Suppression of bladder overactivity by activation of somatic afferent nerves in the foot

Tai, Changfeng; Shen, Bing; Chen, Mang; Wang, Jicheng; Liu, Hailong; Roppolo, James R.; Groat, William C. de

doi:10.1111/j.1464-410x.2010.09358.x

Cited by 30 publications

(41 citation statements)

References 21 publications

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“…Information about TNS inhibition of reflex bladder activity may also provide insights into the mechanisms of action of other types of neuromodulation such as foot stimulation because the latter and TNS exhibit similar properties, including naloxone sensitivity (15,24,25) and prolonged poststimulation inhibition (4,27). Inhibition by TNS or foot stimulation also has similar frequency characteristics during AA CMGs, producing an increase in bladder capacity over a wide range of frequencies (5-30 Hz) (23,26). On the other hand, inhibitory modulation of reflex bladder activity elicited by pudendal nerve stimulation (PNS) in the cat is markedly different than TNS and foot neuromodulation.…”

Section: Discussionmentioning

confidence: 99%

Role of the brain stem in tibial inhibition of the micturition reflex in cats

Ferroni

Slater

Shen

et al. 2015

American Journal of Physiology-Renal Physiology

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This study examined the role of the brain stem in inhibition of bladder reflexes induced by tibial nerve stimulation (TNS) in ␣-chloralose-anesthetized decerebrate cats. Repeated cystometrograms (CMGs) were performed by infusing saline or 0.25% acetic acid (AA) to elicit normal or overactive bladder reflexes, respectively. TNS (5 or 30 Hz) at three times the threshold (3T) intensity for inducing toe movement was applied for 30 min between CMGs to induce post-TNS inhibition or applied during the CMGs to induce acute TNS inhibition. Inhibition was evident as an increase in bladder capacity without a change in amplitude of bladder contractions. TNS applied for 30 min between saline CMGs elicited prolonged (Ͼ2 h) poststimulation inhibition that significantly (P Ͻ 0.05) increased bladder capacity to 30 -60% above control; however, TNS did not produce this effect during AA irritation. TNS applied during CMGs at 5 Hz but not 30 Hz significantly (P Ͻ 0.01) increased bladder capacity to 127.3 Ϯ 6.1% of saline control or 187.6 Ϯ 5.0% of AA control. During AA irritation, naloxone (an opioid receptor antagonist) administered intravenously (1 mg/kg) or directly to the surface of the rostral brain stem (300 -900 g) eliminated acute TNS inhibition and significantly (P Ͻ 0.05) reduced bladder capacity to 62.8 Ϯ 22.6% (intravenously) or 47.6 Ϯ 25.5% (brain stem application). Results of this and previous studies indicate 1) forebrain circuitry rostral to the pons is not essential for TNS inhibition; and 2) opioid receptors in the brain stem have a critical role in TNS inhibition of overactive bladder reflexes but are not involved in inhibition of normal bladder reflexes. neuromodulation; brain stem; opioid; tibial; cat TIBIAL NEUROMODULATION, a Food and Drug Administration (FDA)-approved therapy for overactive bladder (OAB) symptoms, including urgency, frequency, and incontinence (7,19,20,29), is often used to treat patients whose symptoms are not completely controlled by drugs or who have unacceptable drug side effects (1,2,8,18). However, the mechanisms underlying tibial neuromodulation therapy are uncertain. Understanding the site of action and neurotransmitters involved in the inhibition of bladder reflexes by tibial nerve stimulation (TNS) is important for developing new OAB treatments by combining drug therapies with tibial neuromodulation to achieve a higher efficacy with fewer side effects (14,33).Previous studies in cats have demonstrated the inhibitory effect of TNS on bladder reflexes elicited during non-nociceptive saline distention as well as nociceptive acetic acid (AA) irritation (23,27). The failure of TNS to inhibit reflex bladder contractions during AA irritation in animals with acute spinal cord transection at the T9/T10 level (32) indicates that supraspinal neural circuits are necessary for TNS inhibition. However, it is unknown whether these supraspinal circuits are located in the forebrain or in the brain stem.A major clinical benefit of TNS is the long-lasting poststimulation inhibitory effect, which allows...

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Section: Discussionmentioning

confidence: 99%

Role of the brain stem in tibial inhibition of the micturition reflex in cats

Ferroni

Slater

Shen

et al. 2015

American Journal of Physiology-Renal Physiology

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“…Also, electrical stimulation of the foot or posterior tibial nerve can increase bladder capacity and decrease bladder overactivity in both humans and animals. [81][82][83][84][85] Somatosensory feedback during stepping may be similar to foot electrostimulation leading to the measured increase in ICIs. It will be important for subsequent studies to directly explore the impact of training on sphincter and detrusor activity.…”

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confidence: 85%

Novel Multi-System Functional Gains via Task Specific Training in Spinal Cord Injured Male Rats

