Pharmacology of pain processing systems

Schadrack, Jan; Zieglgänsberger, W.

doi:10.1007/s003930050224

Cited by 9 publications

(4 citation statements)

References 13 publications

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“…Several neurotransmitters, including glutamate, aspartate, vasoactive intestinal peptide (VIP), SP, cholecystokinin (CCK), and neurotensin-enhance neural transmission [25]. Inhibitory dorsal horn interneurons that attenuate nociception often produce high concentrations of gammaamino-butyric acid (GABA), an important inhibitor of nocicpetive neurons [26,27]. In addition, cholinergic interneurons, acting through muscarinic and nicotinic receptors, also seem to play an important role in anti-nociception [28].…”

Section: Central Sensitizationmentioning

confidence: 98%

Peripheral and central sensitization in fibromyalgia: Pathogenetic role

Staud

Smitherman

2002

Current Science Inc

151

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Characteristic symptoms of fibromyalgia syndrome include widespread pain, fatigue, sleep abnormalities, and distress. Patients with fibromyalgia show psychophysical evidence of mechanical, thermal, and electrical hyperalgesia. Peripheral and central abnormalities of nociception have been described in fibromyalgia. Important nociceptor systems in the skin and muscles seem to undergo profound changes in patients with fibromyalgia through unknown mechanisms. They include sensitization of vanilloid receptor, acid-sensing ion channel receptors, and purino-receptors. Tissue mediators of inflammation and nerve growth factors can excite these receptors and cause extensive changes in pain sensitivity, but patients with fibromyalgia lack consistent evidence for inflammatory soft tissue abnormalities. Therefore, recent investigations have focused on central nervous system mechanisms of pain in fibromyalgia.

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Section: Central Sensitizationmentioning

confidence: 98%

Peripheral and central sensitization in fibromyalgia: Pathogenetic role

Staud

Smitherman

2002

Current Science Inc

151

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“…Gamma-amino-butyric acid (GABA), a major inhibitory transmitter in the CNS, is localized in high concentration in interneurons of laminae I-III, among others also in islet cells (Fig. 2), and has been implicated in the inhibition of acute and persistent pain (64,89). However, because NO also acts as a crucial transmitter in models for persisting pain, co-localization of GABA with NOS, as it occurs in islet cells, may suggest even opposite functions for these neurons (2).…”

Section: The Dorsal Horn Of the Spinal Cordmentioning

confidence: 99%

Nociception, pain, and antinociception: current concepts

Riedel

Neeck

2001

Zeitschrift f�r Rheumatologie

143

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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. The two most important systems in modulating nociception and antinociception, the N-methyl-D-aspartate (NMDA) and opioid receptor system, show a close distribution pattern in nearly all CNS regions, and activation of NMDA receptors has been found to contribute to the hyperalgesia associated with nerve injury or inflammation. Apart from substance P (SP), the major facilitatory effect in nociception is exerted by glutamate as the natural activator of NMDA receptors. Stimulation of ionotropic NMDA receptors causes intraneuronal elevation of Ca2+ which stimulates nitric oxide synthase (NOS) and the production of nitric oxide (NO). NO as a gaseous molecule diffuses out from the neuron and by action on guanylyl cyclase, NO stimulates in neighboring neurons the formation of cGMP. Depending on the expression of cGMP-controlled ion channels in target neurons, NO may act excitatory or inhibitory. NO has been implicated in the development of hyperexcitability, resulting in hyperalgesia or allodynia, by increasing nociceptive transmitters at their central terminals. Among the three subtypes of opioid receptors, mu- and delta-receptors either inhibit or potentiate NMDA receptor-mediated events, while kappa opioids antagonize NMDA receptor-mediated activity. Recently, CRH has been found to act at all levels of the neuraxis to produce analgesia. Modulation of nociception occurs at all levels of the neuraxis, thus, eliciting the multidimensional experience of pain involving sensory-discriminative, affective-motivational, cognitive and locomotor components.

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“…The organization and physiological properties of primary afferent pathways in the spinal cord have been extensively and authoritatively reviewed elsewhere (Ruda et al, 1986;Willis, Jr. and Coggeshall, 1991;Todd and Spike, 1993;Ribeiro-Da-Silva, 1994;Schadrack and Zieglgansberger, 1998;Millan, 1999;Alvares and Fitzgerald, 1999;Dubner and Ren, 1999;Petersen-Zeitz and Basbaum, 1999;McHugh and McHugh, 2000;Burnstock, 2000;Herrero et al, 2000;Gerber et al, 2000a;Willis, 2001;Hunt and Mantyh, 2001;Ji and Woolf, 2001;Morisset et al, 2001;Mendell and Arvanian, 2002;Willis, 2002), and cutaneous primary afferent fibers (PAFs) have been studied in deeper detail. Therefore, the following short description will be mainly based upon the data available for this type of fibers.…”

Section: Organization Of the Primary Afferent Pathways In The Spinal ...mentioning

confidence: 99%