Functional interaction between GABA receptors and type I benzo-diazepine recognition sites in the spinal cord of the rat

1988 ◽  
Vol 20 (12) ◽  
pp. 1089-1090
Author(s):  
B. Longoni ◽  
M.G. Corda ◽  
G. Biggio
Keyword(s):  
Spinal Cord ◽  
Gaba Receptors ◽  
Type I ◽  
Functional Interaction ◽  
Recognition Sites

Lipomeningocele associated with diplomyelia in a dog

2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze
Keyword(s):  
Spinal Cord ◽  
Neurological Status ◽  
Split Cord Malformation ◽  
Lumbar Spinal Cord ◽  
Histopathological Diagnosis ◽  
Type I ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Subcutaneous Mass ◽  
Lumbar Spinal

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.

Split spinal cord malformations in children

1998 ◽  
Vol 88 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Yusuf Ersşahin ◽  
Saffet Mutluer ◽  
Sevgül Kocaman ◽  
Eren Demirtasş
Keyword(s):  
Spinal Cord ◽  
Neurological Deficits ◽  
Single Type ◽  
Type I ◽  
Type Ii ◽  
Content Type ◽  
Spinal Lesion ◽  
The Mean ◽  
Fine Print

Object. The authors reviewed and analyzed information on 74 patients with split spinal cord malformations (SSCMs) treated between January 1, 1980 and December 31, 1996 at their institution with the aim of defining and classifying the malformations according to the method of Pang, et al. Methods. Computerized tomography myelography was superior to other radiological tools in defining the type of SSCM. There were 46 girls (62%) and 28 boys (38%) ranging in age from less than 1 day to 12 years (mean 33.08 months). The mean age (43.2 months) of the patients who exhibited neurological deficits and orthopedic deformities was significantly older than those (8.2 months) without deficits (p = 0.003). Fifty-two patients had a single Type I and 18 patients a single Type II SSCM; four patients had composite SSCMs. Sixty-two patients had at least one associated spinal lesion that could lead to spinal cord tethering. After surgery, the majority of the patients remained stable and clinical improvement was observed in 18 patients. Conclusions. The classification of SSCMs proposed by Pang, et al., will eliminate the current chaos in terminology. In all SSCMs, either a rigid or a fibrous septum was found to transfix the spinal cord. There was at least one unrelated lesion that caused tethering of the spinal cord in 85% of the patients. The risk of neurological deficits resulting from SSCMs increases with the age of the patient; therefore, all patients should be surgically treated when diagnosed, especially before the development of orthopedic and neurological manifestations.

Effect of spinal cord stimulation in Type I complex regional pain syndrome with 2 rare severe cutaneous manifestations

2009 ◽  
Vol 110 (2) ◽  
pp. 274-278
Author(s):  
Kim Rijkers ◽  
Jasper van Aalst ◽  
Erkan Kurt ◽  
Marc A. Daemen ◽  
Emile A. M. Beuls ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Complex Regional Pain Syndrome ◽  
Female Patient ◽  
Spinal Cord Stimulation ◽  
Scientific Literature ◽  
Pain Syndrome ◽  
Type I ◽  
Syndrome Type ◽  
Cutaneous Manifestations ◽  
Giant Bullae

The authors present the case of a 49-year-old female patient with complex regional pain syndrome–Type I (CRPSI) who was suffering from nonhealing wounds and giant bullae, which dramatically improved after spinal cord stimulation (SCS). The scientific literature concerning severe cutaneous manifestations of CRPS-I and their treatment is reviewed. Nonhealing wounds and bullae are rare manifestations of CRPS-I that are extremely difficult to treat. Immediate improvement of both wounds and bullae after SCS, such as in this case, has not been reported previously in literature. Considering the rapidly progressive nature of these severe skin manifestations, immediate treatment, possibly with SCS, is mandatory.

