<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>Borgognon, Simon</dc:creator>
  <dc:creator>Cottet, Jérôme</dc:creator>
  <dc:creator>Badoud, Simon</dc:creator>
  <dc:creator>Bloch, Jocelyne</dc:creator>
  <dc:creator>Brunet, Jean-François</dc:creator>
  <dc:creator>Rouiller, Eric M.</dc:creator>
  <dc:date>2020-10-26</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Besides the main cortical inputs to the basal ganglia, via the corticostriatal projection,  there is another input via the corticosubthalamic projection (CSTP), terminating in the  subthalamic nucleus (STN). The present study investigated and compared the CSTPs  originating from the premotor cortex (PM) or the primary motor cortex (M1) in two  groups of adult macaque monkeys. The first group includes six intact monkeys,  whereas the second group was made up of four monkeys subjected to 1-methyl-4- phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication producing Parkinson’s disease  (PD)-like symptoms and subsequently treated with an autologous neural cell  ecosystem (ANCE) therapy. The CSTPs were labeled with the anterograde tracer  biotinylated dextran amine (BDA), injected either in PM or in M1. BDA-labeled axonal  terminal boutons in STN were charted, counted, and then normalized based on the  number of labeled corticospinal axons in each monkey. In intact monkeys, the CSTP  from PM was denser than that originating from M1. In two PD monkeys, the CSTP  originating from PM or M1 were substantially increased, as compared to intact  monkeys. In one other PD monkey, there was no obvious change, whereas the last  PD monkey showed a decrease of the CSTP originating from M1. Interestingly, the  linear relationship between CSTP density and PD symptoms yielded a possible  dependence of the CSTP re-organization with the severity of the MPTP lesion. The  higher the PD symptoms, the larger the CSTP densities, irrespective of the origin  (from both M1 or PM). Plasticity of the CSTP in PD monkeys may be related to PD  itself and/or to the ANCE treatment.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/309024</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/309024/files/rou_cpp.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.3389/fncir.2020.528993</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Frontiers in Neural Circuits. - 2020, vol. 14, p. 528993</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Cortical projection from the premotor or primary motor cortex to the subthalamic nucleus in intact and parkinsonian adult macaque monkeys: a pilot tracing study</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
