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Spinal Cord Injury, Corticotropin

Wenling Chen, Yvette Taché, Juan Carlos Marvizón
Latent sensitization is a model of chronic pain in which an injury triggers a period of hyperalgesia followed by an apparent recovery, but in which pain sensitization persists but is suppressed by opioid and adrenergic receptors. One important characteristic of latent sensitization is that hyperalgesia can be triggered by acute stress. To determine whether the effect of stress is mimicked by the activation of corticotropin-releasing factor (CRF) signaling in the brain, rats with latent sensitization induced by injecting complete Freund's adjuvant (CFA, 50 μl) in one hind paw were given an intracerebroventricular (i...
June 15, 2018: Neuroscience
Natasha M Sosanya, Alex V Trevino, Roger L Chavez, Robert J Christy, Bopaiah P Cheppudira
Sound stress (SS) elicits behavioral changes, including pain behaviors. However, the neuronal mechanisms underlying SS-induced pain behaviors remain to be explored. The current study examined the effects of SS on nociceptive behaviors and changes in expression of the spinal corticotropin-releasing factor (CRF) system in male Sprague Dawley rats with and without thermal pain. We also studied the effects of SS on plasma corticosterone and fecal output. Rats were exposed to 3 days of SS protocol (n = 12/group)...
2017: Journal of Pain Research
Matthew Andreoli, Tanvi Marketkar, Eugene Dimitrov
We investigated the role of amygdala corticotropin-releasing factor (CRF) neurons in the perturbations of descending pain inhibition caused by neuropathic pain. Forced swim increased the tail-flick response latency in uninjured mice, a phenomenon known as stress-induced analgesia (SIA) but did not change the tail-flick response latency in mice with neuropathic pain caused by sciatic nerve constriction. Neuropathic pain also increased the expression of CRF in the central amygdala (CeAmy) and ΔFosB in the dorsal horn of the spinal cord...
December 2017: Experimental Neurology
Eun Hyun Kim, Da Hye Ryu, Sejin Hwang
Corticotropin-releasing factor (CRF) is a peptide involved in the activation of the hypothalamic-pituitary-adrenal (HPA) axis. CRF is distributed not only along the HPA axis but also throughout pain-relevant anatomical sites. CRF elicits potent antinociception at the three main levels of pain transmissions: namely, the brain, spinal cord, and peripheral sensory neurons. The widespread distribution of CRF receptors 1 and 2 in the brain offers several targets wherein CRF could alter pain, some of which may be independent of the HPA axis...
March 2011: Anatomy & Cell Biology
Leonardo C Welling, Eberval G Figueiredo
No abstract text is available yet for this article.
October 2010: World Neurosurgery
Michele Hummel, Terri Cummons, Peimin Lu, Lilly Mark, James E Harrison, Jeffrey D Kennedy, Garth T Whiteside
Corticotropin-releasing factor (CRF) plays a major role in controlling the body's response to stress. Because painful conditions are inherently stressful, we hypothesize that CRF may act via CRF-1 receptors to contribute to the pain experience. Studies were designed to investigate whether blocking CRF-1 receptors with selective antagonists or reducing their expression with CRF-Saporin, would attenuate ulcer, inflammatory- and neuropathic-like pain. Five experimental designs were undertaken. In experiment 1, ulcer pain was induced in mice following oral administration of indomethacin, while in experiments 2 and 3, inflammatory pain was induced in rats with either carrageenan or FCA, respectively...
September 2010: Neuropharmacology
H Yuan, S Xu, Y Wang, H Xu, C Wang, Q Zhu, R-K Yang, X Chen, P-C Yang, X Shi
OBJECTIVE: To evaluate the role of corticotrophin-releasing hormone (CRH) in facilitating axon outgrowth. BACKGROUND: Injured neural tissue is difficult to regenerate; the mechanism has not been fully understood. METHODS: A rat model of spinal cord transection injury was developed. Levels of BDNF, CRH and oligodendrocyte glycoprotein (OMgp) in injured spinal cord were monitored dynamically after surgery. Cellular interaction among rat dorsal root ganglia (DRG) cells, oligocondrocytes and microglial cells was observed with a coculture model...
December 2010: Spinal Cord
Dorien H Vrinten, Willem Hendrik Gispen, Cor J Kalkman, Roger A H Adan
BACKGROUND: The authors recently demonstrated that administration of the melanocortin-4 receptor antagonist SHU9119 decreased neuropathic pain symptoms in rats with a sciatic chronic constriction injury. The authors hypothesised that there is a balance between tonic pronociceptive effects of the spinal melanocortin system and tonic antinociceptive effects of the spinal opioid system. Therefore, they investigated a possible interaction between these two systems and tested whether opioid effectiveness could be increased through modulation of the spinal melanocortin system activity...
August 2003: Anesthesiology
Katarzyna Starowicz, Ryszard Przewlocki, Willem Hendrik Gispen, Barbara Przewlocka
Co-localization of opioid and melanocortin receptor expression, especially at the spinal cord level in the dorsal horn and in the gray matter surrounding the central canal led to the suggestion that melanocortins might play a role in nociceptive processes. In the present studies, we aimed to determine the effects of melanocortins, administered intrathecally, on allodynia, and to ascertain whether there is an interaction between opioid and melanocortin systems at the spinal cord level. Neuropathic pain was induced by chronic constriction injury (CCI) of the right sciatic nerve in rats...
