{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:07:14Z","timestamp":1791328034061,"version":"4.3.1"},"reference-count":47,"publisher":"Society for Neuroscience","issue":"7","license":[{"start":{"date-parts":[[2013,8,13]],"date-time":"2013-08-13T00:00:00Z","timestamp":1376352000000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2013,2,13]]},"abstract":"<jats:p>The cellular form of prion protein PrP<jats:sup>C<\/jats:sup>is highly expressed in the brain, where it can be converted into its abnormally folded isoform PrP<jats:sup>Sc<\/jats:sup>to cause neurodegenerative diseases. Its predominant synaptic localization suggests a crucial role in synaptic signaling. Interestingly, PrP<jats:sup>C<\/jats:sup>is developmentally regulated and its high expression in the immature brain could be instrumental in regulating neurogenesis and cell proliferation. Here, PrP<jats:sup>C<\/jats:sup>-deficient (<jats:italic>Prnp<\/jats:italic><jats:sup>0\/0<\/jats:sup>) mice were used to assess whether the prion protein is involved in synaptic plasticity processes in the neonatal hippocampus. To this aim, calcium transients associated with giant depolarizing potentials, a hallmark of developmental networks, were transiently paired with mossy fiber activation in such a way that the two events were coincident. While this procedure caused long-term potentiation (LTP) in wild-type (WT) animals, it caused long-term depression (LTD) in<jats:italic>Prnp<\/jats:italic><jats:sup>0\/0<\/jats:sup>mice. Induction of LTP was postsynaptic and required the activation of cAMP-dependent protein kinase A (PKA) signaling. The induction of LTD was presynaptic and relied on G-protein-coupled GluK1 receptor and protein lipase C. In addition, at emerging CA3-CA1 synapses in WT mice, but not in<jats:italic>Prnp<\/jats:italic><jats:sup>0\/0<\/jats:sup>mice, pairing Schaffer collateral stimulation with depolarization of CA1 principal cells induced LTP, known to be PKA dependent. Postsynaptic infusion of a constitutively active isoform of PKA catalytic subunit C\u03b1 into CA1 and CA3 principal cells in the hippocampus of<jats:italic>Prnp<\/jats:italic><jats:sup>0\/0<\/jats:sup>mice caused a persistent synaptic facilitation that was occluded by subsequent pairing. These data suggest that PrP<jats:sup>C<\/jats:sup>plays a crucial role in regulating via PKA synaptic plasticity in the developing hippocampus.<\/jats:p>","DOI":"10.1523\/jneurosci.4149-12.2013","type":"journal-article","created":{"date-parts":[[2013,2,13]],"date-time":"2013-02-13T17:38:14Z","timestamp":1360777094000},"page":"2973-2983","source":"Crossref","is-referenced-by-count":51,"title":["PrP<sup>C<\/sup>Controls via Protein Kinase A the Direction of Synaptic Plasticity in the Immature Hippocampus"],"prefix":"10.1523","volume":"33","author":[{"given":"Maddalena D.","family":"Caiati","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria 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