<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Roccaro-Waldmeyer, Diana M.</dc:creator>
  <dc:creator>Girard, Franck</dc:creator>
  <dc:creator>Milani, Daniele</dc:creator>
  <dc:creator>Vannoni, Elisabetta</dc:creator>
  <dc:creator>Prétôt, Laurent</dc:creator>
  <dc:creator>Wolfer, David P.</dc:creator>
  <dc:creator>Celio, Marco R.</dc:creator>
  <dc:date>2018</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">The calcium-binding protein parvalbumin (PV) is a recognized marker of short-axon  GABA-ergic neurons in the cortex and the hippocampus. However in addition, PV is  expressed by excitatory, glutamatergic neurons in various areas of the brain and  spinal cord. Depending on the location of these neurons, loading of their synaptic  vesicles with glutamate is mediated by either of three vesicular glutamate transporters  (VGlut): VGlut1, VGlut2 or VGlut3. Driven by our interest in one of these  glutamatergic/PV-expressing cell clusters – the lateral hypothalamic parvafox nucleus  - we investigated the functions of this population of neurons by the selective deletion  of VGlut2 expression in PV-expressing cells according to the Cre/Lox-approach. PV- Cre;VGlut2-Lox mutant mice are phenotypically characterized by deficits in locomotion  and vocalization, by a decreased thermal nociception, and by an increased social  dominance. We conducted a search of the Allen Brain Atlas for regions that might co- express the genes encoding PV and VGlut2, and that might thus contribute to the  manifestation of the observed phenotypes. Our survey revealed several structures  that could contribute to the deficits in locomotion and vocalization, such as the red, the  subthalamic and the deep cerebellar nuclei. It also disclosed that a shift in the balance  of afferental glutamatergic neurotransmission to the periaqueductal grey matter might  be accountable for the decrease in sensitivity to pain and for the increase in social  dominance. As a whole, this study broadens the state of knowledge about PV- expressing excitatory neurons.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/307144</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307144/files/cel_evd.pdf</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307144/files/cel_evd_sm.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.3389/fnbeh.2018.00146</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Frontiers in Behavioral Neuroscience. - 2018, vol. 12, p. 146</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Eliminating the VGlut2-dependent glutamatergic transmission of parvalbumin-expressing neurons leads to deficits in locomotion and vocalization, decreased pain sensitivity, and increased dominance</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