December 20, 2002: Neuroreport
Soon Lee, Richard Miselis, Catherine Rivier
Testosterone (T) secretion is classically considered to be under the primary control of pituitary LH, itself regulated by the hypothalamic peptide LH-releasing hormone. Secretagogues present in the general circulation and/or manufactured in the testis can also alter Leydig cell activity independently of the pituitary. Finally, spanchnic innervation regulates testicular LH receptors and blood flow. In the present work, we provide evidence that, in addition, there may be a neural brain-testicular circuit that regulates T release function independently of LH release...
November 2002: Endocrinology
W Riedel, G Neeck
The physiology of nociception involves a complex interaction of peripheral and central nervous system (CNS) structures, extending from the skin, the viscera and the musculoskeletal tissues to the cerebral cortex. The pathophysiology of chronic pain shows alterations of normal physiological pathways, giving rise to hyperalgesia or allodynia. After integration in the spinal cord, nociceptive information is transferred to thalamic structures before it reaches the somatosensory cortex. Each of these levels of the CNS contain modulatory mechanisms...
December 2001: Zeitschrift Für Rheumatologie
D H Vrinten, R A Adan, G J Groen, W H Gispen
UNLABELLED: We investigated the involvement of the spinal cord melanocortin (MC) system in neuropathic pain. Because we recently demonstrated that MC receptor ligands acutely alter nociception in an animal model of neuropathic pain, in this study we tested whether chronic administration was also effective. We hypothesized that chronic blockade of the spinal MC system might decrease sensory abnormalities associated with this condition. The effects of the MC receptor antagonist SHU9119 (0...
December 2001: Anesthesia and Analgesia
D H Vrinten, W H Gispen, G J Groen, R A Adan
The presence of both pro-opiomelanocortin-derived peptides and melanocortin (MC) receptors in nociception-associated areas in the spinal cord suggests that, at the spinal level, the MC system might be involved in nociceptive transmission. In the present study, we demonstrate that a chronic constriction injury (CCI) to the rat sciatic nerve, a lesion that produces neuropathic pain, results in changes in the spinal cord MC system, as shown by an increased binding of (125)I-NDP-MSH to the dorsal horn. Furthermore, we investigated whether intrathecal administration (in the cisterna magna) of selective MC receptor ligands can affect the mechanical and cold allodynia associated with the CCI...
November 1, 2000: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
E A Joosten, B Majewska, D A Houweling, P R Bär, W H Gispen
Peptides related to melanotropin (alphaMSH) and corticotropin (ACTH), collectively termed melanocortins, are known to improve the postlesion repair of injured peripheral nerves. In addition, melanocortins exert trophic effects on the outgrowth of neurites from central nervous system neurons in vitro. Here we report, for the first time, the stimulation by alpha-MSH of spinal neurite outgrowth in vivo after injury. In the in vivo model, spinal cord trauma was produced at lower thoracic spinal levels of adult rats...
June 1999: Journal of Neurotrauma
M van der Kraan, J B Tatro, M L Entwistle, J H Brakkee, J P Burbach, R A Adan, W H Gispen
Although neurotrophic effects of alpha-melanocyte-stimulating hormone (alpha-MSH) are well established, the mechanism underlying these effects is unknown. To identify candidate components of the signaling system that may mediate these effects, in the present study rat spinal cord, dorsal root ganglia, sciatic nerve and soleus muscle were analysed for the expression of the neural MC3, MC4 and MC5 receptors and for the expression of the melanocortin precursor pro-opiomelanocortin (POMC). In rat lumbar spinal cord, the MC4 receptor was the only MC receptor subtype for which mRNA was detectable using RNAse protection assays...
January 8, 1999: Brain Research. Molecular Brain Research
T S Huang, Y H Wang, S H Lee, J S Lai
Twenty-five men with spinal cord injuries were studied for evaluation of the hypothalamus-pituitary-adrenal axis, using corticotropin-releasing hormone and insulin-induced hypoglycemia. Twenty-five age-matched healthy male volunteers served as controls. Three spinal cord-injured subjects had hyperprolactinemia, three had elevated basal follicle-stimulating hormone levels, one had an elevated basal luteinizing hormone level, and four had hypotestosteronemia. The mean plasma adrenocorticotropin response to corticotropin-releasing hormone of spinal cord-injured subjects was smaller than that of the healthy controls but did not reach a statistical significance...
March 1998: American Journal of Physical Medicine & Rehabilitation
H van de Meent, F P Hamers, A J Lankhorst, E A Joosten, W H Gispen
OBJECTIVE: Melanocortins, peptides related to melanocyte-stimulating hormone (MSH) and corticotropin (ACTH), exhibit neurotrophic and neuroprotective activity in several established models of peripheral and central nervous system damage. The beneficial effects of melanocortins on functional recovery after experimental brain damage and central demyelinating diseases have prompted us to investigate alpha MSH treatment in a weight drop model of traumatic spinal cord injury in rats. METHODS: In two independent randomized blinded experiments, treatment with either alpha MSH (75 micrograms/kg of body weight administered subcutaneously every 48 h for 3 weeks after trauma) or single high-dose (30 mg/kg, 30 min after injury) methylprednisolone was compared with saline treatment in rats subjected to a moderately severe 20-gcm weight drop injury...
January 1997: Neurosurgery
M Palkovits
Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS). Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival. Axotomy induces transient (1-21 d) upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin II, and neuropeptide Y...
April 1995: Molecular Neurobiology
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