scholarly journals Microglial deactivation by adeno‐associated virus expressing small‐hairpin GCH1 has protective effects against neuropathic pain development in a spinothalamic tract‐lesion model

2021 ◽  
Author(s):  
Hyun Ho Jung ◽  
Chin Su Koh ◽  
Minkyung Park ◽  
Ji Hyun Kim ◽  
Ha‐Na Woo ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Protective Effects ◽  
Spinothalamic Tract ◽  
Adeno Associated Virus

scholarly journals Hypersensitivity of Spinothalamic Tract Neurons Associated With Diabetic Neuropathic Pain in Rats

2002 ◽  
Vol 87 (6) ◽  
pp. 2726-2733 ◽  
Author(s):  
Shao-Rui Chen ◽  
Hui-Lin Pan
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Thermal Hyperalgesia ◽  
Diabetic Rats ◽  
Projection Neurons ◽  
Diabetic Neuropathic Pain ◽  
Spinothalamic Tract ◽  
Functional Changes ◽  
Spinal Dorsal

Diabetic neuropathic pain is often considered to be caused by peripheral neuropathy. The involvement of the CNS in this pathological condition has not been well documented. Development of hypersensitivity of spinal dorsal horn neurons is involved in neuropathic pain induced by traumatic nerve injury. In the present study, we determined the functional changes of identified spinothalamic tract (STT) neurons and their correlation to diabetic neuropathic pain. Diabetes was induced in rats by intraperitoneal injection of streptozotocin. Hyperalgesia and allodynia were assessed by the withdrawal responses to pressure, radiant heat, and von Frey filaments applied to the hindpaw. Single-unit activity of STT neurons was recorded from the lumbar spinal cord in anesthetized rats. The responses of STT neurons to mechanical and thermal stimuli and the sensitivity to intravenous morphine were determined in diabetic and normal rats. In 12 diabetic rats, mechanical allodynia and hyperalgesia, but not thermal hyperalgesia, developed within 2 wk after streptozotocin injection and lasted for ≥7 wk. Compared to the 32 STT neurons recorded in normal animals, the 37 STT neurons in diabetic rats displayed a higher spontaneous discharge activity and enlarged receptive fields. Also, the STT neurons in diabetic rats exhibited lower thresholds and augmented responses to mechanical stimulation. Intravenous injection of 2.5 mg/kg of morphine suppressed significantly the responses of STT neurons to noxious stimuli in 12 nondiabetic rats. However, such an inhibitory effect of morphine on the evoked response of STT neurons was diminished in 14 diabetic animals. This electrophysiological study provides new information that development of hypersensitivity of spinal dorsal horn projection neurons may be closely related to neuropathic pain symptoms caused by diabetes. Furthermore, the attenuated inhibitory effects of morphine on evoked responses of STT neurons in diabetes likely accounts for its reduced analgesic efficacy in this clinical form of neuropathic pain.

scholarly journals Protective Effects of Human and Mouse Soluble Scavenger-Like CD6 Lymphocyte Receptor in a Lethal Model of Polymicrobial Sepsis

2016 ◽  
Vol 61 (1) ◽  
Author(s):  
Mario Martínez-Florensa ◽  
Marta Consuegra-Fernández ◽  
Fernando Aranda ◽  
Noelia Armiger-Borràs ◽  
Marianna Di Scala ◽  
...  
Keyword(s):  
Adjunctive Therapy ◽  
Cecal Ligation ◽  
Experimental Models ◽  
Polymicrobial Sepsis ◽  
Soluble Form ◽  
Protective Effects ◽  
Adeno Associated Virus ◽  
Time Points ◽  
Cytokine Levels ◽  
Human And Mouse

ABSTRACT Sepsis still constitutes an unmet clinical need, which could benefit from novel adjunctive strategies to conventional antibiotic therapy. The soluble form of the scavenger-like human CD6 lymphocyte receptor (shCD6) binds to key pathogenic components from Gram-positive and -negative bacteria and shows time- and dose-dependent efficacy in mouse models of monobacterial sepsis. The objective of the present work was to demonstrate the effectiveness of infusing mouse and human sCD6 by different systemic routes, either alone or as adjunctive therapy to gold standard antibiotics, in a lethal model of polymicrobial sepsis. To this end, C57BL/6 mice undergoing high-grade septic shock induced by cecal ligation and puncture (CLP; ≥90% lethality) were infused via the intraperitoneal (i.p.) or intravenous (i.v.) route with shCD6 at different doses and time points, either alone or in combination with imipenem/cilastatin (I/C) at a dose of 33 mg/kg of body weight every 8 h. Significantly reduced mortality and proinflammatory cytokine levels were observed by i.p. infusion of a single shCD6 dose (1.25 mg/kg) 1 h pre- or post-CLP. When using the i.v. route, mice survival was significantly extended by starting shCD6 infusion at later time points post-CLP (up to 6 h after CLP). Significant adjunctive effects on mouse survival were observed by i.p. or i.v. infusion of shCD6 in combination with i.p. I/C post-CLP. Similar results were obtained in mice expressing high sustained levels (5 to 10 μg/ml) of mouse sCD6 in serum by means of transduction with hepatotropic adeno-associated virus (AAV). Taken together, the data support the conserved antibacterial effects of human and mouse sCD6 and their use as adjunctive therapy in experimental models of complex and severe polymicrobial sepsis.

