Region-specific changes in the phosphorylation of ERK1/2 and ERK5 in rat micturition pathways following cyclophosphamide-induced cystitis

2007 ◽  
Vol 292 (3) ◽  
pp. R1368-R1375 ◽  
Author(s):  
Li-Ya Qiao ◽  
Melisa A. Gulick
Keyword(s):  
Spinal Cord ◽  
Urinary Bladder ◽  
Visceral Pain ◽  
Specific Effect ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Bladder Inflammation ◽  
Before And After ◽  
Lumbar Spinal

Chronic inflammation of the urinary bladder generates hyperalgesia and allodynia. Growing evidence suggests a role of ERK in mediating somatic and visceral pain processing. In the present studies, we characterized and compared the activation of two ERK isoforms, ERK1/2 and ERK5, in micturition pathways, including the urinary bladder, lumbosacral dorsal root ganglia (DRG), and spinal cord in adult female and male rats before and after cyclophosphamide (CYP)-induced bladder inflammation. Results showed differential activation of ERK1/2 and ERK5 in these regions following cystitis. The level of phospho-ERK1/2 but not phospho-ERK5 was increased in the urinary bladder; the level of phospho-ERK5 but not phospho-ERK1/2 was increased in DRG; and the level of phospho-ERK1/2 but not phospho-ERK5 was increased in lumbar spinal cord following cystitis compared with control. Cystitis-induced upregulation of phospho-ERK1/2 and phospho-ERK5 was time dependent and showed similar patterns in female and male rats. The level of phospho-ERK1/2 in bladder was increased at 2 and 8 h after CYP injection; the level of phospho-ERK5 in DRG was increased at 8 and 48 h after CYP injection; and the level of phospho-ERK1/2 in lumbar spinal cord was increased at 48 h after CYP injection. The result that phospho-ERK5 was exclusively increased in DRG neurons, while phospho-ERK1/2 was increased in the spinal cord and the urinary bladder after cystitis, suggests a region-specific effect of neurotrophins on micturition pathways following bladder inflammation.

Effects of Glycine Administration on Canine Experimental Spinal Spasticity and the Levels of Glycine, Glutamate, and Aspartate in the Lumbar Spinal Cord

Neurosurgery ◽  
1979 ◽  
Vol 4 (2) ◽  
pp. 152-156 ◽  
Author(s):  
J. E. Smith ◽  
P. V. Hall ◽  
M. R. Galvin ◽  
A. R. Jones ◽  
R. L. Campbell
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Gray Matter ◽  
Clinical Signs ◽  
Spinal Cord Transection ◽  
Lumbar Spinal Cord ◽  
Central Gray Matter ◽  
Central Gray ◽  
Lumbar Spinal

Abstract Twelve female mongrel dogs were made paraplegic by midthoracic spinal cord transection. Beginning at 9 weeks posttransection, either glycine (50 mg/kg) or saline was injected intramuscularly each day and the signs of spinal spasticity were assessed clinically. After treating the dogs for 3 weeks, we removed the lumbar enlargement of each dog and microdissected it into gray and white areas which we assayed for glycine, glutamate, and aspartate content. Some of the clinical signs of spasticity improved in the animals injected with glycine compared to the saline-injected controls. The content of glycine was significantly elevated in the central gray matter and ventral medial white matter of the glycinetreated dogs. The levels of glutamate were also significantly elevated in the central, lateral ventral, and medial ventral gray matter and in the dorsal lateral and ventral medial white matter of the glycine-treated dogs. The possible role of these segmental putative neurotransmitters in spinal spasticity is discussed.

scholarly journals Spinal Cord Injury Causes Reduction of Galanin and Gastrin Releasing Peptide mRNA Expression in the Spinal Ejaculation Generator of Male Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
James W. Wiggins ◽  
Jonathan E. Sledd ◽  
Lique M. Coolen
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Gastrin Releasing Peptide ◽  
Cord Injury ◽  
Contusion Injury ◽  
Spinal Contusion ◽  
Lumbar Spinal ◽  
Injury Causes

Spinal cord injury (SCI) in men is commonly associated with sexual dysfunction, including anejaculation, and chronic mid-thoracic contusion injury in male rats also impairs ejaculatory reflexes. Ejaculation is controlled by a spinal ejaculation generator consisting of a population of lumbar spinothalamic (LSt) neurons that control ejaculation through release of four neuropeptides including galanin and gastrin releasing peptide (GRP) onto lumbar and sacral autonomic and motor nuclei. It was recently demonstrated that spinal contusion injury in male rats caused reduction of GRP-immunoreactivity, but not galanin-immunoreactivity in LSt cells, indicative of reduced GRP peptide levels, but inconclusive results for galanin. The current study further tests the hypothesis that contusion injury causes a disruption of GRP and galanin mRNA in LSt cells. Male rats received mid-thoracic contusion injury and galanin and GRP mRNA were visualized 8 weeks later in the lumbar spinal cord using fluorescent in situ hybridization. Spinal cord injury significantly reduced GRP and galanin mRNA in LSt cells. Galanin expression was higher in LSt cells compared to GRP. However, expression of the two transcripts were positively correlated in LSt cells in both sham and SCI animals, suggesting that expression for the two neuropeptides may be co-regulated. Immunofluorescent visualization of galanin and GRP peptides demonstrated a significant reduction in GRP-immunoreactivity, but not galanin in LSt cells, confirming the previous observations. In conclusion, SCI reduced GRP and galanin expression in LSt cells with an apparent greater impact on GRP peptide levels. GRP and galanin are both essential for triggering ejaculation and thus such reduction may contribute to ejaculatory dysfunction following SCI in rats.