MSC secreted extracellular vesicles carrying TGF-beta upregulate Smad 6 expression and promote the regrowth of neurons in spinal cord injured rats

2021 ◽  
Author(s):  
Tianyu Han ◽  
Peiwen Song ◽  
Zuomeng Wu ◽  
Xiang Xia ◽  
Ying Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Extracellular Vesicles ◽  
Kinase Inhibitor ◽  
Inflammatory Factors ◽  
Type I ◽  
Post Injury ◽  
Cord Injury ◽  
Spinal Cord Injured ◽  
Feedback Regulator

Abstract Mesenchymal stem cells (MSCs) are a promising therapy for spinal cord injury (SCI) as they can provide a favorable environment for the regrowth of neurons and axons by inhibiting receptor-regulated Smads (R-Smads) in endogenous neural stem cells (NSCs). However, their mechanism of action and effect on the expression of inhibitory Smads (I-Smads) remains unclear. Here, we demonstrated that Extracellular vesicles (EVs) from MSCs were able to upregulate the Smad 6 expression by carrying TGF-β. Smad 6 knockdown in NSCs partly weakened the BMSC-EVs-induced effect on neural differentiation. In spinal cord injured rats, we found that in the acute phase of injury, the Smad 6 expression was not reduced by the treatment of TGF-β type I receptor kinase inhibitor SB431542, indicating that the Smad 6 expression was not only mediated TGF-β, the inflammatory factors and BMPs were also involved. However, in the later phase of SCI, the Smad 6 expression was reduced by the addition of SB 431542, suggesting in this phase, TGF-β played a key role on the mediation of Smad 6 expression. In addition, by immunohistochemistry staining, Hematoxylin-eosin staining and BBB scores, we revealed that the early inhibition of TGF-β did not increase the regrowth of neurons. Instead, it increased the volume of cavity and the Caspase-3 expression at 24h post-injury, leading to a wore functional outcome. In contrast the later treatment of the TGF-β inhibitor promoted the regrowth of neurons around the cavity, resulting into a better neurological outcome. Together all these results indicated that Smad 6 acts as a feedback regulator to prevents over-differentiation of NSCs to astrocytes and BMSC-EVs can upregulate Smad 6 expression by the carring TGF-β.

scholarly journals Multiple Sclerosis Of The Spinal Cord: Is Gadolinium Irreplaceable In Assessing Lesion Activity?

2013 ◽  
Vol 59 (3) ◽  
pp. 158-161
Author(s):  
Constantina Andrada Treabă ◽  
M Buruian ◽  
Rodica Bălașa ◽  
Maria Daniela Podeanu ◽  
I P Simu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Magnetic Resonance ◽  
Contrast Enhancement ◽  
Signs And Symptoms ◽  
Magnetic Resonance Images ◽  
Type I ◽  
Focal Lesions ◽  
Spinal Cord Lesions ◽  
Active Lesion

Abstract Purpose: To evaluate the relationship between the T2 patterns of spinal cord multiple sclerosis lesions and their contrast uptake. Material and method: We retrospectively reviewed the appearance of spinal cord lesions in 29 patients (with relapsing-remitting multiple sclerosis) who had signs and symptoms of myelopathy on neurologic examination and at least one active lesion visualized on magnetic resonance examinations performed between 2004 and 2011. We correlated the T2 patterns of lesions with contrast enhancement and calculated sensitivity and specificity in predicting gadolinium enhancement. Results: Only focal patterns consisting of a lesion’s center homogenously brighter than its periphery on T2-weighed images (type I) correlated significantly with the presence of contrast enhancement (p = 0.004). Sensitivity was 0.307 and specificity 0.929. In contrast, enhancement was not significantly related to uniformly hyperintense T2 focal lesions (type II) or diffuse (type III) pattern defined as poorly delineated areas of multiple small, confluent, subtle hyperintense T2 lesions (p > 0.5 for both). Conclusions: We believe that information about the activity of multiple sclerosis spinal cord lesions in patients with myelopathy may be extracted not only from contrast enhanced, but also from non-enhanced magnetic resonance images.

