Changes of Bladder Activity and Glycine Levels in the Spinal Cord and Serum after Spinal Cord Injury in Rats

Nishijima, Saori; Sugaya, Kimio; Miyazato, Minoru; Ashitomi, Katsuhiro; Morozumi, Makoto; Ogawa, Yoshihide

doi:10.2220/biomedres.24.165

Cited by 13 publications

(21 citation statements)

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“…In this phase, the glycine level in the lumbosacral cord showed a reversible decrease at 2-8 weeks in rats with SCI. 17 These findings propose that in the chronic phase of SCI, a decrease in glycinergic neuronal activity in the spinal cord occurred. Reduction in GlyRa1 at day 10 (chronic phase) in our study is in agreement with this Expression of glycine receptor subunit mRNA in spinal cord injury A Esmaeili and SR Zaker finding.…”

Section: Discussionmentioning

confidence: 94%

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Esmaeili

Zaker

2010

Spinal Cord

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Study design: Spinal cord injury (SCI) results in alterations in the regulation of many genes that may influence neuronal death and the subsequent loss of motor function and neuropathic pain. The subtype expression mRNA levels of glycine receptors (GlyRs) after SCI are unknown. Methods: Using real-time reverse transcription PCR, this study analyzed changes in the mRNA abundance of the four major GlyR subunits (a13 and b) at 6, 24 h and 3, 7 and 10 days after SCI in adult male rats. SCI was induced at the T9 level by transection. Results: Our results show a complicated temporal and spatial pattern of alteration in GlyR mRNA expression levels after SCI. Temporal and spatial variations with different degrees and direction (up or downregulation) of expression alteration were observed. The greatest variation was seen in GlyRa1, whereas GlyRa2 was downregulated in all regions following SCI. Conclusion: This study shows that alteration in GlyR expression starts as early as 6 h after SCI. The most significant points of this research are temporal elevation of GlyRa1 and continuous reduction of GlyRa2. Alterations in GlyR expression within the spinal cord may have a key role in the development of pathological pain. Therefore, control of GlyR expression could represent a novel therapeutic avenue for the development of new painkiller agents in SCI.

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Section: Discussionmentioning

confidence: 94%

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Esmaeili

Zaker

2010

Spinal Cord

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“…When the spinal cord is transected at the lower thoracic level, the lower extremities and bladder develop flaccid paralysis. At this time, the glycine level increases in the lumbosacral cord (Nishijima et al, 2003a). In rats with chronic spinal cord injury, bladder activity increases and urinary frequency develops.…”

Section: Spinal Amino Acid Neurons and The Micturition Reflex Pathwaymentioning

confidence: 97%

“…At this time, the glycine level in the lumbosacral cord conversely shows a decrease. The changes of glycine in the lumbosacral cord after spinal cord injury are reflected by the serum glycine level with a delay of 1-2 weeks (Nishijima et al, 2003a). On the other hand, cerebral infarction induces urinary frequency in rats and humans.…”

Section: Spinal Amino Acid Neurons and The Micturition Reflex Pathwaymentioning

confidence: 99%

Central nervous control of micturition and urine storage

Sugaya

Nishijima

Miyazato

et al. 2005

J. Smooth Muscle Res.

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101

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The micturition reflex is one of the autonomic reflexes, but the release of urine is regulated by voluntary neural mechanisms that involve centers in the brain and spinal cord. The micturition reflex is a bladder-to-bladder contraction reflex for which the reflex center is located in the rostral pontine tegmentum (pontine micturition center: PMC). There are two afferent pathways from the bladder to the brain. One is the dorsal system and the other is the spinothalamic tract. Afferents to the PMC ascend in the spinotegmental tract, which run through the lateral funiculus of the spinal cord. The efferent pathway from the PMC also runs through the lateral funiculus of the spinal cord to inhibit the thoracolumbar sympathetic nucleus and the sacral pudendal nerve nucleus, while promoting the activity of the sacral parasymapathetic nucleus. Inhibition of the sympathetic nucleus and pudendal nerve nucleus induces relaxation of the bladder neck and the external urethral sphincter, respectively. There are two centers that inhibit micturition in the pons, which are the pontine urine storage center and the rostral pontine reticular formation. In the lumbosacral cord, excitatory glutamatergic and inhibitory glycinergic/GABAergic neurons influence both the afferent and efferent limbs of the micturition reflex. The activity of these neurons is affected by the pontine activity. There are various excitatory and inhibitory areas co-existing in the brain, but the brain has an overall inhibitory effect on micturition, and thus maintains continence. For micturition to occur, the cerebrum must abate its inhibitory influence on the PMC.

