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Cord Segments (cord + segment)
Kinds of Cord Segments Selected AbstractsEarly Embryonic Development of the Camel Lumbar Spinal Cord SegmentANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005M. E. Abd Elmonem The lumbar spinal cord segment of the camel embryo at CVRL 2.4 to 28 cm was examined. Major changes are occurring in the organization of the lumbar spinal cord segments during this early developmental period. At the CVRL 2.4, 2.7 and 3.6 cm the three primary layers, ependymal cells layer, mantle cells layer, marginal cells layer in the developing lumber spinal cord segment were demonstrated. The mantle layer is the first to show striking differentiation, while the marginal layer is represented by thin outer rim. Proliferation and differentiation of the neuroepithelial cells in the developing spinal cord produce the thick lateral walls, thin roof and floor plates. The spinal ganglion and dorsal root of the spinal nerve are differentiated. At 2.7 cm CVRL differential thickening of the lateral walls produces a shallow longitudinal groove called sulcus limitans, which separates the dorsal part (alar plate) from ventral part (basal plate). The ventral root of the spinal nerve, the spinal cord and ganglion are embedded in loose mesenchyme, which tends to differentiate into spinal meninges. At 3.6 cm CVRL the basal plate, which is the future ventral gray horn, seem to be quite voluminous and the dorsal and ventral roots unite to form the beginning of the spinal nerve. At 5.5 cm CVRL the alar plates enlarge forming the dorsal septum. At 8.4 cm to 10.5 cm CVRL the basal plates enlarge, and bulge ventrally on each side of the midline producing the future ventral medium fissure, and the white and gray matters can be recognized. At 28 cm CVRL the lumen of the spinal cord is differentiated into the central canal bounded dorsally and ventrally by dorsal and ventral gray commissures, and therefore the gray matter takes the appearance of a butterfly. The lumber spinal nerve and their roots are well distinguished. [source] A study of juvenile rat spinal cord injuryJOURNAL OF NEUROCHEMISTRY, Issue 2002J. M. Wingrave Greater than 5% of all spinal cord injuries (SCI) in the US occur in people younger than 16, although a minority, children will require extended attention during their lifetime. While facing increased mortality in the initial 24 h after trauma, children with incomplete injuries seem to have a greater capacity for recovery of function compared to adults suggesting that there is a difference in injury tolerance in the young over the adult. Knowledge of the factors involved in this difference would not only increase understanding of SCI, but also potentiate new avenues for SCI treatment. Yet there has not been a model for the study of youth SCI. For these reasons, we developed a model of SCI in juvenile rats equivalent to an adult injury of 25 g cm force (GCF). To do so, we recorded spinal cord masses of Sprague,Dawley rats at 21, 30, 45, and 60 days of age, compared them to adult cord masses, and assembled a conversion factor that provides youth injuries comparable to adult. To investigate the pathophysiology in juvenile SCI, two cord segments, 1 cm long, were removed from animals 24 h following injury. One segment was centered at the impact site, the other immediately caudal. After homogenization, the samples were assayed by Western blot analysis for calpain content and degradation of 68K Neuro-Filament Protein (68K NFP), a neuronal structural protein. mCalpain expression, a neutral protease previously implicated in secondary SCI, was reduced in juvenile animals relative to adult cohorts. The degradation of 68K NFP was also found to be reduced in juvenile animals. From these analyses, it seems plausible that calpain expression and pathogenic activity is abated in the setting of young rat SCI. Acknowledgements:, Supported by grants from NIH-NINDS. [source] Glucose-dependent insulinotropic polypeptide (GIP) and its receptor (GIPR): Cellular localization, lesion-affected expression, and impaired regenerative axonal growthJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2009Bettina A. Buhren Abstract Glucose-dependent insulinotropic polypeptide (GIP) was initially described to be rapidly regulated by endocrine cells in response to nutrient ingestion, with stimulatory effects on insulin synthesis and release. Previously, we demonstrated a significant up-regulation of GIP mRNA in the rat subiculum after fornix injury. To gain more insight into the lesion-induced expression of GIP and its receptor (GIPR), expression profiles of the mRNAs were studied after rat sciatic nerve crush injury in 1) affected lumbar dorsal root ganglia (DRG), 2) spinal cord segments, and 3) proximal and