Neuropathic pain

2011 ◽  
Author(s):  
John Scadding
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Sensory System ◽  
Diagnostic Category ◽  
Sensory Loss ◽  
Clinical Feature ◽  
Tissue Destruction ◽  
Spinothalamic Tract ◽  
Protective Function ◽  
Paradoxical Situation

Pain signalled by a normal sensory system, nociceptive pain, serves a vital protective function. The peripheral and central nervous somatosensory systems permit rapid localization and identification of the nature of painful stimuli, prior to appropriate action to minimize or avoid potentially tissue damaging events. A reduction or absence of pain resulting from neurological disease emphasizes the importance of this normal protective function of pain. For example, tissue destruction occurs frequently in peripheral nerve diseases which cause severe sensory loss such as leprosy, and in central disorders such as syringomyelia. Neuropathic pain results from damage to somatosensory pathways and serves no protective function. This chapter provides an overview of neuropathic pain, considering its context, clinical features, pathophysiology, and treatment.In the peripheral nervous system, neuropathic pain is caused by conditions affecting small nerve fibres, and in the central nervous system by lesions of the spinothalamic tract and thalamus, and rarely by subcortical and cortical lesions. The clinical feature common to virtually all conditions leading to the development of neuropathic pain is the perception of pain in an area of sensory impairment, an apparently paradoxical situation. The exception is trigeminal neuralgia.Neuropathic pain is heterogeneous clinically, aetiologically, and pathophysiologically. Within a given diagnostic category, whether defined clinically or aetiologically, there are wide variations in reports of pain by patients. This heterogeneity poses one of the greatest challenges in understanding the mechanisms of neuropathic pain. Knowledge of the pathophysiology is an obvious pre-requisite to the development of effective treatments. The goal of a pathophysiologically based understanding of the symptoms and signs of neuropathic pain is, of course, just such a rational and specific approach to treatment. While this is not yet achievable, clinical-pathophysiological correlations have led to some recent advances in treatment.

scholarly journals Changes in Diffuse Tensor Imaging and Therapeutic Effect of Repetitive Transcranial Magnetic Stimulation in Traumatic Brain Injury with Central Pain

2020 ◽  
Vol 10 (12) ◽  
pp. 929
Author(s):  
Dong-Ha Kang ◽  
Gi-Wook Kim
Keyword(s):  
Traumatic Brain Injury ◽  
Neuropathic Pain ◽  
Diffusion Tensor Imaging ◽  
Magnetic Stimulation ◽  
Diffusion Tensor ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Central Pain ◽  
Spinothalamic Tract ◽  
Before And After ◽  
Diffusion Tensor Imaging Dti

Post-trauma chronic pain characterized by central pain is a symptom following traumatic brain injury (TBI). Studies on the effect of repetitive transcranial magnetic stimulation (rTMS) on central pain and the association between central pain and spinothalamic tract (STT) have been reported, but few studies have examined the effect of rTMS in patients with mild TBI with central pain through changes in diffusion tensor imaging (DTI)-based metrics of STT before and after rTMS. This case series aimed to investigate the therapeutic effect of rTMS in TBI with central pain and the changes in diffusion tensor imaging (DTI)-based metrics of the spinothalamic tract (STT) before and after rTMS. This study included four patients who complained of severe pain in the left or right side of the body below the neck area after a car accident. We performed numeric rating scale (NRS), bedside sensory examination, electrodiagnostic study, and DTI-based metrics of the STT before and after rTMS. According to the guidelines of the diagnosis and grading for neuropathic pain, all patients had neuropathic pain corresponding to “probable grade.” In all patients, rTMS was applied to the contralateral M1 cortex on the more painful side. There were no medication changes and other interventions during the rTMS. After rTMS, NRS decreased, bed sensory testing improved, and DTI-based STT metrics increased in all patients compared to before rTMS.

scholarly journals In vivo and in vitro protective effects of omeprazole against neuropathic pain

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Sanjay K. Chanchal ◽  
Umesh B. Mahajan ◽  
Sumit Siddharth ◽  
Navyya Reddy ◽  
Sameer N. Goyal ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Protective Effects

Neurotrophin-3 Has Protective Effects in a Neuropathic Pain Rat Model

Neurosurgery ◽  
2009 ◽  
Vol 65 (2) ◽  
pp. 414-415
Author(s):  
Gabriel Claudiu Tender ◽  
Jian-Guo Cui
Keyword(s):  
Neuropathic Pain ◽  
Rat Model ◽  
Protective Effects ◽  
Neurotrophin 3
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