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  • 1
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    Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain (2016)
    Springer Nature
    In: Nature
    Details
    Publication Date: 2016-06-23
    Description: Selective spider toxins reveal a role for the Nav1.1 channel in mechanical pain Nature 534, 7608 (2016). doi:10.1038/nature17976 Authors: Jeremiah D. Osteen, Volker Herzig, John Gilchrist, Joshua J. Emrick, Chuchu Zhang, Xidao Wang, Joel Castro, Sonia Garcia-Caraballo, Luke Grundy, Grigori Y. Rychkov, Andy D. Weyer, Zoltan Dekan, Eivind A. B. Undheim, Paul Alewood, Cheryl L. Stucky, Stuart M. Brierley, Allan I. Basbaum, Frank Bosmans, Glenn F. King & David Julius Voltage-gated sodium (Nav) channels initiate action potentials in most neurons, including primary afferent nerve fibres of the pain pathway. Local anaesthetics block pain through non-specific actions at all Nav channels, but the discovery of selective modulators would facilitate the analysis of
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 2
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    Impaired nociception and pain sensation in mice lacking the capsaicin receptor (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (〉43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caterina, M J -- Leffler, A -- Malmberg, A B -- Martin, W J -- Trafton, J -- Petersen-Zeitz, K R -- Koltzenburg, M -- Basbaum, A I -- Julius, D -- NS07265/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):306-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764638" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Temperature/drug effects ; Calcium/metabolism ; Capsaicin/metabolism/*pharmacology ; Cells, Cultured ; Diterpenes/pharmacology ; Ganglia, Spinal/cytology ; Gene Targeting ; Hot Temperature ; Hydrogen-Ion Concentration ; Inflammation/physiopathology ; Mice ; Mice, Knockout ; Nerve Fibers/physiology ; Neurons/physiology ; Neurons, Afferent/*physiology ; Nociceptors/*physiology ; Pain/*physiopathology ; Pain Threshold ; Receptors, Drug/*physiology ; Spinal Cord/cytology/physiology ; TRPV Cation Channels
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Injury-induced mechanical hypersensitivity requires C-low threshold mechanoreceptors (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-17
    Description: Mechanical pain contributes to the morbidity associated with inflammation and trauma, but primary sensory neurons that convey the sensation of acute and persistent mechanical pain have not been identified. Dorsal root ganglion (DRG) neurons transmit sensory information to the spinal cord using the excitatory transmitter glutamate, a process that depends on glutamate transport into synaptic vesicles for regulated exocytotic release. Here we report that a small subset of cells in the DRG expresses the low abundance vesicular glutamate transporter VGLUT3 (also known as SLC17A8). In the dorsal horn of the spinal cord, these afferents project to lamina I and the innermost layer of lamina II, which has previously been implicated in persistent pain caused by injury. Because the different VGLUT isoforms generally have a non-redundant pattern of expression, we used Vglut3 knockout mice to assess the role of VGLUT3(+) primary afferents in the behavioural response to somatosensory input. The loss of VGLUT3 specifically impairs mechanical pain sensation, and in particular the mechanical hypersensitivity to normally innocuous stimuli that accompanies inflammation, nerve injury and trauma. Direct recording from VGLUT3(+) neurons in the DRG further identifies them as a poorly understood population of unmyelinated, low threshold mechanoreceptors (C-LTMRs). The analysis of Vglut3(-/-) mice now indicates a critical role for C-LTMRs in the mechanical hypersensitivity caused by injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810205/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810205/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seal, Rebecca P -- Wang, Xidao -- Guan, Yun -- Raja, Srinivasa N -- Woodbury, C Jeffery -- Basbaum, Allan I -- Edwards, Robert H -- F32 MH068085/MH/NIMH NIH HHS/ -- F32 MH068085-02/MH/NIMH NIH HHS/ -- R01 MH050712/MH/NIMH NIH HHS/ -- R01 MH050712-17/MH/NIMH NIH HHS/ -- R01 NS044094/NS/NINDS NIH HHS/ -- R01 NS044094-06/NS/NINDS NIH HHS/ -- England -- Nature. 2009 Dec 3;462(7273):651-5. doi: 10.1038/nature08505. Epub 2009 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco School of Medicine, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19915548" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Transport Systems, Acidic/genetics/*metabolism ; Animals ; Behavior, Animal/physiology ; Female ; Ganglia, Spinal/*metabolism ; Gene Expression Regulation ; Hypersensitivity/*genetics/*physiopathology ; Mechanoreceptors/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pain/*genetics ; Wounds and Injuries/*physiopathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Interneurons from embryonic development to cell-based therapy (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-04-12
