ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2013
Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Trial
- Review
- Article
- Tibial nerve stimulation for overactive bladder: a literature review of stimulation parameters.Translational andrology and urology · 2026Review
- Efficacy and sex-specific outcomes after six episodes of percutaneous tibial nerve stimulation treatment on overactive bladder syndrome symptoms.Frontiers in urology · 2024Article
- Real-time changes in brain activity during tibial nerve stimulation for overactive bladder: Evidence from functional near-infrared spectroscopy hype scanning.Frontiers in neuroscience · 2023Article
- Recruitment of unmyelinated C-fibers mediates the bladder-inhibitory effects of tibial nerve stimulation in a continuous-fill anesthetized rat model.American journal of physiology. Renal physiology · 2019Article
- Glutamatergic Mechanisms Involved in Bladder Overactivity and Pudendal Neuromodulation in Cats.The Journal of pharmacology and experimental therapeutics · 2017Article
- Sex difference in the contribution of GABAAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Neurotransmitter Mechanisms Underlying Sacral Neuromodulation of Bladder Overactivity in Cats.Neuromodulation : journal of the International Neuromodulation Society · 2017Article
- Role of µ, κ, and δ opioid receptors in tibial inhibition of bladder overactivity in cats.The Journal of pharmacology and experimental therapeutics · 2015Article
- Role of the brain stem in tibial inhibition of the micturition reflex in cats.American journal of physiology. Renal physiology · 2015Article
- Neurophysiological modeling of bladder afferent activity in the rat overactive bladder model.The journal of physiological sciences : JPS · 2015Article
- Impact of Bioelectronic Medicine on the Neural Regulation of Pelvic Visceral Function.Bioelectronic medicine · 2015Article
- Does our limited knowledge of the mechanisms of neural stimulation limit its benefits for patients with overactive bladder? ICI-RS 2013.Neurourology and urodynamics · 2014Review
- The mouse cyclophosphamide model of bladder pain syndrome: tissue characterization, immune profiling, and relationship to metabotropic glutamate receptors.Physiological reports · 2014Article
- Poststimulation inhibition of the micturition reflex induced by tibial nerve stimulation in rats.Physiological reports · 2014Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
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 α-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 < 0.0001) reduced bladder capacity to 26.6 ± 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 ± 8.3% at 2T (P < 0.01) and 80.8 ± 9.2% at 4T (P = 0.0001) of saline control capacity. LY341495 (0.1-5 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.