-1205.
Purpose
We assessed the effect of ovariectomy and estrogen replacement on nociceptive responses to bladder distention in a rat model.
Materials and Methods
Female Sprague-Dawley rats (Harlan™) underwent ovariectomy or sham surgery. Visceromotor responses (abdominal contractions) to bladder distention were determined 3 to 4 weeks later under isoflurane anesthesia. In rat subsets estrogen was chronically replaced with a subcutaneous estrogen pellet vs a placebo pellet or acutely replaced by subcutaneous injection 24 hours before testing. Effects of estrogen withdrawal were examined in another group of rats by implanting a pellet and explanting the pellet 24 hours before testing. Uterine weight was measured to assess the estrogen dose.
Results
Visceromotor responses to bladder distention were significantly less vigorous in ovariectomized rats vs controls. Acute estrogen replacement increased visceromotor responses in these rats but chronic estrogen replacement did not. Sudden chronic estrogen withdrawal resulted in increased visceromotor responses. Uterine weight was consistent with the physiological estrogen dose.
Conclusions
Estrogen alone was not sufficient to produce increased nociceptive responses but an acute decrease in estrogen resulted in increased visceromotor responses. These data suggest that the pronociceptive effects of estrogen may be due to a mismatch between peripheral vs central and/or genomic vs nongenomic effects of the hormone, which occur during rapidly decreasing estrogen levels.
doi:10.1016/j.juro.2009.11.003
PMCID: PMC3094858  PMID: 20096872
estrogens; ovary; pain; ovariectomy; rats; Sprague-Dawley
3.  Serotonergic and Noradrenergic Facilitation of the Visceromotor Reflex Evoked by Urinary Bladder Distension in Rats with Inflamed Bladders 
Neuroscience letters  2008;442(3):253-256.
Bladder inflammation resulting from intravesical administration of zymosan significantly enhances the visceromotor reflex (VMR) evoked by urinary bladder distension (UBD). The present study examined whether intrathecal (i.t.) administration of receptor antagonists to either noreprinephrine (NE) or serotonin (5-HT) altered this enhancement effect. I.t. administration of the non-specific 5-HT receptor antagonist methysergide (30 μg), the 5-HT3 receptor antagonist ondansetron, or the 5-HT1A receptor antagonist WAY 100635 eliminated the enhancement effect produced by intravesical zymosan and also tended to reduce EMG responses to UBD in non-inflamed rats. I.t. administration of either the non-specific NE receptor antagonist phentolamine (30 μg) or the α1 antagonist WB4101 also eliminated the enhancement effect, whereas i.t. administration of the α2 antagonist yohimbine failed to significantly affect the enhancement effect. The effects of phentolamine and methysergide were not mediated by changes in bladder compliance. This is the first study to demonstrate that bladder hypersensitivity resulting from bladder inflammation is partly mediated by 5-HT and NE facilitatory effects. Based on these and previous findings we conclude that the net nociceptive response to bladder distension under conditions of bladder inflammation represents a complex interaction of facilitatory influences of spinal 5-HT and NE, and inhibitory influences of spinal opioids.
doi:10.1016/j.neulet.2008.07.031
PMCID: PMC2553514  PMID: 18647638
bladder; serotonin; norepinephrine; visceromotor reflex; pain; facilitation

Results 1-3 (3)