distal nerve fragments by means of quantitative RT-PCR. Our results clearly identified lesion-induced as well as tissue type-specific mRNA regulation of GIP and its receptor. Furthermore, comprehensive immunohistochemical stainings not only confirmed and exceeded the previous observation of neuronal GIP expression but also revealed corresponding GIPR expression, implying putative modulatory functions of GIP/GIPR signaling in adult neurons. In complement, we also observed expression of GIP and its receptor in myelinating Schwann cells and oligodendrocytes. Polarized localization of GIPR in the abaxonal Schwann cell membranes, plasma membrane-associated GIPR expression of satellite cells, and ependymal GIPR expression strongly suggests complex cell type-specific functions of GIP and GIPR in the adult nervous system that are presumably mediated by autocrine and paracrine interactions, respectively. Notably, in vivo analyses with GIPR-deficient mice suggest a critical role of GIP/GIPR signal transduction in promoting spontaneous recovery after nerve crush, insofar as traumatic injury of GIPR-deficient mouse sciatic nerve revealed impaired axonal regeneration compared with wild-type mice. © 2009 Wiley-Liss, Inc. [source] Extradural spinal juxtafacet (synovial) cysts in three dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 2 2007C. S. H. Sale Three dogs were presented for investigation of spinal disease and were diagnosed with extradural spinal juxtafacet cysts of synovial origin. Two dogs that were presented with clinical signs consistent with pain in the lumbosacral region associated with bilateral hindlimb paresis were diagnosed using magnetic resonance imaging. Both cysts were solitary and associated with the L6-7 dorsal articulations; both the dogs had a transitional vertebra in the lumbosacral region. A third dog that was presented with progressive paraparesis localised to T3-L3 spinal cord segments and compression of the spinal cord at T13-L1 was diagnosed using myelography. A solitary multiloculated cyst was found at surgery. Decompressive surgery resulted in resolution of the clinical signs in all three dogs. Immunohistological findings indicated that one to two layers of vimentin-positive cells consistent with synovial origin lined the cysts. [source] Spinal arachnoid pseudocysts in 10 rottweilersJOURNAL OF SMALL ANIMAL PRACTICE, Issue 1 2004K. Jurina Ten rottweilers presenting with spinal arachnoid pseudocysts were investigated. In six dogs, the lesions were localised dorsally at C2-C3; in three dogs, dorsally and ventrally at C5-C6; and, in one dog, dorsally and ventrally at C6-C7. Clinical signs were consistent with focal compression of the affected spinal cord segments. The animals showed ataxia of all four limbs, with truncal ataxia and marked hypermetria in cases of C2-C3 involvement, or ambulatory tetraparesis in cases of C5-C6 or C6-C7 involvement. Other than signs indicative of spina bifida in one dog, no abnormalities could detected on plain radiographs. Myelography was used to define the localisation and extent of the pseudocysts. Additional information was obtained using magnetic resonance imaging in five dogs. Five dogs underwent a dorsal laminectomy; in three cases, the pseudocyst was treated by marsupialisation and, in two, by durectomy. [source] fMRI of the lumbar spinal cord during a lower limb motor taskMAGNETIC RESONANCE IN MEDICINE, Issue 2 2004J. Kornelsen Abstract This study applied spinal fMRI to the lumbar spinal cord during lower limb motor activity. During active ankle movement, activity was detected in the lumbar spinal cord motor areas and sensory areas bilaterally. During passive ankle movement, activity was detected in the motor and sensory areas in lower lumbar spinal cord segments and motor activity in higher lumbar spinal cord segments. Spinal fMRI detects patterns of activity consistent with known physiology and can be used to reliably assess activity in the lumbar spinal cord during lower limb motor stimulation. This study affirms spinal fMRI as an effective tool for assessing spinal cord function and increases its potential as a clinical tool. Magn Reson Med 52:411,414, 2004. © 2004 Wiley-Liss, Inc. [source] Venous congestive myelopathy of the cervical spinal cord: An autopsy case showing a rapidly progressive clinical courseNEUROPATHOLOGY, Issue 3 2007Akio Kimura We report a rapidly progressive myelopathy in a 74-year-old Japanese man who was admitted to our hospital with a 4-month history of progressive gait disturbance and died of pneumonia followed by respiratory failure on the 22nd day of admission. During the course of his illness, magnetic resonance imaging (MRI) revealed intramedullary lesions with edematous swelling from the medulla oblongata to the spinal cord at the level of