Mo1869 Increased Substance P Immunoreactivity in the Dorsal Horn of the Thoracic Spinal Cord is Sustained Following Acute and Chronic Colitis

2012 ◽  
Vol 142 (5) ◽  
pp. S-704
Author(s):  
Jessica Benson ◽  
Stephen J. Vanner ◽  
Alan Lomax
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Dorsal Horn ◽  
Chronic Colitis ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

Myocardial ischemia induces the release of substance P from cardiac afferent neurons in rat thoracic spinal cord

2004 ◽  
Vol 286 (5) ◽  
pp. H1654-H1664 ◽  
Author(s):  
Fang Hua ◽  
Brian A. Ricketts ◽  
Angela Reifsteck ◽  
Jeffrey L. Ardell ◽  
Carole A. Williams
Keyword(s):  
Spinal Cord ◽  
Coronary Artery ◽  
Substance P ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Afferent Neurons ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cardiac Afferents ◽  
Stimulation Of

Antibody-coated microprobes were inserted into the thoracic (T3–4) spinal cord in urethane-anesthetized Sprague-Dawley rats to detect the differences in the release of immunoreactive substance P-like (irSP) substances in response to differential activation of cardiac nociceptive sensory neurons (CNAN). CNAN were stimulated either by intrapericardial infusion of an inflammatory ischemic exudate solution (IES) containing algogenic substances (i.e., 10 mM each of adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine), or by transient occlusion of the left anterior descending coronary artery (CoAO). There was widespread basal release of irSP from the thoracic spinal cord. Stimulation of the CNAN by IES did not alter the pattern of release of irSP. Conversely, CoAO augmented the release of irSP from T3–4 spinal segments from laminae I–VII. This CoAO-induced irSP release was eliminated after thoracic dorsal rhizotomy. These results indicate that heterogeneous activation of cardiac afferents, as with focal coronary artery occlusion, represents an optimum input for activation of the cardiac neuronal hierarchy and for the resultant perception of angina. Excessive stimulation of cardiac nociceptive afferent neurons elicited during regional coronary artery occlusion involves the release of SP in the thoracic spinal cord and suggests that local spinal cord release of SP may be involved in the neural signaling of angina.

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.

Left vagal stimulation induces dynorphin release and suppresses substance P release from the rat thoracic spinal cord during cardiac ischemia

2004 ◽  
Vol 287 (6) ◽  
pp. R1468-R1477 ◽  
Author(s):  
Fang Hua ◽  
Jeffrey L. Ardell ◽  
Carole A. Williams
Keyword(s):  
Spinal Cord ◽  
Coronary Artery ◽  
Substance P ◽  
Vagal Stimulation ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Vagal Afferents ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Vagal Afferent

Electrostimulatory forms of therapy can reduce angina that arises from activation of cardiac nociceptive afferent fibers during transient ischemia. This study sought to determine the effects of electrical stimulation of left thoracic vagal afferents (C8–T1 level) on the release of putative nociceptive [substance P (SP)] and analgesic [dynorphin (Dyn)] peptides in the dorsal horn at the T4 spinal level during coronary artery occlusion in urethane-anesthetized Sprague-Dawley rats. Release of Dyn and SP was measured by using antibody-coated microprobes. While Dyn and SP had a basal release, occlusion of the left anterior descending coronary artery only affected SP release, causing an increase from lamina I-VII. Left vagal stimulation increased Dyn release, inhibited basal SP release, and blunted the coronary artery occlusion-induced release of SP. Dyn release reflected activation of descending pathways in the thoracic spinal cord, because vagal afferent stimulation still increased the release of Dyn after bilateral dorsal rhizotomy of T2–T5. These results indicate that electrostimulatory therapy, using vagal afferent excitation, may induce analgesia, in part, via inhibition of the release of SP in the spinal cord, possibly through a Dyn-mediated neuronal interaction.

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