scholarly journals Suppression of detrusor-sphincter dysynergia by GABA-receptor activation in the lumbosacral spinal cord in spinal cord-injured rats

2008 ◽  
Vol 295 (1) ◽  
pp. R336-R342 ◽  
Author(s):  
Minoru Miyazato ◽  
Kurumi Sasatomi ◽  
Shiro Hiragata ◽  
Kimio Sugaya ◽  
Michael B. Chancellor ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Receptor Activation ◽  
Urethral Pressure ◽  
Sprague Dawley ◽  
Lumbosacral Spinal Cord ◽  
Detrusor Sphincter Dyssynergia ◽  
Sprague Dawley Rats ◽  
Spinal Cord Injured ◽  
Awake Condition ◽  
Intact Rats

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.

scholarly journals α1D-Adrenoceptor blockade increases voiding efficiency by improving external urethral sphincter activity in rats with spinal cord injury

2016 ◽  
Vol 311 (5) ◽  
pp. R971-R978 ◽  
Author(s):  
Hirokazu Ishida ◽  
Hiroki Yamauchi ◽  
Hideaki Ito ◽  
Hironobu Akino ◽  
Osamu Yokoyama
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lower Urinary Tract Dysfunction ◽  
Urethral Sphincter ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Detrusor Sphincter Dyssynergia ◽  
Sphincter Electromyography ◽  
Sprague Dawley Rats ◽  
Cord Injury

Ideal therapy for lower urinary tract dysfunction in patients with spinal cord injury (SCI) should decrease detrusor overactivity, thereby promoting urine storage at low intravesical pressure and promoting efficient voiding at low pressure by decreasing detrusor-sphincter dyssynergia. Here we investigated blockade of various α-adrenoceptors to determine the subtype that was principally responsible for improving the voiding dysfunction. The effects of the intravenous α-blocker naftopidil, the α-blocker BMY 7378, and the α-blocker silodosin were evaluated using cystometrography and external urethral sphincter-electromyography (EMG) in decerebrated, unanesthetized female Sprague-Dawley rats with chronic SCI following transection at Th8. Parameters measured included the voided volume, residual volume, voiding efficiency, and burst and silent periods on EMG. Compared with values in decerebrated non-SCI rats, EMG of decerebrated SCI rats revealed more prominent tonic activity, significantly shorter periods of bursting activity, and a reduced ratio of the silent to active period during bursting. Compared with the value before drug administration (control), the voiding efficiency was significantly increased by naftopidil (1 and 3 mg/kg) (<0.05 each), and the burst (<0.01 and <0.05, respectively) and silent periods (<0.01 each) on EMG were significantly lengthened. BMY 7378 (1 mg/kg) significantly increased voiding efficiency and lengthened the burst periods (<0.05 each). Silodosin did not affect any parameters. These results suggest that α-blockade reduces the urethral resistance associated with detrusor-sphincter dyssynergia, thus improving voiding efficiency in SCI rats.

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 ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Detrusor Overactivity ◽  
Gaba Receptor ◽  
Receptor Activation ◽  
Lumbosacral Spinal Cord ◽  
Spinal Cord Injured

Visualizing lower urinary tract afferent projections in the lumbosacral spinal cord in rats v1

2021 ◽  
Author(s):  
John-Paul Fuller-Jackson ◽  
Peregrine B Osborne ◽  
Janet R Keast
Keyword(s):  
Spinal Cord ◽  
Urinary Tract ◽  
3D Reconstruction ◽  
Lower Urinary Tract ◽  
Sprague Dawley ◽  
Lumbosacral Spinal Cord ◽  
Afferent Projections ◽  
Sprague Dawley Rats ◽  
Stage 1 ◽  
Lower Urinary

This collection includes the protocols required to map the lower urinary tract afferent projections to the lumbosacral spinal cord of male and female Sprague-Dawley rats. Afferents can be visualized using 3D reconstruction of alternating sections in TissueMaker (MBF Bioscience), or through the immunolabelling and clearing method, iDISCO. The following protocols are performed, regardless of endpoint: STAGE 1: Use of cholera toxin subunit B to label neural projections to lower urinary tract organs. STAGE 2: Intracardiac perfusion with fixative for anatomical studies. The next set of protocols pertain to the 3D reconstruction of spinal cord from alternating sections. STAGE 3: Immunohistochemical labelling of lower urinary tract afferents in spinal cord. STAGE 4: Quantitation of lower urinary tract afferents in 3D reconstruction of lumbosacral spinal cord sections For the visualization of lower urinary tract afferents in the intact spinal cord, skip Stages 3 and 4, and instead use Stage 5: STAGE 5: Immunolabelling and clearing of intact spinal cord for visualization of lower urinary tract afferents