Ward

Herrity

Smith

et al. 2014

Journal of Neurotrauma

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Locomotor training (LT) after spinal cord injury (SCI) is a rehabilitative therapy used to enhance locomotor recovery. There is evidence, primarily anecdotal, also associating LT with improvements in bladder function and reduction in some types of SCI-related pain. In the present study, we determined if a step training paradigm could improve outcome measures of locomotion, bladder function, and pain/allodynia. After a T10 contusive SCI trained animals (adult male Wistar rats), trained animals began quadrupedal step training beginning 2 weeks post-SCI for 1 h/day. End of study experiments (3 months of training) revealed significant changes in limb kinematics, gait, and hindlimb flexor-extensor bursting patterns relative to non-trained controls. Importantly, micturition function, evaluated with terminal transvesical cystometry, was significantly improved in the step trained group (increased voiding efficiency, intercontraction interval, and contraction amplitude). Because both SCI and LT affect neurotrophin signaling, and neurotrophins are involved with post-SCI plasticity in micturition pathways, we measured bladder neurotrophin mRNA. Training regulated the expression of nerve growth factor (NGF) but not BDNF or NT3. Bladder NGF mRNA levels were inversely related to bladder function in the trained group. Monitoring of overground locomotion and neuropathic pain throughout the study revealed significant improvements, beginning after 3 weeks of training, which in both cases remained consistent for the study duration. These novel findings, improving non-locomotor in addition to locomotor functions, demonstrate that step training post-SCI could contribute to multiple quality of life gains, targeting patient-centered high priority deficits.

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“…Fur was removed from the right hindfoot, and two self-adhesive pad electrodes (diameter: 1 cm, Grass FE10ND, Astro-Medical, Mentor, OH) were attached to the skin at the bottom of the foot. One electrode was at the front of the foot, and the other was at the heel (6,33).…”

Section: Methodsmentioning

confidence: 99%

“…The stimulation intensity threshold was defined as the minimal intensity to induce a toe twitch. Foot stimulation of two and four times the stimulation intensity threshold (2T and 4T, respectively) was used in this study since our previous studies (6,18,33) demonstrated that this intensity range was effective in inhibiting reflex bladder contractions.…”

Section: Methodsmentioning

confidence: 99%

“…Our previous studies in cats have revealed a novel, noninvasive method to suppress bladder overactivity by stimulating somatic afferent nerves in the foot with skin surface electrodes. Although foot stimulation alone does not completely suppress bladder overactivity (6,33), we have recently identified another treatment strategy that combines foot stimulation with low doses of drugs such as tolterodine or tramadol to enhance OAB treatment efficacy while lowering the potential for unwanted side effects (18,27). The additive effect of neuromodulation and drug therapy has also been demonstrated clinically in patients who had incomplete responses to neuromodulation therapy alone (13).…”

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confidence: 99%

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Inhibition of bladder overactivity by duloxetine in combination with foot stimulation or WAY-100635 treatment in cats

Schwen

Matsuta

Shen

et al. 2013

American Journal of Physiology-Renal Physiology

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The purpose of this study was to determine whether duloxetine [a serotonin (5-HT)-norepinephrine reuptake inhibitor] combined with transcutaneous foot stimulation or WAY-100635 (a 5-HT1A antagonist) can enhance inhibition of bladder overactivity in cats. Cystometrograms were performed on eight cats under α-chloralose anesthesia by infusing saline and then 0.25% acetic acid (AA) to induce bladder overactivity. To inhibit bladder overactivity, foot stimulation (5 Hz) was applied via transcutaneous pad electrodes to the right hindfoot at two and four times the threshold intensity for inducing a toe twitch. Duloxetine (0.003-3 mg/kg) was administered intravenously to determine the effect of combination treatment. After the 3 mg/kg dose of duloxetine, WAY-100635 (0.5 mg/kg) was given intravenously. AA irritation significantly (P < 0.0001) reduced bladder capacity to 42.7 ± 7.4% of the saline control capacity. Foot stimulation alone at both two and four times the threshold intensity significantly (P < 0.0001) inhibited bladder overactivity and increased bladder capacity to 66.7 ± 6.3% and 85.7 ± 6.5% of the saline control, respectively. Duloxetine alone dose dependently inhibited bladder overactivity and completely restored bladder capacity to the saline control (109 ± 15.5%) at 3 mg/kg. Although duloxetine combined with foot stimulation did not further enhance inhibition, WAY-100635 (0.5 mg/kg) given after 3 mg/kg duloxetine further increased (P = 0.008) bladder capacity to 162.2 ± 22.5% of the saline control. Although duloxetine and foot stimulation independently inhibited bladder overactivity, combined treatment did not enhance inhibition. Duloxetine combined with WAY-100635, however, synergistically enhanced bladder inhibition, indicating a potential novel treatment for overactive bladder if duloxetine is combined with a 5-HT1A receptor antagonist drug.

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Suppression of bladder overactivity by activation of somatic afferent nerves in the foot

Cited by 30 publications

References 21 publications

Role of the brain stem in tibial inhibition of the micturition reflex in cats

Role of the brain stem in tibial inhibition of the micturition reflex in cats

Novel Multi-System Functional Gains via Task Specific Training in Spinal Cord Injured Male Rats

Inhibition of bladder overactivity by duloxetine in combination with foot stimulation or WAY-100635 treatment in cats

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