    Description: Many neurologic and psychiatric disorders are marked by imbalances between neural excitation and inhibition. In the cerebral cortex, inhibition is mediated largely by GABAergic (gamma-aminobutyric acid-secreting) interneurons, a cell type that originates in the embryonic ventral telencephalon and populates the cortex through long-distance tangential migration. Remarkably, when transplanted from embryos or in vitro culture preparations, immature interneurons disperse and integrate into host brain circuits, both in the cerebral cortex and in other regions of the central nervous system. These features make interneuron transplantation a powerful tool for the study of neurodevelopmental processes such as cell specification, cell death, and cortical plasticity. Moreover, interneuron transplantation provides a novel strategy for modifying neural circuits in rodent models of epilepsy, Parkinson's disease, mood disorders, and chronic pain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056344/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056344/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Nicholas, Cory R -- Basbaum, Allan I -- Stryker, Michael P -- Kriegstein, Arnold R -- Rubenstein, John L -- Alvarez-Buylla, Arturo -- HD032116/HD/NICHD NIH HHS/ -- MH049428/MH/NIMH NIH HHS/ -- NS14627/NS/NINDS NIH HHS/ -- NS28478/NS/NINDS NIH HHS/ -- NS78326/NS/NINDS NIH HHS/ -- R01 EY002874/EY/NEI NIH HHS/ -- R01 MH049428/MH/NIMH NIH HHS/ -- R01 NS014627/NS/NINDS NIH HHS/ -- R01 NS028478/NS/NINDS NIH HHS/ -- R01 NS078326/NS/NINDS NIH HHS/ -- R01-EY02874/EY/NEI NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- T32 GM008568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):1240622. doi: 10.1126/science.1240622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24723614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Separation ; *Cell- and Tissue-Based Therapy ; Cerebral Cortex/cytology/growth & development/physiology ; *Embryonic Development ; Humans ; Interneurons/*physiology/*transplantation ; Mental Disorders/*therapy ; Mice ; Nervous System Diseases/*therapy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Preserved acute pain and reduced neuropathic pain in mice lacking PKCgamma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack protein kinase C gamma (PKCgamma) displayed normal responses to acute pain stimuli, but they almost completely failed to develop a neuropathic pain syndrome after partial sciatic nerve section, and the neurochemical changes that occurred in the spinal cord after nerve injury were blunted. Also, PKCgamma was shown to be restricted to a small subset of dorsal horn neurons, thus identifying a potential biochemical target for the prevention and therapy of persistent pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malmberg, A B -- Chen, C -- Tonegawa, S -- Basbaum, A I -- DA08377/DA/NIDA NIH HHS/ -- NS 14627/NS/NINDS NIH HHS/ -- NS 21445/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):279-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, CA 92143, USA. annikam@phy.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ganglia, Spinal/metabolism ; Gene Deletion ; Hyperalgesia/physiopathology/*therapy ; Inflammation/physiopathology/therapy ; Interneurons/*enzymology ; Isoenzymes/deficiency/genetics/*metabolism ; Ligation ; Mice ; Mice, Knockout ; Neuropeptide Y/metabolism ; Pain/physiopathology ; *Pain Management ; Pain Threshold ; Protein Kinase C/deficiency/genetics/*metabolism ; Receptors, Neurokinin-1/metabolism ; Sciatic Nerve/surgery ; Signal Transduction ; Spinal Cord/cytology/*enzymology/metabolism ; Substance P/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    A heteromeric Texas coral snake toxin targets acid-sensing ion channels to produce pain (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-19
    Description: Natural products that elicit discomfort or pain represent invaluable tools for probing molecular mechanisms underlying pain sensation. Plant-derived irritants have predominated in this regard, but animal venoms have also evolved to avert predators by targeting neurons and receptors whose activation produces noxious sensations. As such, venoms provide a rich and varied source of small molecule and protein pharmacophores that can be exploited to characterize and manipulate key components of the pain-signalling pathway. With this in mind, here we perform an unbiased in vitro screen to identify snake venoms capable of activating somatosensory neurons. Venom from the Texas coral snake (Micrurus tener tener), whose bite produces intense and unremitting pain, excites a large cohort of sensory neurons. The purified active species (MitTx) consists of a heteromeric complex between Kunitz- and phospholipase-A2-like proteins that together function as a potent, persistent and selective agonist for acid-sensing ion channels (ASICs), showing equal or greater efficacy compared with acidic pH. MitTx is highly selective for the ASIC1 subtype at neutral pH; under more acidic conditions (pH 〈 6.5), MitTx massively potentiates (〉100-fold) proton-evoked activation of ASIC2a channels. These observations raise the possibility that ASIC channels function as coincidence detectors for extracellular protons and other, as yet unidentified, endogenous factors. Purified MitTx elicits robust pain-related behaviour in mice by activation of ASIC1 channels on capsaicin-sensitive nerve fibres. These findings reveal a mechanism whereby snake venoms produce pain, and highlight an unexpected contribution of ASIC1 channels to nociception.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226747/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohlen, Christopher J -- Chesler, Alexander T -- Sharif-Naeini, Reza -- Medzihradszky, Katalin F -- Zhou, Sharleen -- King, David -- Sanchez, Elda E -- Burlingame, Alma L -- Basbaum, Allan I -- Julius, David -- F31NS065597/NS/NINDS NIH HHS/ -- P40 RR018300-09/RR/NCRR NIH HHS/ -- P40RR018300-09/RR/NCRR NIH HHS/ -- P41 GM103481/GM/NIGMS NIH HHS/ -- P41RR001614/RR/NCRR NIH HHS/ -- R01NS065071/NS/NINDS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Nov 16;479(7373):410-4. doi: 10.1038/nature10607.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, California 94158-2517, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22094702" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Sensing Ion Channels ; Amino Acid Sequence ; Animals ; Capsaicin/pharmacology ; Cells, Cultured ; Elapid Venoms/*chemistry/*pharmacology ; *Elapidae ; Hindlimb/drug effects/physiopathology ; Humans ; Hydrogen-Ion Concentration ; Ion Channel Gating/drug effects ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Nerve Tissue Proteins/agonists/deficiency/genetics/*metabolism ; Nociception/drug effects/physiology ; Oocytes ; Pain/*chemically induced/metabolism/physiopathology ; *Protein Multimerization ; Protein Structure, Quaternary ; Protons ; Rats ; Sensory Receptor Cells/drug effects/metabolism ; Sodium Channel Agonists ; Sodium Channels/deficiency/genetics/*metabolism ; TRPV Cation Channels/metabolism ; Xenopus laevis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Receptor endocytosis and dendrite reshaping in spinal neurons after somatosensory stimulation (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-16