the fourth vertebra. After administration of contrast medium, the ventral portion of the lesion was mildly and irregularly enhanced and a dilated vessel was recognized along the ventral surface of the upper cervical cord. At autopsy, ischemic changes were observed in the upper-to-middle cervical cord segments, with so-called arterialized veins in the subarachnoid space. No neoplastic lesions were found within or outside the brain and spinal cord. These pathological findings were essentially those of venous congestive myelopathy (VCM) associated with dural arteriovenous fistulae (AVF), formerly known as Foix,Alajouanine syndrome. VCM associated with dural AVF, which is now considered to be treatable in the early stages, is rare found in the cervical spinal cord. The present autopsy case, with MRI findings, provides further information that might be useful for recognition and diagnosis. [source] Morphine tolerance increases [3H]MK-801 binding affinity and constitutive neuronal nitric oxide synthase expression in rat spinal cord. (National Medical Defense Center, Taipei, Taiwan) Br J Anaesth 2000;85:587,591.PAIN PRACTICE, Issue 2 2001Chih-Shung Wong N -Methyl-D-aspartate (NMDA) receptor antagonists and nitric oxide synthase (NOS) inhibitors inhibit morphine tolerance. In the present study, a lumbar subarachnoid polyethylene (PE10) catheter was implanted for drug administration to study alterations in NMDA receptor activity and NOS protein expression in a morphine-tolerant rat spinal model. Antinociceptive tolerance induced by intrathecal morphine infusion (10 ,g h,1) for 5 days. Co-administered MK801 with morphine was used to inhibit the development of morphine tolerance. Lumbar spinal cord segments were removed and prepared for [3H]MK-801 binding assays and NOS western blotting. The binding affinity of [3H]MK-801 was higher in spinal cords of morphine-related rats than in control rats. There was no difference in Bmax. Western blot analysis showed that constitutive expression of neuronal NOS protein in the morphine-tolerant group was twice that in the control group. This up-regulation was partially prevented by MK-801. The results suggest that morphine tolerance affects NMDA receptor binding activity and increases nNOS expression in the rat spinal cord. Comment by Octavio Calvillo, M.D., Ph.D. Morphine tolerance may be due to receptor down-regulation or receptor uncoupling; activation of the NMDA-dependent pain-facilitatory system may also play a role. It has been proposed that NMDA receptor activation may play a role in morphine tolerance. NMDA receptor antagonists and nitric oxide synthase [NOS] inhibitors may prevent morphine tolerance. Tolerance was induced in rats by intrathecal injection of morphine [10 ug/h] for 5 days, co-administration of MK801 [NMDA antagonist] with morphine was used to prevent morphine tolerance. Lumbar spinal cord segments were removed and prepared for [H3]MK801 binding assays and NOS western blotting. The binding affinity of labeled MK801 was higher in spinal cords of morphine tolerant rats than in control rats. Western blot analysis showed that constitutive expression of neuronal NOS protein in the morphine tolerant rats was twice that in the control group, thus, up-regulation was prevented by MK801. The results suggest that morphine tolerance affect NMDA receptor binding activity and increase neuronal protein expression in rat the spinal cord. [source] Hind-limb paraparesis in a rat model for neurolathyrism associated with apoptosis and an impaired vascular endothelial growth factor system in the spinal cordTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2010Kuniko Kusama-Eguchi Abstract Neurolathyrism is a motor neuron disease characterized by lower limb paraparesis. It is associated with ingestion of a plant excitotoxin, ,-N-oxalyl-L-,,-diaminopropionic acid (L -,-ODAP), an agonist of ,-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate-type glutamatergic receptors. Previously, a limited model of neurolathyrism was reported for the rat. To improve upon the model, we stressed rat pups by separation from their mothers, followed by the subcutaneous L -,-ODAP treatment, resulting in a 4.6-fold higher incidence (14.0,15.6%) of the paraparesis compared with the prior study. The number and size of motor neurons in these rats were decreased only in the lumbar and sacral cord segments, at approximately 13,36 weeks after treatment. Only lumbar and sacral spinal cord tissue revealed pathological insults typical of physical and ischemic spinal cord injury in the surviving motor neurons. In addition, extensive but transient hemorrhage occurred in the ventral spinal cord parenchyma of the rat, and numerous TdT-mediated dUTP-biotin nick end-labeling (TUNEL)-positive cells were also observed. In parallel, vascular endothelial growth factor receptor (VEGFR)-2 (Flk-1) levels were significantly lowered in the lumbosacral spinal cord of the paraparetic rats compared with their controls, suggesting a failure of the VEGF system to protect neurons against L -,-ODAP toxicity. We propose, based on these data, a novel pathological process of motor neuron death induced by peripheral L -,-ODAP. For the first time, we present a model of the early molecular events that occur during chemically induced spinal cord injury, which can potentially be applied to other neurodegenerative disorders. J. Comp. Neurol. 