scholarly journals C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons

2008 ◽  
Vol 295 (5) ◽  
pp. R1519-R1528 ◽  
Author(s):  
XiaoHui Ding ◽  
Fang Hua ◽  
Kristopher Sutherly ◽  
Jeffrey L. Ardell ◽  
Carole A. Williams
Keyword(s):  
Spinal Cord ◽  
Myocardial Ischemia ◽  
Dorsal Horn ◽  
Cervical Spinal Cord ◽  
Ibotenic Acid ◽  
Opioid Antagonist ◽  
Sprague Dawley ◽  
Thoracic Spinal Cord ◽  
Central Processing ◽  
Thoracic Spinal

During myocardial ischemia, the cranial cervical spinal cord (C1–C2) modulates the central processing of the cardiac nociceptive signal. This study was done to determine 1) whether C2 SCS-induced release of an analgesic neuropeptide in the dorsal horn of the thoracic (T4) spinal cord; 2) if one of the sources of this analgesic peptide was cervical propriospinal neurons, and 3) if chemical inactivation of C2 neurons altered local T4 substance P (SP) release during concurrent C2 SCS and cardiac ischemia. Ischemia was induced by intermittent occlusion of the left anterior descending coronary artery (CoAO) in urethane-anesthetized Sprague-Dawley rats. Release of dynorphin A (1-13), (DYN) and SP was determined using antibody-coated microprobes inserted into T4. SCS alone induced DYN release from laminae I–V in T4, and this release was maintained during CoAO. C2 injection of the excitotoxin, ibotenic acid, prior to SCS, inhibited T4 DYN release during SCS and ischemia; it also reversed the inhibition of SP release from T4 dorsal laminae during C2 SCS and CoAO. Injection of the κ-opioid antagonist, nor-binaltorphimine, into T4 also allowed an increased SP release during SCS and CoAO. CoAO increased the number of Fos-positive neurons in T4 dorsal horns but not in the intermediolateral columns (IML), while SCS (either alone or during CoAO) minimized this dorsal horn response to CoAO alone, while inducing T4 IML neuronal recruitment. These results suggest that activation of cervical propriospinal pathways induces DYN release in the thoracic spinal cord, thereby modulating nociceptive signals from the ischemic heart.

Responses of T2-4 spinal cord neurons to irritation of the lower airways in the rat

1997 ◽  
Vol 273 (3) ◽  
pp. R1147-R1157 ◽  
Author(s):  
T. Hummel ◽  
J. N. Sengupta ◽  
S. T. Meller ◽  
G. F. Gebhart
Keyword(s):  
Spinal Cord ◽  
Afferent Input ◽  
Sprague Dawley ◽  
Spinal Neurons ◽  
Thoracic Spinal Cord ◽  
Spinal Cord Neurons ◽  
Thoracic Spinal ◽  
Balloon Distension ◽  
Sprague Dawley Rats ◽  
Lower Airways

The aim of the study was to investigate the information processing in the thoracic spinal cord (T2-4) after chemical irritation of the lower airways. Experiments were performed in pentobarbital sodium-anesthetized and pancuronium-paralyzed male Sprague-Dawley rats. Balloon distension of the esophagus was used as the search stimulus. Ammonia and smoke were applied by means of a tracheal cannula; they produced excitatory, inhibitory, and biphasic responses in a concentration-related manner (ammonia 39/39; smoke 23/ 39). Inhaled irritant-responsive neurons exhibited a number of similarities that have been described for neurons responding to stimulation of other thoracic viscera. These similarities relate to the distribution of neurons in the deeper laminae of the thoracic spinal cord, the relatively small number of neurons receiving input from the lower airways, the extensive convergent input from the skin and other thoracic viscera, and the pattern of responses. In addition, both stimulus-induced responses and spontaneous activity are subject to modulation from supraspinal sites. On the basis of responses to inhaled irritants after either spinal cord or vagus nerve block/transection, these T2-4 spinal neurons are likely to receive spinal afferent input that is modulated by vagal-brain stem input.

