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  • 1
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    Broad-spectrum, non-opioid analgesic activity by selective modulation of neuronal nicotinic acetylcholine receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: Development of analgesic agents for the treatment of severe pain requires the identification of compounds that are devoid of opioid receptor liabilities. A potent (inhibition constant = 37 picomolar) neuronal nicotinic acetylcholine receptor (nAChR) ligand called ABT-594 was developed that has antinociceptive properties equal in efficacy to those of morphine across a series of diverse animal models of acute thermal, persistent chemical, and neuropathic pain states. These effects were blocked by the nAChR antagonist mecamylamine. In contrast to morphine, repeated treatment with ABT-594 did not appear to elicit opioid-like withdrawal or physical dependence. Thus, ABT-594 may be an analgesic that lacks the problems associated with opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bannon, A W -- Decker, M W -- Holladay, M W -- Curzon, P -- Donnelly-Roberts, D -- Puttfarcken, P S -- Bitner, R S -- Diaz, A -- Dickenson, A H -- Porsolt, R D -- Williams, M -- Arneric, S P -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):77-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurological and Urological Diseases Research, Pharmaceutical Products Division, Abbott Laboratories, Abbott Park, IL 60064-3500, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417028" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Non-Narcotic/chemical synthesis/metabolism/*pharmacology ; Animals ; Azetidines/chemical synthesis/metabolism/*pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Capsaicin/pharmacology ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Ligands ; Mecamylamine/pharmacology ; Morphine/pharmacology ; Nerve Fibers/drug effects/metabolism/physiology ; Neuromuscular Junction/metabolism ; Neurons/drug effects/metabolism/physiology ; Nicotine/pharmacology ; Nicotinic Agonists/chemical synthesis/metabolism/*pharmacology ; Nicotinic Antagonists/pharmacology ; Pain/drug therapy ; Pain Measurement ; Pyridines/chemical synthesis/metabolism/*pharmacology ; Rats ; Receptors, Nicotinic/*metabolism ; Spinal Cord/drug effects/metabolism/physiology ; Substance Withdrawal Syndrome/etiology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The cell and molecular basis of mechanical, cold, and inflammatory pain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: Peripheral pain pathways are activated by a range of stimuli. We used diphtheria toxin to kill all mouse postmitotic sensory neurons expressing the sodium channel Nav1.8. Mice showed normal motor activity and low-threshold mechanical and acute noxious heat responses but did not respond to noxious mechanical pressure or cold. They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammatory insults. In contrast, nerve injury led to heightened pain sensitivity to thermal and mechanical stimuli indistinguishable from that seen with normal littermates. Pain behavior correlates well with central input from sensory neurons measured electrophysiologically in vivo. These data demonstrate that Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abrahamsen, Bjarke -- Zhao, Jing -- Asante, Curtis O -- Cendan, Cruz Miguel -- Marsh, Steve -- Martinez-Barbera, Juan Pedro -- Nassar, Mohammed A -- Dickenson, Anthony H -- Wood, John N -- BB/F000227/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G9717869/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):702-5. doi: 10.1126/science.1156916.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Nociception Group, University College London (UCL), Gower Street, London, WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cold Temperature ; Electrophysiology ; Freund's Adjuvant ; Hot Temperature ; Inflammation/*physiopathology ; Mice ; Mice, Knockout ; NAV1.8 Voltage-Gated Sodium Channel ; Neurons, Afferent/*physiology ; Nociceptors/physiology ; Pain/*physiopathology ; Pain Measurement ; Pain Threshold ; Pressure ; Sodium Channels/genetics/*metabolism ; TRPV Cation Channels/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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    PAPER CURRENT
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