518:928,942, 2010. © 2009 Wiley-Liss, Inc. [source] Early Embryonic Development of the Camel Lumbar Spinal Cord SegmentANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005M. E. Abd Elmonem The lumbar spinal cord segment of the camel embryo at CVRL 2.4 to 28 cm was examined. Major changes are occurring in the organization of the lumbar spinal cord segments during this early developmental period. At the CVRL 2.4, 2.7 and 3.6 cm the three primary layers, ependymal cells layer, mantle cells layer, marginal cells layer in the developing lumber spinal cord segment were demonstrated. The mantle layer is the first to show striking differentiation, while the marginal layer is represented by thin outer rim. Proliferation and differentiation of the neuroepithelial cells in the developing spinal cord produce the thick lateral walls, thin roof and floor plates. The spinal ganglion and dorsal root of the spinal nerve are differentiated. At 2.7 cm CVRL differential thickening of the lateral walls produces a shallow longitudinal groove called sulcus limitans, which separates the dorsal part (alar plate) from ventral part (basal plate). The ventral root of the spinal nerve, the spinal cord and ganglion are embedded in loose mesenchyme, which tends to differentiate into spinal meninges. At 3.6 cm CVRL the basal plate, which is the future ventral gray horn, seem to be quite voluminous and the dorsal and ventral roots unite to form the beginning of the spinal nerve. At 5.5 cm CVRL the alar plates enlarge forming the dorsal septum. At 8.4 cm to 10.5 cm CVRL the basal plates enlarge, and bulge ventrally on each side of the midline producing the future ventral medium fissure, and the white and gray matters can be recognized. At 28 cm CVRL the lumen of the spinal cord is differentiated into the central canal bounded dorsally and ventrally by dorsal and ventral gray commissures, and therefore the gray matter takes the appearance of a butterfly. The lumber spinal nerve and their roots are well distinguished. [source] The effect of intravesical electrical stimulation on bladder function and synaptic neurotransmission in the rat spinal cord after spinal cord injuryBJU INTERNATIONAL, Issue 8 2009Chang Hee Hong OBJECTIVE To investigate the effects of intravesical electrical stimulation (IVES) on bladder function and synaptic neurotransmission in the lumbosacral spinal cord in the spinalized rat, as the clinical benefits of IVES in patients with increased residual urine or reduced bladder capacity have been reported but studies on the mechanism of IVES have mainly focused on bladder A, afferents in central nervous system-intact rats. MATERIALS AND METHODS In all, 30 female Sprague-Dawley rats were divided equally into three groups: normal control rats, sham-stimulated spinalized rats and IVES-treated spinalized rats. IVES was started 5 weeks after spinal cord injury (SCI) and was performed 20 min a day for 5 consecutive days. At 7 days after IVES, conscious filling cystometry was performed. Sections from the L6 and S1 spinal cord segments were examined for n -methyl- d -aspartic acid receptor 1 (NMDAR1) subunit and ,-aminobutyric acid (GABA) immunoactivity. RESULTS In IVES-treated spinalized rats, the number and maximal pressure of nonvoiding detrusor contractions were significantly less than in sham-stimulated spinalized rats. The mean maximal voiding pressure was also lower in IVES-treated than in sham-stimulated spinalized rats. IVES significantly reduced the interval between voiding contractions compared with the untreated spinalized rats. There was an overall increase in NMDAR1 immunoactivity after SCI, which was significantly lower in IVES-treated spinalized rats. Immunoactivity of GABA after SCI was significantly lower than in the control group and was significantly higher in IVES-treated spinalized rats. CONCLUSION Our results suggest that IVES might affect voiding contractions in addition to inhibiting C-fibre activity and that IVES seems to have a more complex effect on the bladder control pathway. For synaptic neurotransmission in the spinal cord, IVES could possibly shift the balance between excitation and inhibition towards inhibition. [source] | |||||||||||||