Control of abdominal and expiratory intercostal muscle activity during vomiting: role of ventral respiratory group expiratory neurons

1987 ◽  
Vol 57 (6) ◽  
pp. 1854-1866 ◽  
Author(s):  
A. D. Miller ◽  
L. K. Tan ◽  
I. Suzuki
Keyword(s):  
Muscle Activity ◽  
Discharge Rate ◽  
Abdominal Muscle ◽  
Lumbar Spinal Cord ◽  
Abdominal Muscles ◽  
Ventral Respiratory Group ◽  
Before And After ◽  
The One ◽  
Lumbar Spinal

The role of ventral respiratory group (VRG) expiratory (E) neurons in the control of abdominal and internal intercostal (expiratory) muscle activity during vomiting was examined in decerebrate cats by recording from these neurons during fictive vomiting in paralyzed animals and comparing abdominal muscle activity during vomiting before and after sectioning the axons of these descending neurons. Fictive vomiting was defined by a series of bursts of coactivation of abdominal and phrenic nerves elicited by either subdiaphragmatic vagus nerve stimulation or emetic drugs. Such coordinated activity would be expected to produce vomiting if the animals were not paralyzed. Data were recorded from 27 VRG E neurons that were antidromically activated from the lower thoracic (T13) or lumbar spinal cord. During fictive vomiting, almost two-thirds of these neurons (17/27) were mainly active in between periods of abdominal and phrenic nerve coactivation, when the internal intercostal motoneurons are known to be active. This group of neurons was termed INT neurons. INT neurons were subdivided according to whether they were active between every burst of phrenic and abdominal nerve coactivation (INTa neurons, n = 10) or only between some bursts (INTb neurons, n = 7). Another one-third of the VRG E neurons had normal or increased levels of activity when the abdominal nerves were active during fictive vomiting (ABD neurons). The one remaining neuron was mainly silent throughout fictive vomiting. ABD neurons were indistinguishable from INT neurons on the basis of their location in the VRG, type of firing pattern (ramp versus step ramp), conduction velocity, or extent of projection in the lumbar cord. However, INTa neurons had a significantly higher discharge rate during respiration than either ABD or INTb neurons. Abdominal muscle EMG and nerve activity were recorded from six unparalyzed cats before and after cutting the axons of VRG E neurons as they cross the midline between C1 and the obex. The lesions abolished or almost eliminated expiratory modulation of abdominal muscle activity. In contrast, the abdominal muscles were always active during vomiting; however, the amplitude of postlesion abdominal activity varied from approximately 70-100% of prelesion values in three cats to 60-70% of normal in a fourth animal to only approximately 20% of prelesion values in two other cats.(ABSTRACT TRUNCATED AT 400 WORDS)

The exercise pressor reflex is attenuated by intrathecal oxytocin

1994 ◽  
Vol 267 (4) ◽  
pp. R909-R915 ◽  
Author(s):  
C. L. Stebbins ◽  
A. Ortiz-Acevedo
Keyword(s):  
Spinal Cord ◽  
Pressor Response ◽  
Intrathecal Injection ◽  
Sensory Nerve ◽  
Lumbar Spinal Cord ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Before And After ◽  
Pressor Reflex ◽  
Lumbar Spinal

We tested the hypothesis that oxytocin (Oxt) acts in the lumbar spinal cord to attenuate reflex pressor (mean arterial pressure, MAP) and heart rate (HR) responses to static hindlimb contraction (i.e., the exercise pressor reflex). Thus we compared MAP and HR responses to electrically stimulated hindlimb static contraction in the anesthetized cat before and after intrathecal injection of Oxt (30 pmol, n = 3; 300 pmol, n = 6; or 3 nmol, n = 6). The 300-pmol dose was most effective; it attenuated the pressor response to static contraction by 39 +/- 10% but had no effect on HR. In three other cats, contraction-induced increases in MAP and HR were monitored before and after intrathecal injection of 300 pmol of Oxt + 300 nmol of the selective Oxt receptor antagonist [d(CH2)5(1),O-Me-Tyr2,Thr4,Tyr9,Orn8]vasotocin. Pretreatment with the antagonist eliminated the effect of Oxt on MAP. In an additional 10 cats, increases in these same variables in response to static contraction were compared before and after intrathecal injection of the Oxt antagonist (30 nmol, n = 3 or 300 nmol, n = 7) into the lumbar spinal cord (L1-L7). Whereas 30 nmol of the Oxt antagonist had no effect, the 300-nmol dose augmented the contraction-induced pressor and HR responses by 28 +/- 7 and 32 +/- 17%, respectively. These data imply that endogenous Oxt modulates the exercise pressor reflex by its action on Oxt receptors in the lumbar spinal cord that can attenuate sensory nerve transmission from skeletal muscle.