Selective cephalic upregulation of p-ERK, CamKII and p-CREB in response to glyceryl trinitrate infusion

Cephalalgia ◽  
2017 ◽  
Vol 38 (6) ◽  
pp. 1057-1070 ◽  
Author(s):  
Roshni Ramachandran ◽  
Sara Hougaard Pedersen ◽  
Dipak Vasantrao Amrutkar ◽  
Steffen Petersen ◽  
Julie Mie Jacobsen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglion ◽  
Dorsal Horn ◽  
Trigeminal Ganglion ◽  
Dura Mater ◽  
Dorsal Root ◽  
Spinal Cord Dorsal Horn ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Extracellular Signal

Background A common characteristic of migraine-inducing substances is that they cause headache and no pain in other areas of the body. Few studies have compared pain mechanisms in the trigeminal and spinal systems and, so far, no major differences have been noted. We compared signalling molecules in the trigeminal and spinothalamic system after infusion of the migraine-provoking substance glyceryltrinitrate. Method A catheter was placed in the femoral vein of rats and one week later glyceryltrinitrate 4 µg/kg/min was infused for 20 min. Protein expression in the dura mater, trigeminal ganglion, nucleus caudalis, dorsal root ganglion and the dorsal horn of the thoracic spinal cord was analysed at different time points using western blotting and immunohistochemistry. Results Glyceryltrinitrate caused a threefold increase in expression of phosphorylated extracellular signal-regulated kinases at 30 min in the dura mater and nucleus caudalis ( P < 0.05) and at 2 h in the trigeminal ganglion with very few expressions in the dorsal root ganglion. In the nucleus caudalis, expression of phosphorylated extracellular signal-regulated kinases and Cam KII increased 2.6-fold and 3.2-fold, respectively, at 2 h after glycerytrinitrate infusion ( P < 0.01). p-CREB/ATF-1 upregulation was observed only at 30 min ( P < 0.05) in the nucleus caudalis. None of these markers showed increased expression in the regions of thoracic spinal cord dorsal horn. Conclusion The dura, trigeminal ganglion and nucleus caudalis are activated shortly after glycerytrinitrate infusion with long-lasting expression of phosphorylated extracellular signal-regulated kinases observed in the nucleus caudalis. These activations were not observed at the spinal level.

scholarly journals Spinal cord neural network interactions: implications for sympathetic control of the porcine heart

2020 ◽  
Vol 318 (4) ◽  
pp. H830-H839
Author(s):  
Erica A. Dale ◽  
Jasmine Kipke ◽  
Yukiko Kubo ◽  
Michael D. Sunshine ◽  
Peter A. Castro ◽  
...  
Keyword(s):  
Neural Network ◽  
Spinal Cord ◽  
Myocardial Ischemia ◽  
Autonomic Response ◽  
Electrode Arrays ◽  
Vessel Occlusion ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cross Correlation Analysis ◽  
Ischemic Stress

Inherent and acquired factors determine the integrated autonomic response to cardiovascular stressors. Excessive sympathoexcitation to ischemic stress is a major contributor to the potential for sudden cardiac death. To define fundamental aspects of cardiac-related autonomic neural network interactions within the thoracic cord, specifically as related to modulating sympathetic preganglionic (SPN) neural activity. Adult, anesthetized Yorkshire pigs ( n = 10) were implanted with penetrating high-density microarrays (64 electrodes) at the T2 level of the thoracic spinal cord to record extracellular potentials concurrently from left-sided dorsal horn (DH) and SPN neurons. Electrical stimulation of the T2 paravertebral chain allowed for antidromic identification of SPNs located in the intermediolateral cell column (57 of total 1,760 recorded neurons). Cardiac stressors included epicardial touch, occlusion of great vessels to transiently alter preload/afterload, and transient occlusion of the left anterior descending coronary artery (LAD). Spatial/temporal assessment of network interactions was characterized by cross-correlation analysis. While some DH neurons responded solely to changes in preload/afterload (8.5 ± 1.9%) or ischemic stress (10.5 ± 3.9%), the majority of cardiovascular-related DH neurons were multimodal (30.2 ± 4.7%) with ischemia sensitivity being one of the modalities (26.1 ± 4.7%). The sympathoexcitation associated with transient LAD occlusion was associated with increased correlations from baseline within DH neurons (2.43 ± 0.61 to 7.30 ± 1.84%, P = 0.04) and between SPN to DH neurons (1.32 ± 0.78 to 7.24 ± 1.84%, P = 0.02). DH to SPN network correlations were reduced during great vessel occlusion. In conclusion, increased intrasegmental network coherence within the thoracic spinal cord contributes to myocardial ischemia-induced sympathoexcitation. NEW & NOTEWORTHY In an in vivo pig model, we demonstrate using novel high-resolution neural electrode arrays that increased intrasegmental network coherence within the thoracic spinal cord contributes to myocardial ischemia-induced sympathoexcitation.