Epididymal Sperm Transport in Normal and Recent Spinal Cord Injured Sprague Dawley Rats

1999 ◽  
Vol 22 (2) ◽  
pp. 102-106 ◽  
Author(s):  
T.A. Linsenmeyer ◽  
J.E. Ottenweller ◽  
J.S. D’lmperio ◽  
L.M. Pogach ◽  
H.F.S. Huang
Keyword(s):  
Spinal Cord ◽  
Epididymal Sperm ◽  
Sprague Dawley ◽  
Sperm Transport ◽  
Sprague Dawley Rats ◽  
Spinal Cord Injured

scholarly journals Characterization of ultrasound-mediated delivery of trastuzumab to normal and pathologic spinal cord tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paige Smith ◽  
Natalia Ogrodnik ◽  
Janani Satkunarajah ◽  
Meaghan A. O’Reilly
Keyword(s):  
Drug Delivery ◽  
Spinal Cord ◽  
Focused Ultrasound ◽  
Healthy Tissue ◽  
Spinal Cord Tissue ◽  
Sprague Dawley ◽  
Intense Staining ◽  
Her2 Breast Cancer ◽  
Sprague Dawley Rats ◽  
Blood Spinal Cord Barrier

AbstractExtensive studies on focused ultrasound (FUS)-mediated drug delivery through the blood–brain barrier have been published, yet little work has been published on FUS-mediated drug delivery through the blood-spinal cord barrier (BSCB). This work aims to quantify the delivery of the monoclonal antibody trastuzumab to rat spinal cord tissue and characterize its distribution within a model of leptomeningeal metastases. 10 healthy Sprague–Dawley rats were treated with FUS + trastuzumab and sacrificed at 2-h or 24-h post-FUS. A human IgG ELISA (Abcam) was used to measure trastuzumab concentration and a 12 ± fivefold increase was seen in treated tissue over control tissue at 2 h versus no increase at 24 h. Three athymic nude rats were inoculated with MDA-MB-231-H2N HER2 + breast cancer cells between the meninges in the thoracic region of the spinal cord and treated with FUS + trastuzumab. Immunohistochemistry was performed to visualize trastuzumab delivery, and semi-quantitative analysis revealed similar or more intense staining in tumor tissue compared to healthy tissue suggesting a comparable or greater concentration of trastuzumab was achieved. FUS can increase the permeability of the BSCB, improving drug delivery to specifically targeted regions of healthy and pathologic tissue in the spinal cord. The achieved concentrations within the healthy tissue are comparable to those reported in the brain.

Mineralocorticoid Receptor Activation by Aldosterone or Corticosterone Induces Hypertension, Myocardial Infarction and Proteinuria

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-723
Author(s):  
Qing-Feng Tao ◽  
Diego Martinez vasquez ◽  
Ricardo Rocha ◽  
Gordon H Williams ◽  
Gail K Adler
Keyword(s):  
Myocardial Infarction ◽  
Drinking Water ◽  
Mineralocorticoid Receptor ◽  
Critical Role ◽  
Weight Ratio ◽  
Myocardial Necrosis ◽  
Receptor Activation ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

P165 Aldosterone through its interaction with the mineralocorticoid receptor (MR) plays a critical role in the development of hypertension and cardiovascular injury (CVI). Normally, MR is protected by 11β-hydroxysteroid dehydrogenase (11β-HSD) which inactivates glucocorticoids preventing their binding to MR. We hypothesis that if activation of MR by either aldosterone or glucocorticoids induces hypertension and CVI, then the inhibition of 11β-HSD with glycyrrhizin (GA), a natural inhibitor of 11β-HSD, should induce damage similar to that observed with aldosterone. Sprague-Dawley rats were uninephrectomized, and treated for 4 weeks with 1% NaCl (in drinking water) for the control group, 1% NaCl + aldosterone infusion (0.75 μg/h), or 1% NaCl + GA (3.5 g/l in drinking water). After 4 weeks, aldosterone and GA caused significant increases in blood pressure compared to control rats ([mean ± SEM] 211± 9, 205 ± 12, 120 ± 9 mmHg, respectively, p<0.001). Both aldosterone- and GA-treated rats had a significant increase in proteinuria (152.2 ± 8.7 and 107.7 ± 19.5 mg/d, respectively) versus controls (51.2 ± 9.5 mg/d). There was a significant increase (p<0.001) in heart to body weight ratio in the rats treated with aldosterone or GA compared with control (3.92 ± 0.10, 3.98 ± 0.88, and 3.24 ± 0.92 mg/g, respectively). Hearts of GA and aldosterone treated rats showed similar histological changes consisting of biventricular myocardial necrosis and fibrinoid necrosis of small coronary arteries and arterioles. These data suggests that in rodents activation of MR by either aldosterone or corticosterone leads to severe hypertension, vascular injury, proteinuria and myocardial infarction. Thus, 11β-HSD plays an important role in protecting the organism from injury.

