Changes in G proteins genes expression in rat lumbar spinal cord support the inhibitory effect of chronic pain on the development of tolerance to morphine analgesia

2005 ◽  
Vol 53 (3) ◽  
pp. 250-256 ◽  
Author(s):  
Mohammad Javan ◽  
Abolhassan Ahmadiani ◽  
Fereshteh Motamadi ◽  
Bahram Kazemi
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
G Proteins ◽  
Inhibitory Effect ◽  
Lumbar Spinal Cord ◽  
Morphine Analgesia ◽  
Genes Expression ◽  
Lumbar Spinal ◽  
Development Of Tolerance

scholarly journals Alterations in the Anandamide Metabolism in the Development of Neuropathic Pain

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Natalia Malek ◽  
Mateusz Kucharczyk ◽  
Katarzyna Starowicz
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Mrna Level ◽  
Inhibitory Effect ◽  
Lumbar Spinal Cord ◽  
Local Synthesis ◽  
Time Points ◽  
Pain Pathways ◽  
Lumbar Spinal ◽  
Synthesis And Degradation

Endocannabinoids (EC), particularly anandamide (AEA), released constitutively in pain pathways might be accountable for the inhibitory effect on nociceptors. Pathogenesis of neuropathic pain may reflect complex remodeling of the dorsal root ganglia (DRGs) and spinal cord EC system. Multiple pathways involved both in the biosynthesis and degradation of AEA have been suggested. We investigated the local synthesis and degradation features of AEA in DRGs and spinal cord during the development and maintenance of pain in a model of chronic constriction injury (CCI). All AEA synthesis and degradation enzymes are present on the mRNA level in DRGs and lumbar spinal cord of intact as well as CCI-treated animals. Deregulation of EC system components was consistent with development of pain phenotype at days 3, 7, and 14 after CCI. The expression levels of enzymes involved in AEA degradation was significantly upregulated ipsilateral in DRGs and spinal cord at different time points. Expression of enzymes of the alternative, sPLA2-dependent and PLC-dependent, AEA synthesis pathways was elevated in both of the analyzed structures at all time points. Our data have shown an alteration of alternative AEA synthesis and degradation pathways, which might contribute to the variation of AEA levels and neuropathic pain development.

Differential Spinal Cord Gene Expression in Rodent Models of Radicular and Neuropathic Pain

2006 ◽  
Vol 104 (6) ◽  
pp. 1283-1292 ◽  
Author(s):  
Michael L. LaCroix-Fralish ◽  
Vivianne L. Tawfik ◽  
Flobert Y. Tanga ◽  
Kevin F. Spratt ◽  
Joyce A. DeLeo
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Chronic Pain ◽  
Polymerase Chain Reaction ◽  
Mechanical Allodynia ◽  
Lumbar Spinal Cord ◽  
Chain Reaction ◽  
Pain Models ◽  
Polymerase Chain ◽  
Lumbar Spinal

Background Neuropathic pain and radicular low back pain both have a major impact on human health worldwide. Microarray gene analysis on central nervous system tissues holds great promise for discovering novel targets for persistent pain modulation. Methods Rat models of lumbar radiculopathy (L5 nerve root ligation) and neuropathy (L5 spinal nerve transection) were used for these studies. The authors measured mechanical allodynia followed by analysis of global gene expression in the lumbar spinal cord at two time points (7 days and 14 days) after surgery using the Affymetrix RAE230A GeneChip(R) (Santa Clara, CA). The expression patterns of several genes of interest were subsequently confirmed using real-time reverse transcriptase polymerase chain reaction. Results The authors observed similarly robust mechanical allodynia in both models. Second, they observed significant differences in lumbar spinal cord gene expression across chronic pain models. There was little overlap between genes altered in each injury model, suggesting that the site and type of injury produce distinct spinal mechanisms mediating the observed mechanical allodynia. The authors further confirmed a subset of the genes using reverse transcriptase polymerase chain reaction and identified several genes as either neuropathy-associated genes or radiculopathy-associated genes. Conclusions These two models of persistent pain produce similar allodynic outcomes but produce differential gene expression. These results suggest that diverging mechanisms lead to a common behavioral outcome in these pain models. Furthermore, these distinct pathophysiologic mechanisms in neuropathic versus radicular pain may implicate unique drug therapies for these types of chronic pain syndromes.

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.

Aging process of the human lumbar spinal cord: A morphometric analysis

1996 ◽  
Vol 16 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Ming Zhou ◽  
Noboru Goto ◽  
Chen Zhang ◽  
Wei Tang
Keyword(s):  
Spinal Cord ◽  
Morphometric Analysis ◽  
Aging Process ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal

scholarly journals Multi-pronged neuromodulation intervention engages the residual motor circuitry to facilitate walking in a rat model of spinal cord injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marco Bonizzato ◽  
Nicholas D. James ◽  
Galyna Pidpruzhnykova ◽  
Natalia Pavlova ◽  
Polina Shkorbatova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Stress Responses ◽  
Learning Algorithm ◽  
Lumbar Spinal Cord ◽  
Cord Injury ◽  
Potential Synergy ◽  
Lumbar Spinal ◽  
Deep Brain

AbstractA spinal cord injury usually spares some components of the locomotor circuitry. Deep brain stimulation (DBS) of the midbrain locomotor region and epidural electrical stimulation of the lumbar spinal cord (EES) are being used to tap into this spared circuitry to enable locomotion in humans with spinal cord injury. While appealing, the potential synergy between DBS and EES remains unknown. Here, we report the synergistic facilitation of locomotion when DBS is combined with EES in a rat model of severe contusion spinal cord injury leading to leg paralysis. However, this synergy requires high amplitudes of DBS, which triggers forced locomotion associated with stress responses. To suppress these undesired responses, we link DBS to the intention to walk, decoded from cortical activity using a robust, rapidly calibrated unsupervised learning algorithm. This contingency amplifies the supraspinal descending command while empowering the rats into volitional walking. However, the resulting improvements may not outweigh the complex technological framework necessary to establish viable therapeutic conditions.

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