Stimulation of the Posterior Hypothalamus Produces Analgesia in Nociceptive and Neuropathic Pain

2.50
Hdl Handle:
http://hdl.handle.net/10755/161098
Type:
Presentation
Title:
Stimulation of the Posterior Hypothalamus Produces Analgesia in Nociceptive and Neuropathic Pain
Abstract:
Stimulation of the Posterior Hypothalamus Produces Analgesia in Nociceptive and Neuropathic Pain
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2006
Author:Jeong, Younhee, PhDc, RN
P.I. Institution Name:University of Illinois at Chicago
Title:Research Assistant
Contact Address:College of Nursing, 845 S. Damen Ave. #232, Chicago, IL, 60612, USA
Contact Telephone:312-996-3935
Co-Authors:Janean E. Holden, PhD, RN, Associate Professor
While all pain should be aggressively treated, neuropathic pain from damage to central or peripheral nerves often does not respond to standard treatments. One way to identify better treatments is to understand how the body process neuropathic pain. We showed that stimulating the posterior hypothalamus (PH) produces analgesia in acute, nociceptive pain. Using neuroanatomical techniques, we identified neurons in the PH that project to the A7 catecholamine cell group in the pons. The A7 cells project to the spinal cord dorsal horn and produce analgesia through release of norepinephrine. To investigate the role of A7 cells in PH-induced analgesia, we measured tail flick (TFL) and foot withdrawal latencies (FWL) in female Sprague-Dawley rats. Lightly anesthetized rats received microinjection of carbachol (125 nmol/0.05 ¦l normal saline) or normal saline for control into the left PH and analgesia was obtained. The alpha1-adrenoceptor antagonist WB4101 (97nmol), alpha2-adrenoceptor antagonist yohimbine (97nmol), or normal saline was given intrathecally following PH stimulation. WB4101 increased both TFL and FWL compared to controls, while yohimbine decreased both TFL and FWL. These data suggest that stimulating the PH produces analgesia mediated by alpha2-adrenoceptors while alpha1-adrenoceptors mediate a concomitant increased response to pain in the dorsal horn. To test whether the PH modifies neuropathic pain, we ligated the left sciatic nerve of rats to induce neuropathic pain. Rats that received carbachol (125 nmol) in the left PH had significantly longer latencies on the FWL for the affected left paw than rats that received saline (p < 0.05), suggesting that PH-induced analgesia occurs in neuropathic as well as nociceptive pain. Studies are ongoing to determine the role of A7 noradrenergic neurons in the neuropathic model. Such findings will lead to better treatments for neuropathic pain used by nurses.
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleStimulation of the Posterior Hypothalamus Produces Analgesia in Nociceptive and Neuropathic Painen_GB
dc.identifier.urihttp://hdl.handle.net/10755/161098-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Stimulation of the Posterior Hypothalamus Produces Analgesia in Nociceptive and Neuropathic Pain</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2006</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Jeong, Younhee, PhDc, RN</td></tr><tr class="item-institute"><td class="label">P.I. Institution Name:</td><td class="value">University of Illinois at Chicago</td></tr><tr class="item-author-title"><td class="label">Title:</td><td class="value">Research Assistant</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">College of Nursing, 845 S. Damen Ave. #232, Chicago, IL, 60612, USA</td></tr><tr class="item-phone"><td class="label">Contact Telephone:</td><td class="value">312-996-3935</td></tr><tr class="item-email"><td class="label">Email:</td><td class="value">yjeong2@uic.edu</td></tr><tr class="item-co-authors"><td class="label">Co-Authors:</td><td class="value">Janean E. Holden, PhD, RN, Associate Professor</td></tr><tr><td colspan="2" class="item-abstract">While all pain should be aggressively treated, neuropathic pain from damage to central or peripheral nerves often does not respond to standard treatments. One way to identify better treatments is to understand how the body process neuropathic pain. We showed that stimulating the posterior hypothalamus (PH) produces analgesia in acute, nociceptive pain. Using neuroanatomical techniques, we identified neurons in the PH that project to the A7 catecholamine cell group in the pons. The A7 cells project to the spinal cord dorsal horn and produce analgesia through release of norepinephrine. To investigate the role of A7 cells in PH-induced analgesia, we measured tail flick (TFL) and foot withdrawal latencies (FWL) in female Sprague-Dawley rats. Lightly anesthetized rats received microinjection of carbachol (125 nmol/0.05 &brvbar;l normal saline) or normal saline for control into the left PH and analgesia was obtained. The alpha1-adrenoceptor antagonist WB4101 (97nmol), alpha2-adrenoceptor antagonist yohimbine (97nmol), or normal saline was given intrathecally following PH stimulation. WB4101 increased both TFL and FWL compared to controls, while yohimbine decreased both TFL and FWL. These data suggest that stimulating the PH produces analgesia mediated by alpha2-adrenoceptors while alpha1-adrenoceptors mediate a concomitant increased response to pain in the dorsal horn. To test whether the PH modifies neuropathic pain, we ligated the left sciatic nerve of rats to induce neuropathic pain. Rats that received carbachol (125 nmol) in the left PH had significantly longer latencies on the FWL for the affected left paw than rats that received saline (p &lt; 0.05), suggesting that PH-induced analgesia occurs in neuropathic as well as nociceptive pain. Studies are ongoing to determine the role of A7 noradrenergic neurons in the neuropathic model. Such findings will lead to better treatments for neuropathic pain used by nurses.</td></tr></table>en_GB
dc.date.available2011-10-26T23:15:52Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T23:15:52Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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