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However, increasing knowledge about the participation of PrP\n                      <jats:sup>C<\/jats:sup>\n                      in prion pathogenesis contrasts with puzzling data regarding its natural physiological role. PrP\n                      <jats:sup>C<\/jats:sup>\n                      is expressed in a number of tissues, including at high levels in the nervous system, especially in neurons and glial cells, and while previous studies have established a neuroprotective role, conflicting evidence for a synaptic function has revealed both reduced and enhanced long-term potentiation, and variable observations on memory, learning, and behavior. Such evidence has been confounded by the absence of an appropriate knock-out mouse model to dissect the biological relevance of PrP\n                      <jats:sup>C<\/jats:sup>\n                      , with some functions recently shown to be misattributed to PrP\n                      <jats:sup>C<\/jats:sup>\n                      due to the presence of genetic artifacts in mouse models. Here we elucidate the role of PrP\n                      <jats:sup>C<\/jats:sup>\n                      in the hippocampal circuitry and its related functions, such as learning and memory, using a recently available strictly co-isogenic\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>0\/0<\/jats:italic>\n                      <\/jats:sup>\n                      mouse model (\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>ZH3\/ZH3<\/jats:italic>\n                      <\/jats:sup>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We performed behavioral and operant conditioning tests to evaluate memory and learning capabilities, with results showing decreased motility, impaired operant conditioning learning, and anxiety-related behavior in\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>ZH3\/ZH3<\/jats:italic>\n                      <\/jats:sup>\n                      animals. We also carried in vivo electrophysiological recordings on CA3-CA1 synapses in living behaving mice and monitored spontaneous neuronal firing and network formation in primary neuronal cultures of\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>ZH3\/ZH3<\/jats:italic>\n                      <\/jats:sup>\n                      vs wildtype mice. PrP\n                      <jats:sup>C<\/jats:sup>\n                      absence enhanced susceptibility to high-intensity stimulations and kainate-induced seizures. However, long-term potentiation (LTP) was not enhanced in the\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>ZH3\/ZH3<\/jats:italic>\n                      <\/jats:sup>\n                      hippocampus. In addition, we observed a delay in neuronal maturation and network formation in\n                      <jats:italic>Prnp<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>ZH3\/ZH3<\/jats:italic>\n                      <\/jats:sup>\n                      cultures.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our results demonstrate that PrP\n                      <jats:sup>C<\/jats:sup>\n                      promotes neuronal network formation and connectivity. PrP\n                      <jats:sup>C<\/jats:sup>\n                      mediates synaptic function and protects the synapse from excitotoxic insults. Its deletion may underlie an epileptogenic-susceptible brain that fails to perform highly cognitive-demanding tasks such as associative learning and anxiety-like behaviors.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12915-021-01203-0","type":"journal-article","created":{"date-parts":[[2022,1,13]],"date-time":"2022-01-13T13:02:55Z","timestamp":1642078975000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Analysis of co-isogenic prion protein deficient mice reveals behavioral deficits, learning impairment, and enhanced hippocampal excitability"],"prefix":"10.1186","volume":"20","author":[{"given":"A.","family":"Matamoros-Angles","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Hervera","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Soriano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Mart\u00ed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Carulla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Llorens","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Nuvolone","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Aguzzi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Ferrer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Gruart","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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CEEA of the University of Barcelona approved the protocol for using animals in this study (CEEA approval #276\/16 and 141\/15). Behavioral and electrophysiological studies were performed following the guidelines of the European Union Council (2010\/276:33-79\/EU) and current Spanish regulations (BOE 34:11370-421, 2013) for the use of laboratory animals in chronic experiments. Experiments were also approved by the Ethics Committee for Animal Care and Handling of the Pablo de Olavide University (UPO-JA 06\/03\/2018\/025).","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"The authors declare that they have no competing interests.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"17"}}