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“…Microinjection of carbachol into the rostral pontine reticular formation in rats, corresponding to the PoO in cats, inhibits bladder contraction and induces an increase of glycine level in the lumbosacral cord (11). Spinal glycinergic neurons are major inhibitory interneurons involved in the control of lower urinary tract function (9,10). Therefore, the inhibitory effects of the PoO may be mediated via spinal inhibitory glycinergic interneurons.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of the nucleus reticularis pontis oralis on the pontine micturition center and pontine urine storage center in decerebrate cats

Sugaya¹,

Nishijima²,

Miyazato³

et al. 2006

Biomed. Res.

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The infl uence of the nucleus reticularis pontis oralis (PoO) on the pontine micturition center (PMC) and pontine urine storage center (PUSC) was examined in decerebrate cats by electrical and chemical stimulations of the PMC, PUSC or PoO. Microinjection of carbachol into the rostral and dorsolateral part of the PoO rapidly inhibited refl ex micturition and external urethral sphincter (EUS) activity. After confi rming the inhibition of refl ex micturition and EUS activity by microinjection of carbachol into the PoO, intravenous injection of atropine sulfate or its microinjection into the PoO recovered both refl ex micturition and EUS activity. Microinjection of carbachol into the PMC evoked micturition and then inhibited refl ex micturition, but intravenous injection of atropine or its microinjection into the PoO recovered refl ex micturition. After confi rming the inhibition of refl ex micturition and EUS activity by microinjection of carbachol into the PoO, electrical stimulation of the PUSC enhanced EUS activity, but electrical stimulation of the PMC failed to evoke micturition. However, electrical stimulation of the PMC evoked micturition after microinjection of atropine into the PoO. These results suggest that the PoO strongly inhibits the PMC and less strongly inhibits the PUSC. Therefore, the PoO seems to be the pontine micturition inhibitory area.The pontine micturition center (PMC) is the site where electrical stimulation evokes micturition, and it corresponds to the nucleus locus coeruleus alpha (LCa) in cats (16) and dogs (13). Electrical stimulation of the region ventrolateral to the PMC enhances external urethral sphincter (EUS) activity and inhibits bladder contraction (2,6,12). This region is called the pontine urine storage center (PUSC) or L-region, and it corresponds to the nucleus locus subcoeruleus (LSC) in cats (2, 6) and dogs (12). The third pontine region controlling lower urinary tract function is located at a ventromedial site to the locus coeruleus complex. Electrical stimulation or microinjection of carbachol (a long-acting cholinomimetic agent that is resistant to acetylcholinesterase) into the third pontine region inhibits both bladder contraction and EUS activity (3,17), and this region corresponds to the nucleus reticularis pontis oralis (PoO). While, microinjection of fl avoxate hydrochloride into the PoO only inhibits bladder contraction without affecting EUS activity (3). Thus, the infl uence of the PoO on EUS activity was uncertain.In this study using cats, we examined the relationship among the PMC, PUSC, and PoO with respect to bladder and EUS activity, especially the infl uence of the PoO on the function of the PMC and PUSC, by a combination of electrical and chemical stimulation of the PMC, PUSC, or PoO, as well as a urodynamic study that included cystome-

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Changes of Bladder Activity and Glycine Levels in the Spinal Cord and Serum after Spinal Cord Injury in Rats

Cited by 13 publications

References 0 publications

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Central nervous control of micturition and urine storage

Inhibitory effect of the nucleus reticularis pontis oralis on the pontine micturition center and pontine urine storage center in decerebrate cats

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