scholarly journals Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management

1999 ◽  
Vol 6 (1) ◽  
pp. E6 ◽  
Author(s):  
Fernando L. Vale ◽  
Jennifer Burns ◽  
Amie B. Jackson ◽  
Mark N. Hadley
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Cervical Spinal Cord ◽  
Bladder Function ◽  
Thoracic Spinal Cord ◽  
Arterial Blood ◽  
Thoracic Spinal ◽  
Cord Injury

The optimal management of acute spinal cord injuries remains to be defined. The authors prospectively applied resuscitation principles of volume expansion and blood pressure maintenance to 77 patients who presented with acute neurological deficits as a result of spinal cord injuries occurring from C-1 through T-12 in an effort to maintain spinal cord blood flow and prevent secondary injury. According to the Intensive Care Unit protocol, all patients were managed by Swan-Ganz and arterial blood pressure catheters and were treated with immobilization and fracture reduction as indicated. Intravenous fluids, colloid, and vasopressors were administered as necessary to maintain mean arterial blood pressure above 85 mm Hg. Surgery was performed for decompression and stabilization, and fusion in selected cases. Sixty-four patients have been followed at least 12 months postinjury by means of detailed neurological assessments and functional ability evaluations. Sixty percent of patients with complete cervical spinal cord injuries improved at least one Frankel or American Spinal Injury Association (ASIA) grade at the last follow-up review. Thirty percent regained the ability to walk and 20% had return of bladder function 1 year postinjury. Thirty-three percent of the patients with complete thoracic spinal cord injuries improved at least one Frankel or ASIA grade. Approximately 10% of the patients regained the ability to walk and had return of bladder function. As of the 12-month follow-up review, 92% of patients demonstrated clinical improvement after sustaining incomplete cervical spinal cord injuries compared to their initial neurological status. Ninety-two percent regained the ability to walk and 88% regained bladder function. Eighty-eight percent of patients with incomplete thoracic spinal cord injuries demonstrated significant improvements in neurological function 1 year postinjury. Eighty-eight percent were able to walk and 63% had return of bladder function. The authors conclude that the enhanced neurological outcome that was observed in patients after spinal cord injury in this study was in addition to, and/or distinct from, any potential benefit provided by surgery. Early and aggressive medical management (volume resuscitation and blood pressure augmentation) of patients with acute spinal cord injuries optimizes the potential for neurological recovery after sustaining trauma.

scholarly journals Sulcal artery syndrome presenting as an incomplete Brown–Sequard syndrome – Report of an unusual case and review of the literature

2020 ◽  
Vol 29 (1) ◽  
pp. 59-63
Author(s):  
May Myat Win ◽  
Monica Saini ◽  
Shrikant Digambarrao Pande ◽  
Kappaganthu Venkatesh Prasanna
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Vertebral Artery Dissection ◽  
Artery Occlusion ◽  
Sudden Onset ◽  
Artery Dissection ◽  
Spinal Cord Infarction ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Brown Sequard Syndrome

Sulcal arteries perfuse the anterior two-thirds of the spinal cord, and spinal cord infarction as a result of sulcal artery occlusion is rare. Most reported cases are associated with vertebral artery dissection, and commonly involve the cervical spinal cord. A 74-year-old man presented with sudden onset weakness and numbness after a brief bout of abdominal pain. Further investigations concluded that this was sulcal artery syndrome. We report a case of sulcal artery syndrome affecting the thoracic spinal cord presenting as Brown–Sequard syndrome. Sulcal artery syndrome usually has good prognoses, unlike anterior spinal artery infarction.

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