Pudendal-to-bladder reflex in chronic spinal-cord-injured cats

Tai, Changfeng; Smerin, Stanley E.; Groat, William C. de; Roppolo, James R.

doi:10.1016/j.expneurol.2005.09.013

Cited by 70 publications

(129 citation statements)

References 29 publications

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“…Excitation of the bladder was evoked at stimulus strengths of 0.5-4 times the threshold of the pudendal-EUS reflex, whereas previous reports of inhibition in rat used stimuli (0.8 mA) that were sixteen times our measured threshold . Similarly, large amplitude stimulation of pudendal afferents produced bladder inhibition in both cat (Lindstrom et al 1983, Mazieres et al 1998, Tai et al 2006 and human (Vodusek et al 1986, Ohlsson et al 1989, although both frequency and stimulus train duration also play an important role in determining the response polarity in cat (Boggs et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

et al. 2008

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Urinary retention is the inability to empty the bladder completely, and may result from bladder hypocontractility, increases in outlet resistance, or both. Chronic urinary retention can lead to several urological complications and is often refractory to pharmacologic, behavioral, and surgical treatments. We sought to determine whether electrical stimulation of sensory fibers in the pudendal nerve could engage an augmenting reflex and thereby improve bladder emptying in an animal model of urinary retention. We measured the efficiency of bladder emptying with and without concomitant electrical stimulation of pudendal nerve afferents in urethane anesthetized rats. Voiding efficiency (VE=voided volume/initial volume) was reduced from 72±7% to 29±7% following unilateral transection of the sensory branch of the pudendal nerve (UST) and from 70±5% to 18±4% following bilateral transection (BST). Unilateral electrical stimulation of the proximal transected sensory pudendal nerve during distention-evoked voiding contractions significantly improved VE. Low intensity stimulation at frequencies of 1-50 Hz increased VE to 40-51% following UST and to 39-49% following BST, while high intensity stimulation was ineffective at increasing VE. The increase in VE was mediated by increases in the duration of distention-evoked voiding bladder contractions, rather than increases in contraction amplitude. These results are consistent with an essential role for pudendal sensory feedback in efficient bladder emptying, and raise the possibility that electrical activation of pudendal nerve afferents may provide a new approach to restore efficient bladder emptying in persons with urinary retention.

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Section: Discussionmentioning

confidence: 99%

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

et al. 2008

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“…This view of an inhibited spinal or supraspinal drive to the urinary bladder as being the main reason for inefficient distension evoked voiding is supported by the continuous stream of fluid observed during stimulation (Figure 6), which offered no evidence of dyssynergic EUS activity. As previously discussed ,Tai, et al, 2006, α-chloralose is the most appropriate anesthetic for demonstrating the physiological effects of electrical nerve stimulation in the lower urinary tract.…”

Section: Effects Of Anesthesia On Bladder Voidingmentioning

confidence: 99%

“…Conversely, activation of an excitatory pudendo-vesicle response has been studied as a means of restoring functional micturition (i.e., bladder emptying) in spinal intact and acute SCI , Gustafson, et al, 2003, Shefchyk and Buss, 1998, and chronic SCI cats (Tai, et al, 2006). Electrical stimulation of the pudendal nerve at 20 -50 Hz evoked robust sustained bladder contractions and voiding.…”

Section: Introductionmentioning

confidence: 99%

Bladder activation by selective stimulation of pudendal nerve afferents in the cat

Yoo

Woock

Grill

2008

Experimental Neurology

114

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Bladder contractions evoked by pudendal nerve stimulation in both spinal intact and spinal transected cats support the possibility of restoring urinary function in persons with chronic spinal cord injury (SCI). However, electrically evoked bladder responses in persons with SCI were limited to transient contractions at relatively low pressures. This prompted the present study, which presents a detailed quantification of the responses evoked by selective stimulation of individual branches of the pudendal nerve at different stimulation frequencies. In spinal intact cats anesthetized with α-chloralose, selective frequency dependent electrical activation of the sensory (2 Hz ≤ f ≤ 50 Hz), cranial sensory (f ≤ 5 Hz), dorsal genital (f ≥ 20 Hz) and rectal perineal (f ≤ 10 Hz) branches of the pudendal nerve evoked sustained bladder contractions dependent on the stimulation frequency. Contractions evoked by selective electrical stimulation resulted in significant increases in voiding efficiency compared to bladder emptying by distension evoked contractions (p ANOVA < 0.05). Acute spinal transection abolished reflex bladder contractions evoked by low frequency stimulation of the cranial sensory or rectal perineal branches, whereas contractions evoked by high frequency stimulation of the dorsal genital branch remained intact. This study presents evidence for two distinct micturition pathways (spino-bulbo-spinal vs. spinal reflexes) activated by selective afferent pudendal nerve stimulation, the latter of which may be applied to restore bladder function in persons with SCI. Keywords electrical stimulation; cranial sensory nerve; deep perineal branch; lower urinary tract physiology; external urethral sphincter; spinal cord injury; pudendo-pudendal reflex; spinal-bulbo-spinal; prostatic urethra; dorsal nerve of penis