    Description: In vivo somatosensory stimuli evoked the release of substance P from primary afferent neurons that terminate in the spinal cord and stimulated endocytosis of substance P receptors in rat spinal cord neurons. The distal dendrites that showed substance P receptor internalization underwent morphological reorganization, changing from a tubular structure to one characterized by swollen varicosities connected by thin segments. This internalization and dendritic structural reorganization provided a specific image of neurons activated by substance P. Thus receptor internalization can drive reversible structural changes in central nervous system neurons in vivo. Both of these processes may be involved in neuronal plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- DeMaster, E -- Malhotra, A -- Ghilardi, J R -- Rogers, S D -- Mantyh, C R -- Liu, H -- Basbaum, A I -- Vigna, S R -- Maggio, J E -- NS14627/NS/NINDS NIH HHS/ -- NS21445/NS/NINDS NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jun 16;268(5217):1629-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Veterans Administration Medical Center, Minneapolis, MN 55417, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7539937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin/pharmacology ; Dendrites/metabolism/*ultrastructure ; *Endocytosis ; GTP-Binding Proteins/metabolism ; Male ; Neuronal Plasticity ; Neurons/*metabolism/ultrastructure ; Physical Stimulation ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/*metabolism ; Spinal Cord/cytology/*metabolism ; Substance P/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Intraneuronal substance P contributes to the severity of experimental arthritis (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-02
    Description: There is evidence that substance P is a peptide neurotransmitter of some unmyelinated primary afferent nociceptors and that its release from the peripheral terminals of primary afferent fibers mediates neurogenic inflammation. The investigators examined whether substance P also contributes to the severity of adjuvant-induced arthritis, an inflammatory disease in rats. They found that, in the rat, joints that developed more severe arthritis (ankles) were more densely innervated by substance P-containing primary afferent neurons than were joints that developed less severe arthritis (knees). Infusion of substance P into the knee increased the severity of arthritis; injection of a substance P receptor antagonist did not. These results suggest a significant physiological difference between joints that develop mild and severe arthritis and indicate that release of intraneuronal substance P in joints contributes to the severity of the arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, J D -- Clark, R -- Devor, M -- Helms, C -- Moskowitz, M A -- Basbaum, A I -- AM 32634/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):547-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6208609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/chemically induced/*physiopathology ; Double-Blind Method ; Hindlimb ; Joints/drug effects/innervation/physiopathology ; Neurons, Afferent/physiology ; Rats ; Substance P/pharmacology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Leucine enkephalin: localization in and axoplasmic transport by sacral parasympathetic preganglionic neurons (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-06-27
    Description: Nerve processes and cell bodies containing leucine enkephalin were demonstrated in the sacral autonomic nucleus of the cat by immunocytochemical methods. Enkephalinergic preganglionic perikarya were seen only when axonal transport was blocked either by colchicine or by ventral root ligation. Ligation of the sacral ventral roots also produced damming of enkephalin immunoreactivity proximal to the S2 ligature. These data indicate that parasympathetic preganglionic neurons synthesize and transport enkephalin or enkephalin-like immunoreactive compounds to the periphery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glazer, E J -- Basbaum, A I -- New York, N.Y. -- Science. 1980 Jun 27;208(4451):1479-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6155697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Axonal Transport ; Cats ; Enkephalin, Leucine ; Enkephalins/analysis/metabolism ; Histocytochemistry ; Immunoassay ; Neurons/*analysis ; Spinal Cord/analysis/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Lys49 myotoxin from the Brazilian lancehead pit viper elicits pain through regulated ATP release [Physiology] (2017)
    National Academy of Sciences
    Details
    Publication Date: 2017-03-22
    Description: Pain-producing animal venoms contain evolutionarily honed toxins that can be exploited to study and manipulate somatosensory and nociceptive signaling pathways. From a functional screen, we have identified a secreted phospholipase A2 (sPLA2)-like protein, BomoTx, from the Brazilian lancehead pit viper (Bothrops moojeni). BomoTx is closely related to a group of...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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