{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:14:00Z","timestamp":1790036040742,"version":"4.0.1"},"reference-count":49,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2013,7,15]]},"abstract":"<jats:p>The contribution of metabotropic glutamate receptors (mGluR) and opioid receptors to inhibition of bladder overactivity by tibial nerve stimulation (TNS) was investigated in cats under \u03b1-chloralose anesthesia using LY341495 (a group II mGluR antagonist) and naloxone (an opioid receptor antagonist). Slow infusion cystometry was used to measure the volume threshold (i.e., bladder capacity) for inducing a large bladder contraction. After measuring the bladder capacity during saline infusion, 0.25% acetic acid (AA) was infused to irritate the bladder, activate the nociceptive C-fiber bladder afferents, and induce bladder overactivity. AA significantly ( P &lt; 0.0001) reduced bladder capacity to 26.6 \u00b1 4.7% of saline control capacity. TNS (5 Hz, 0.2 ms) at 2 and 4 times the threshold (T) intensity for inducing an observable toe movement significantly increased bladder capacity to 62.2 \u00b1 8.3% at 2T ( P &lt; 0.01) and 80.8 \u00b1 9.2% at 4T ( P = 0.0001) of saline control capacity. LY341495 (0.1\u20135 mg\/kg iv) did not change bladder overactivity, but completely suppressed the inhibition induced by TNS at a low stimulus intensity (2T) and partially suppressed the inhibition at high intensity (4T). Following administration of LY341495, naloxone (0.01 mg\/kg iv) completely eliminated the high-intensity TNS-induced inhibition. However, without LY341495 treatment a 10 times higher dose (0.1 mg\/kg) of naloxone was required to completely block TNS inhibition. These results indicate that interactions between group II mGluR and opioid receptor mechanisms contribute to TNS inhibition of AA-induced bladder overactivity. Understanding neurotransmitter mechanisms underlying TNS inhibition of bladder overactivity is important for the development of new treatments for bladder disorders.<\/jats:p>","DOI":"10.1152\/ajpregu.00572.2012","type":"journal-article","created":{"date-parts":[[2013,4,11]],"date-time":"2013-04-11T03:00:31Z","timestamp":1365649231000},"page":"R126-R133","source":"Crossref","is-referenced-by-count":23,"title":["Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation"],"prefix":"10.1152","volume":"305","author":[{"given":"Yosuke","family":"Matsuta","sequence":"first","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, Pennsylvania;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abhijith D.","family":"Mally","sequence":"additional","affiliation":[{"name":"Department of Urology, University of Pittsburgh, Pittsburgh, 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