{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T18:26:28Z","timestamp":1783103188869,"version":"3.54.6"},"reference-count":32,"publisher":"National Academy of Sciences","issue":"14","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,4,5]]},"abstract":"<jats:p>\n                    Ablating or functionally compromising sets of sensory neurons has provided important insights into peripheral modality-specific wiring in the somatosensory system. Inflammatory hyperalgesia, cold pain, and noxious mechanosensation have all been shown to depend upon Na\n                    <jats:sub>v<\/jats:sub>\n                    1.8-positive sensory neurons. The release of fast-acting neurotransmitters, such as glutamate, and more slowly released neuropeptides, such as substance P (SP), contribute to the diversified responses to external stimuli. Here we show that deleting\n                    <jats:italic>Vglut2<\/jats:italic>\n                    in\n                    <jats:italic>\n                      Na\n                      <jats:sub>v<\/jats:sub>\n                      1.8\n                      <jats:sup>Cre<\/jats:sup>\n                    <\/jats:italic>\n                    -positive neurons compromised mechanical pain and NGF-induced thermal hyperalgesia, whereas tactile-evoked sensation, thermal, formalin-evoked, and chronic neuropathic pain were normal. However, when\n                    <jats:italic>\n                      Vglut2\n                      <jats:sup>f\/f<\/jats:sup>\n                      ;Na\n                      <jats:sub>v<\/jats:sub>\n                      1.8\n                      <jats:sup>Cre<\/jats:sup>\n                    <\/jats:italic>\n                    mice were injected with a SP antagonist before the formalin test, the second phase pain response was nearly completely abolished, whereas in control mice, the pain response was unaffected. Our results suggest that VGLUT2-dependent signaling originating from Na\n                    <jats:sub>v<\/jats:sub>\n                    1.8-positive neurons is a principal sensing mechanism for mechanical pain and, together with SP, inflammatory pain. These data define sets of primary afferents associated with specific modalities and provide useful genetic tools with which to analyze the pathways that are activated by functionally distinct neuronal populations and transmitters.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1013602108","type":"journal-article","created":{"date-parts":[[2011,3,18]],"date-time":"2011-03-18T00:25:44Z","timestamp":1300407944000},"page":"5789-5794","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":44,"title":["A sensory subpopulation depends on vesicular glutamate transporter 2 for mechanical pain, and together with substance P, inflammatory pain"],"prefix":"10.1073","volume":"108","author":[{"given":"Malin C.","family":"Lagerstr\u00f6m","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katarzyna","family":"Rogoz","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bjarke","family":"Abrahamsen","sequence":"additional","affiliation":[{"name":"Molecular Nociception Group, University College London, London WC1E 6BT, United Kingdom; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne-Li","family":"Lind","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline","family":"\u00d6lund","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Casey","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 Alfredo","family":"Mendez","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c5sa","family":"Wall\u00e9n-Mackenzie","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John N.","family":"Wood","sequence":"additional","affiliation":[{"name":"Molecular Nociception Group, University College London, London WC1E 6BT, United Kingdom; and"},{"name":"Department of Molecular Medicine and Biopharmaceutical Chemistry, Seoul National University, Seoul 151-742, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klas","family":"Kullander","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2011,3,17]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0901507106"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0361-9230(98)00159-2"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/379257a0"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/jn.2001.86.2.629"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.11.5953"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature05880"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1156916"},{"key":"e_1_3_3_8_2","volume-title":"Textbook of Pain","author":"McMahon S","year":"2006","unstructured":", eds S McMahon, M Koltzenburg (Elsevier, 5th Ed, Churchill Livingstone, New York Textbook of Pain, 2006).","edition":"5"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2007.02.068"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.2003.02406.x"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3855-06.2006"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5851-08.2009"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature08505"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2556-06.2006"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejpain.2008.12.001"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2004.08.015"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pbio.0030159"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00483-4"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2005.09.003"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2009.09.006"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1038\/328632a0"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1023\/B:NEUR.0000044193.31523.a1"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2010.09.016"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(92)90003-T"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(95)12157-Y"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.20.7820"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(91)90175-N"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1237-04.2004"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1993.73.2.229"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3959(80)90088-3"},{"key":"e_1_3_3_31_2","first-page":"114","article-title":"Role of calcitonin gene-related peptide and substance P in different models of pain","volume":"28","author":"Greco R","year":"2008","unstructured":"R Greco, et al., Role of calcitonin gene-related peptide and substance P in different models of pain. 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