scholarly journals Androgen Regulates the Sexually Dimorphic Gastrin-Releasing Peptide System in the Lumbar Spinal Cord that Mediates Male Sexual Function

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3672-3679 ◽  
Author(s):  
Hirotaka Sakamoto ◽  
Keiko Takanami ◽  
Damian G. Zuloaga ◽  
Ken-ichi Matsuda ◽  
Cynthia L. Jordan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Real Time ◽  
Quantitative Pcr ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Testicular Feminization ◽  
Western Blots ◽  
Gastrin Releasing Peptide ◽  
Real Time Quantitative Pcr ◽  
Lumbar Spinal

A collection of neurons in the upper lumbar spinal cord of male rats projects to the lower lumbar spinal cord, releasing gastrin-releasing peptide (GRP) onto somatic and autonomic centers known to regulate male sexual reflexes such as erection and ejaculation. Because these reflexes are androgen dependent, we asked whether manipulating levels of androgen in adult rats would affect GRP expression in this spinal center. We found that castration resulted, 28 d later, in a profound decrease in the expression of GRP in the spinal cord, as reflected in immunocytochemistry and competitive ELISA for the protein as well as real-time quantitative PCR for the transcript. These effects were prevented if the castrates were treated with testosterone propionate. Genetically male (XY) rats with the dysfunctional testicular feminization allele for the androgen receptor (AR) displayed GRP mRNA and protein levels in the spinal cord similar to those of females, indicating that androgen normally maintains the system through AR. We saw no effect of castration or the testicular feminization allele on expression of the receptor for GRP in the spinal cord, but castration did reduce expression of AR transcripts within the spinal cord as revealed by real-time quantitative PCR and Western blots. Taken together, these results suggest that androgen signaling plays a pivotal role in the regulation of GRP expression in male lumbar spinal cord. A greater understanding of how androgen modulates the spinal GRP system might lead to new therapeutic approaches to male sexual dysfunction.

Supraspinal projections to the ventromedial lumbar spinal cord in adult male rats

1990 ◽  
Vol 300 (2) ◽  
pp. 263-272 ◽  
Author(s):  
Peter Shen ◽  
Arthur P. Arnold ◽  
Paul E. Micevych
Keyword(s):  
Spinal Cord ◽  
Adult Male ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal

Afferent Fibers of the Hypogastric Nerves Are Involved in the Facilitating Effects of Chemical Bladder Irritation in Rats

2001 ◽  
Vol 86 (5) ◽  
pp. 2276-2284 ◽  
Author(s):  
Takahiko Mitsui ◽  
Hidehiro Kakizaki ◽  
Shinobu Matsuura ◽  
Kaname Ameda ◽  
Mitsuhiro Yoshioka ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Acetic Acid ◽  
Marked Decrease ◽  
Lumbar Spinal Cord ◽  
Urinary Frequency ◽  
Acid Infusion ◽  
Afferent Fibers ◽  
Fos Expression ◽  
Lumbar Spinal

To evaluate the role of bladder afferent fibers in the hypogastric nerves (HGN) in modulation of the micturition reflex induced by chemical bladder irritation, voiding behavior, continuous cystometry, and spinal c-fos expression following intravesical acetic acid instillation were investigated in rats with or without HGN transection. Voiding behavior and continuous cystometry were examined in unanesthetized conscious rats. Following chemical bladder irritation, a significant increase in urinary frequency associated with a marked decrease in the voided volume per micturition, was noted in control rats with the intact HGN, but not in HGN-transected rats. Continuous infusion of acetic acid in control rats elicited irritative bladder responses characterized by a marked decrease in the intercontraction interval and a marked increase in maximal vesical pressure, both of which were absent in capsaicin-desensitized rats. HGN transection prevented the decrease in the intercontraction interval but not an increase in maximal vesical pressure following chemical bladder irritation. Compared with saline infusion, acetic acid infusion caused a significant increase in c-fos expression at L1 and L6 of the spinal cord, and HGN transection significantly reduced c-fos expression in the dorsal horn of the spinal cord at L1 but not at L6. These results suggest that capsaicin-sensitive bladder afferent fibers in the HGN, which travel through the rostral lumbar spinal cord, have a role in urinary frequency caused by chemical bladder irritation.

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