scholarly journals Olfactory bulb transplantation in complete spinal cord injury: axonal regeneration and locomotor recovery

2015 ◽  
Vol 14 (1) ◽  
pp. 50-52
Author(s):  
Carlos Abraham Arellanes-Chávez ◽  
Ariana Martínez Bojórquez ◽  
Ernesto Ramos Martínez
Keyword(s):  
Spinal Cord ◽  
Axonal Regeneration ◽  
Sufficient Evidence ◽  
Spinal Cord Regeneration ◽  
Sprague Dawley ◽  
Locomotor Recovery ◽  
Randomized Controlled ◽  
Sprague Dawley Rats ◽  
Cord Injury ◽  
Complete Spinal Cord Injury

OBJECTIVES: To determine whether the intervention in rats is effective in terms of spinal cord regeneration and locomotor recovery, in order to obtain sufficient evidence to apply the therapy in humans. METHODS: a randomized, controlled, experimental, prospective, randomized trial was conducted, with a sample of 15 adult female Sprague-Dawley rats weighing 250 gr. They were divided into three equal groups, and trained for 2 weeks based on Pavlov's classical conditioning method, to strengthen the muscles of the 4 legs, stimulate the rats mentally, and keep them healthy for the surgery. RESULTS: It was observed that implantation of these cells into the site of injury may be beneficial to the process of spinal cord regeneration after spinal trauma, to mediate secretion of neurotrophic and neuroprotective chemokines, and that the OECs have the ability to bridge the repair site and decrease the formation of gliosis, creating a favorable environment for axonal regeneration. CONCLUSION: It is emphasized that the olfactory ensheathing glial cells possess unique regenerative properties; however, it was not until recently that the activity of promoting central nervous system regeneration was recognized.

scholarly journals Selected Contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia

2001 ◽  
Vol 90 (5) ◽  
pp. 2001-2006 ◽  
Author(s):  
D. D. Fuller ◽  
A. G. Zabka ◽  
T. L. Baker ◽  
G. S. Mitchell
Keyword(s):  
Receptor Antagonist ◽  
Phrenic Nerve ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sprague Dawley Rats ◽  
Episodic Hypoxia ◽  
Baseline Levels ◽  
Long Term Facilitation

Episodic hypoxia evokes a sustained augmentation of respiratory motor output known as long-term facilitation (LTF). Phrenic LTF is prevented by pretreatment with the 5-hydroxytryptamine (5-HT) receptor antagonist ketanserin. We tested the hypothesis that 5-HT receptor activation is necessary for the induction but not maintenance of phrenic LTF. Peak integrated phrenic nerve activity (∫Phr) was monitored for 1 h after three 5-min episodes of isocapnic hypoxia (arterial Po 2 = 40 ± 2 Torr; 5-min hyperoxic intervals) in four groups of anesthetized, vagotomized, paralyzed, and ventilated Sprague-Dawley rats [ 1) control ( n = 11), 2) ketanserin pretreatment (2 mg/kg iv; n = 7), and ketanserin treatment 0 and 45 min after episodic hypoxia ( n = 7 each)]. Ketanserin transiently decreased ∫Phr, but it returned to baseline levels within 10 min. One hour after episodic hypoxia, ∫Phr was significantly elevated from baseline in control and in the 0- and 45-min posthypoxia ketanserin groups. Conversely, ketanserin pretreatment abolished phrenic LTF. We conclude that 5-HT receptor activation is necessary to initiate (during hypoxia) but not maintain (following hypoxia) phrenic LTF.

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