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Chronic pain states: Pharmacological strategies to restore diminished inhibitory spinal pain control


Zeilhofer, H U; Benke, D; Yevenes, G E (2012). Chronic pain states: Pharmacological strategies to restore diminished inhibitory spinal pain control. Annual Review of Pharmacology and Toxicology, 52(1):111-133.

Abstract

Potentially noxious stimuli are sensed by specialized nerve cells named nociceptors, which convey nociceptive signals from peripheral tissues to the central nervous system. The spinal dorsal horn and the trigeminal nucleus serve as first relay stations for incoming nociceptive signals. At these sites, nociceptor terminals contact a local neuronal network consisting of excitatory and inhibitory interneurons as well as of projection neurons. Blockade of neuronal inhibition in this network causes an increased sensitivity to noxious stimuli (hyperalgesia), painful sensations occurring after activation of non-nociceptive fibers (allodynia), and spontaneous pain felt in the absence of any sensory stimulation. It thus mimics the major characteristics of chronic pain states. Diminished inhibitory pain control in the spinal dorsal horn occurs naturally, e.g., through changes in the function of inhibitory neurotransmitter receptors or through altered chloride homeostasis in the course of inflammation or nerve damage. This review summarizes our current knowledge about endogenous mechanisms leading to diminished spinal pain control and discusses possible ways that could restore proper inhibition through facilitation of fast inhibitory neurotransmission. Expected final online publication date for the Annual Review of Pharmacology and Toxicology Volume 52 is January 06, 2012. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.

Potentially noxious stimuli are sensed by specialized nerve cells named nociceptors, which convey nociceptive signals from peripheral tissues to the central nervous system. The spinal dorsal horn and the trigeminal nucleus serve as first relay stations for incoming nociceptive signals. At these sites, nociceptor terminals contact a local neuronal network consisting of excitatory and inhibitory interneurons as well as of projection neurons. Blockade of neuronal inhibition in this network causes an increased sensitivity to noxious stimuli (hyperalgesia), painful sensations occurring after activation of non-nociceptive fibers (allodynia), and spontaneous pain felt in the absence of any sensory stimulation. It thus mimics the major characteristics of chronic pain states. Diminished inhibitory pain control in the spinal dorsal horn occurs naturally, e.g., through changes in the function of inhibitory neurotransmitter receptors or through altered chloride homeostasis in the course of inflammation or nerve damage. This review summarizes our current knowledge about endogenous mechanisms leading to diminished spinal pain control and discusses possible ways that could restore proper inhibition through facilitation of fast inhibitory neurotransmission. Expected final online publication date for the Annual Review of Pharmacology and Toxicology Volume 52 is January 06, 2012. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.

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39 citations in Web of Science®
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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:12 Oct 2011 11:31
Last Modified:05 Apr 2016 15:02
Publisher:Annual Reviews
ISSN:1941-1383
Publisher DOI:10.1146/annurev-pharmtox-010611-134636
PubMed ID:21854227
Permanent URL: http://doi.org/10.5167/uzh-49977

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