Ketamine, an N -methyl-d-aspartate Receptor Antagonist, Inhibits the Spinal Neuronal Responses to Distension of the Rat Urinary Bladder

2002 ◽  
Vol 96 (6) ◽  
pp. 1410-1419 ◽  
Author(s):  
Pablo J. Castroman ◽  
Timothy J. Ness
Keyword(s):  
Spinal Cord ◽  
Urinary Bladder ◽  
Spinal Dorsal Horn ◽  
Type I ◽  
Type Ii ◽  
Neuronal Responses ◽  
Spinal Dorsal ◽  
Aspartate Receptor ◽  
Dose Dependent ◽  
Intravenous Ketamine

Background The effect of ketamine as a treatment of visceral pain is not known. The current study investigated the effect of ketamine on spinal dorsal horn neurons excited by urinary bladder distension (UBD). The effect of other clinically available N-methyl-D-aspartate receptor antagonists on these responses was also studied. Methods Extracellular recordings of neurons located in the L6-S2 spinal dorsal horn of cervical spinal cord-transected, decerebrate female rats were obtained. Cutaneous receptive fields of neuronal units excited by UBD were characterized for responses to segmental noxious and nonnoxious stimuli. Nonsegmental noxious stimuli were also applied, and neurons were classified as type I (inhibited) and type II (noninhibited) by the stimulus. The effect of intravenous ketamine (1, 3, and 10 mg/kg), dextromethorphan (5 mg/kg), and memantine (16 mg/kg) on neuronal responses of these units was measured. Results Spontaneous and evoked neuronal activity to UBD was reduced in a dose-dependent fashion by ketamine. Responses to nonnoxious cutaneous stimuli were also significantly reduced after treatment. Dextromethorphan inhibited neuronal activity evoked by UBD in type I neurons. A similar selective effect of treatment on type I versus type II neurons was observed after intravenous ketamine and memantine. Conclusions Intravenous ketamine produces dose-dependent inhibition of the spinal cord neuronal responses evoked by UBD. All three N-methyl-D-aspartate receptor antagonists showed selective effects on spinal cord neurons subject to counterirritation. This neurophysiologic evidence supports a spinally mediated analgesic effect of ketamine in this model of urinary bladder nociception, an effect likely caused by N-methyl-D-aspartate receptor antagonism.

Regulation of neuropeptide release

1980 ◽  
Vol 210 (1178) ◽  
pp. 91-111 ◽  
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Gaba Receptors ◽  
Opiate Receptors ◽  
Sensory Nerve ◽  
Substantia Gelatinosa ◽  
Nerve Terminals ◽  
Analgesic Effects ◽  
Spinal Cord Level

The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulusevoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic γ -aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.

Bladder function after incomplete spinal cord injury in mice: quantifiable outcomes associated with bladder function and efficiency of dehydroepiandrosterone as a therapeutic adjunct

2004 ◽  
Vol 100 (1) ◽  
pp. 56-61
Author(s):  
Pierre-Yves Mure ◽  
Mark Galdo ◽  
Nathalie Compagnone
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mouse Model ◽  
Collagen Type ◽  
Neurological Recovery ◽  
Bladder Function ◽  
Type I ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

Object. The authors conducted a study to establish outcomes associated with bladder function in a mouse model of spinal cord injury (SCI) and to assess the sensitivity of these outcomes in determining the efficacy of pharmacological treatments. Methods. A mouse model of moderate contusive SCI was used. Outcome parameters included physiological, behavioral, and morphological measurements. To test the sensitivity of these outcomes, the authors used a dehydroepiandrosterone (DHEA) treatment that they had previously shown to promote neurological recovery effectively after SCI. A behavioral scale was used to identify the day at which autonomic function of the bladder was recovered. The reduction in the daily volume of urine during the period of functional recovery paralleled this scale. They then determined the day postinjury at which the functional differences between the vehicle- and DHEA-treated mice exhibited the maximal amplitude. Changes were measured in the composition of the extracellular matrix relative to collagen expression in the layer muscularis of the detrusor at this time point. They found that SCI increases the ratio of collagen type III to collagen type I in the detrusor. Moreover, in the DHEA-treated group, this ratio was similar to that demonstrated in sham-operated mice, establishing the sensitivity of this outcome to assess therapeutic benefits to the bladder function. They next examined the relationship between measurements of neurological recovery and controlled voiding by using cluster analysis. Conclusions. The authors found that early recovery of controlled voiding is predictive of motor recovery.

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