scholarly journals GABA Receptor Activation in the Lumbosacral Spinal Cord Decreases Detrusor Overactivity in Spinal Cord Injured Rats

2008 ◽  
Vol 179 (3) ◽  
pp. 1178-1183 ◽  
Author(s):  
Minoru Miyazato ◽  
Kurumi Sasatomi ◽  
Shiro Hiragata ◽  
Kimio Sugaya ◽  
Michael B. Chancellor ◽  
...  
2008 ◽  
Vol 295 (1) ◽  
pp. R336-R342 ◽  
Author(s):  
Minoru Miyazato ◽  
Kurumi Sasatomi ◽  
Shiro Hiragata ◽  
Kimio Sugaya ◽  
Michael B. Chancellor ◽  
...  

We investigated the effects of intrathecal application of GABAA- or GABAB-receptor agonists on detrusor-sphincter dyssynergia (DSD) in spinal cord transection (SCT) rats. Adult female Sprague-Dawley rats were used. At 4 wk after Th9-10 SCT, simultaneous recordings of intravesical pressure and urethral pressure were performed under an awake condition to examine the effect of intrathecal application of GABAA and GABAB agonists (muscimol and baclofen, respectively) or GABAA and GABAB antagonists (bicuculline and saclofen, respectively) at the level of L6-S1 spinal cord. In spinal-intact rats, the effects of bicuculline and saclofen on bladder and urethral activity were also examined. During urethral pressure measurements, DSD characterized by urethral pressure increases during isovolumetric bladder contractions were observed in 95% of SCT rats. However, after intrathecal application of muscimol or baclofen, urethral pressure showed urethral relaxation during isovolumetric bladder contractions. The effective dose to induce inhibition of urethral activity was lower compared with the dose that inhibited bladder contractions. The effect of muscimol and baclofen was antagonized by intrathecal bicuculline and saclofen, respectively. In spinal-intact rats, intrathecal application of bicuculline induced DSD-like changes. These results indicate that GABAA- and GABAB-receptor activation in the spinal cord exerts the inhibitory effects on DSD after SCT. Decreased activation of GABAA receptors due to hypofunction of GABAergic mechanisms in the spinal cord might be responsible, at least in part, for the development of DSD after SCT.


2008 ◽  
Vol 214 (2) ◽  
pp. 301-308 ◽  
Author(s):  
Célia D. Cruz ◽  
Ana Charrua ◽  
Eva Vieira ◽  
João Valente ◽  
António Avelino ◽  
...  

2009 ◽  
Vol 104 (10) ◽  
pp. 1531-1537 ◽  
Author(s):  
Hitoshi Masuda ◽  
Nobutaka Ichiyanagi ◽  
Minato Yokoyama ◽  
Yasuyuki Sakai ◽  
Kazunori Kihara ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Shauh-Der Yeh ◽  
Bor-Shing Lin ◽  
Shih-Ching Chen ◽  
Chih-Hwa Chen ◽  
Kenneth J. Gustafson ◽  
...  

Background/Purpose. Few studies have investigated the effects of changing the amplitude of dorsal genital nerve stimulation (GNS) on the inhibition of neurogenic detrusor overactivity in individuals with spinal cord injury (SCI). The present study determined the acute effects of changes in GNS amplitude on bladder capacity gain in individuals with SCI and neurogenic detrusor overactivity. Methods. Cystometry was used to assess the effects of continuous GNS on bladder capacity during bladder filling. The cystometric trials were conducted in a randomized sequence of cystometric fills with continuous GNS at stimulation amplitudes ranging from 1 to 4 times of threshold (T) required to elicit the genitoanal reflex. Results. The bladder capacity increased minimally and maximally by approximately 34% and 77%, respectively, of the baseline bladder capacity at 1.5 T and 3.2 T, respectively. Stimulation amplitude and bladder capacity were significantly correlated (R = 0.55, P = 0.01). Conclusion. This study demonstrates a linear correlation between the stimulation amplitude ranging from 1 to 4T and bladder capacity gain in individuals with SCI in acute GNS experiments. However, GNS amplitude out of the range of 1-4T might not be exactly a linear relationship due to subthreshold or saturation factors. Thus, further research is needed to examine this issue. Nevertheless, these results may be critical in laying the groundwork for understanding the effectiveness of acute GNS in the treatment of neurogenic detrusor overactivity.


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