Stimulation of the Lateral Hypothalamus Produces Analgesia Mediated by the A7 Catecholamine Cell Group in the Pons

2.50
Hdl Handle:
http://hdl.handle.net/10755/149368
Type:
Presentation
Title:
Stimulation of the Lateral Hypothalamus Produces Analgesia Mediated by the A7 Catecholamine Cell Group in the Pons
Abstract:
Stimulation of the Lateral Hypothalamus Produces Analgesia Mediated by the A7 Catecholamine Cell Group in the Pons
Conference Sponsor:Sigma Theta Tau International
Conference Year:2001
Conference Date:November 10 - 14, 2001
Author:Naleway, Erin
P.I. Institution Name:University of Illinois at Chicago
Pain is a clinical problem that cuts across all age groups. Although clinicians are becoming increasingly more aware of the need to treat pain aggressively, many pain conditions respond poorly to current therapies. An understanding of endogenous pain modulatory systems may promote more effective treatments for clinical pain states. The lateral hypothalamus (LH) receives pain stimuli through the spinohypothalamic tract, which implies that the LH is part of the endogenous pain modulation system. Electrical, but not glutamate, stimulation of the LH produces analgesia that is partially blocked by intrathecal noradrenergic antagonists, indicating that fibers of passage rather than neurons in the LH produce this analgesic effect. However, the LH contains neurons immunoreactive for the excitatory neurotransmitters substance P and neurotensin that project to the A7 catecholamine cell group in the pons. The A7 cell group sends axons to the spinal cord dorsal horn and, when stimulated, produces analgesia blocked by intrathecal noradrenergic antagonists. The existence of an excitatory connection between the LH and the A7 cell group suggests an active role for the LH in this pathway. To investigate the role of the LH in analgesia mediated by the A7 cell group, 125 nmol solution of the cholinergic agonist carbachol was microinjected into the LH at the level of the dorsal hippocampus in female Sprague-Dawley rats and compared to saline microinjection for controls. Analgesia was obtained on the tail flick test (6.40 ± 0.4 vs. 3.30 ± 0.14, carbachol and saline respectively) that lasted for almost 30minutes. Intrathecal administration of 194 nmol solution of yohimbine following carbachol microinjection in the LH resulted in a significant hyperalgesic response, returning the response to baseline levels (p<0.05). Intrathecal administration of WB4101 (194 nmol) facilitated analgesia. These findings suggest that stimulation of neurons in the LH activates a bidirectional pathway in the A7 cell group in which: (1) analgesia occurs from the actions of alpha2 andreoceptors and, (2) pain facilitation occurs from the actions of alpha1 adrenoceptors in the dorsal horn. These findings suggest that the LH and/or the A7 cell group may be sites for the development of tolerance to pain medication.
Repository Posting Date:
26-Oct-2011
Date of Publication:
10-Nov-2001
Sponsors:
Sigma Theta Tau International

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleStimulation of the Lateral Hypothalamus Produces Analgesia Mediated by the A7 Catecholamine Cell Group in the Ponsen_GB
dc.identifier.urihttp://hdl.handle.net/10755/149368-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Stimulation of the Lateral Hypothalamus Produces Analgesia Mediated by the A7 Catecholamine Cell Group in the Pons</td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Sigma Theta Tau International</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2001</td></tr><tr class="item-conference-date"><td class="label">Conference Date:</td><td class="value">November 10 - 14, 2001</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Naleway, Erin</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-email"><td class="label">Email:</td><td class="value">enalew1@uic.edu</td></tr><tr><td colspan="2" class="item-abstract">Pain is a clinical problem that cuts across all age groups. Although clinicians are becoming increasingly more aware of the need to treat pain aggressively, many pain conditions respond poorly to current therapies. An understanding of endogenous pain modulatory systems may promote more effective treatments for clinical pain states. The lateral hypothalamus (LH) receives pain stimuli through the spinohypothalamic tract, which implies that the LH is part of the endogenous pain modulation system. Electrical, but not glutamate, stimulation of the LH produces analgesia that is partially blocked by intrathecal noradrenergic antagonists, indicating that fibers of passage rather than neurons in the LH produce this analgesic effect. However, the LH contains neurons immunoreactive for the excitatory neurotransmitters substance P and neurotensin that project to the A7 catecholamine cell group in the pons. The A7 cell group sends axons to the spinal cord dorsal horn and, when stimulated, produces analgesia blocked by intrathecal noradrenergic antagonists. The existence of an excitatory connection between the LH and the A7 cell group suggests an active role for the LH in this pathway. To investigate the role of the LH in analgesia mediated by the A7 cell group, 125 nmol solution of the cholinergic agonist carbachol was microinjected into the LH at the level of the dorsal hippocampus in female Sprague-Dawley rats and compared to saline microinjection for controls. Analgesia was obtained on the tail flick test (6.40 &plusmn; 0.4 vs. 3.30 &plusmn; 0.14, carbachol and saline respectively) that lasted for almost 30minutes. Intrathecal administration of 194 nmol solution of yohimbine following carbachol microinjection in the LH resulted in a significant hyperalgesic response, returning the response to baseline levels (p&lt;0.05). Intrathecal administration of WB4101 (194 nmol) facilitated analgesia. These findings suggest that stimulation of neurons in the LH activates a bidirectional pathway in the A7 cell group in which: (1) analgesia occurs from the actions of alpha2 andreoceptors and, (2) pain facilitation occurs from the actions of alpha1 adrenoceptors in the dorsal horn. These findings suggest that the LH and/or the A7 cell group may be sites for the development of tolerance to pain medication.</td></tr></table>en_GB
dc.date.available2011-10-26T10:01:01Z-
dc.date.issued2001-11-10en_GB
dc.date.accessioned2011-10-26T10:01:01Z-
dc.description.sponsorshipSigma Theta Tau Internationalen_GB
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