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“…Low-frequency (ϳ10 Hz) pudendal afferent stimulation inhibits bladder contractions, thereby promoting continence in preclinical animal studies (4,46,52). Inhibition of bladder contractions and increased bladder capacities elicited by low-frequency pudendal afferent stimulation can also be achieved after chronic spinal cord injury (43,47).…”

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confidence: 99%

A spinal GABAergic mechanism is necessary for bladder inhibition by pudendal afferent stimulation

McGee

Danziger

Bamford

et al. 2014

American Journal of Physiology-Renal Physiology

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McGee MJ, Danziger ZC, Bamford JA, Grill WM. A spinal GABAergic mechanism is necessary for bladder inhibition by pudendal afferent stimulation. Am J Physiol Renal Physiol 307: F921-F930, 2014. First published August 20, 2014 doi:10.1152/ajprenal.00330.2014.-Electrical stimulation of pudendal afferents can inhibit bladder contractions and increase bladder capacity. Recent results suggest that stimulation-evoked bladder inhibition is mediated by a mechanism other than activation of sympathetic bladder efferents in the hypogastric nerve, generating ␣-adrenergic receptor-mediated inhibition at the vesical ganglia and/or ␤-adrenergic receptor-mediated direct inhibition of the detrusor muscle. We investigated several inhibitory neurotransmitters that may instead be necessary for stimulation-evoked inhibition and found that intravenous picrotoxin, a noncompetitive GABAA antagonist, significantly and reversibly blocked pudendal afferent stimulation-evoked inhibition of bladder contractions in a dose-dependent manner. Similarly, intravenous picrotoxin also blocked pudendal afferent stimulation-evoked inhibition of nociceptive bladder contractions evoked by acetic acid infusion. Furthermore, intrathecal administration of picrotoxin at the lumbosacral spinal cord also blocked bladder inhibition by pudendal afferent stimulation. On the other hand, glycinergic, adrenergic, or opioidergic mechanisms were not necessary for bladder inhibition evoked by pudendal afferent stimulation. These results identify a lumbosacral spinal GABAergic mechanism of bladder inhibition evoked by pudendal afferent stimulation. electrical stimulation; bladder inhibition; pudendal nerve; dorsal nerve of the penis; GABA; picrotoxin IMPROVED BLADDER CONTROL IS an unmet need in persons with urinary incontinence (1) and in persons with neurological disease or injury, such as spinal cord injury (9). Electrical stimulation is a promising approach to treat overactive bladder (OAB), which can produce urgency and incontinence and impair quality of life (8, 32). In particular, pudendal afferent stimulation inhibits distension-evoked bladder contractions and improves continence (51). We sought to identify the mechanism(s) of bladder inhibition by pudendal afferent stimulation.Pudendal nerve (PN) stimulation may be an alternative to sacral nerve stimulation to improve continence (33), and in patients who do not respond to sacral neuromodulation it may be a successful treatment option (29,34,41). Low-frequency (ϳ10 Hz) pudendal afferent stimulation inhibits bladder contractions, thereby promoting continence in preclinical animal studies (4, 46, 52). Inhibition of bladder contractions and increased bladder capacities elicited by low-frequency pudendal afferent stimulation can also be achieved after chronic spinal cord injury (43, 47). However, the mechanisms of action of PN stimulation-mediated bladder inhibition are unclear, and such knowledge may improve patient selection and enable improvements in therapy.Initial studies suggested that pudendal afferent stimu...

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Pudendal-to-bladder reflex in chronic spinal-cord-injured cats

Cited by 70 publications

References 29 publications

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Bladder activation by selective stimulation of pudendal nerve afferents in the cat

A spinal GABAergic mechanism is necessary for bladder inhibition by pudendal afferent stimulation

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