<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Caballero E</submitter><funding>Junta de Castilla y León</funding><funding>Ministerio de Ciencia e Innovación, Spain</funding><funding>Junta de Castilla y León, Spain</funding><pagination>1153</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9138537</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(5)</volume><pubmed_abstract>The molecular basis of amyloid toxicity in Alzheimer's disease (AD) remains controversial. Amyloid β (Aβ) oligomers promote Ca&lt;sup>2+&lt;/sup> influx, mitochondrial Ca&lt;sup>2+&lt;/sup> overload and apoptosis in hippocampal neurons in vivo and in vitro, but the primary Ca&lt;sup>2+&lt;/sup> entry pathways are unclear. We studied Ca&lt;sup>2+&lt;/sup> entry pathways induced by Aβ oligomers in rat hippocampal and cerebellar neurons. Aβ oligomers induce Ca&lt;sup>2+&lt;/sup> entry in neurons. Ca&lt;sup>2+&lt;/sup> responses to Aβ oligomers are large after synaptic networking and prevented by blockers of synaptic transmission. In contrast, in neurons devoid of synaptic connections, Ca&lt;sup>2+&lt;/sup> responses to Aβ oligomers are small and prevented only by blockers of amyloid channels (NA7) and NMDA receptors (MK801). A combin</pubmed_abstract><journal>Biomedicines</journal><pubmed_title>Amyloid Beta Oligomers-Induced Ca&lt;sup>2+&lt;/sup> Entry Pathways: Role of Neuronal Networks, NMDA Receptors and Amyloid Channel Formation.</pubmed_title><pmcid>PMC9138537</pmcid><funding_grant_id>CCVC8485</funding_grant_id><funding_grant_id>VA294P18</funding_grant_id><funding_grant_id>RTI2018-099298-B-10</funding_grant_id><pubmed_authors>Nunez L</pubmed_authors><pubmed_authors>Villalobos C</pubmed_authors><pubmed_authors>Hernando-Perez E</pubmed_authors><pubmed_authors>Calvo-Rodriguez M</pubmed_authors><pubmed_authors>Tapias V</pubmed_authors><pubmed_authors>Caballero E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Amyloid Beta Oligomers-Induced Ca&lt;sup>2+&lt;/sup> Entry Pathways: Role of Neuronal Networks, NMDA Receptors and Amyloid Channel Formation.</name><description>The molecular basis of amyloid toxicity in Alzheimer's disease (AD) remains controversial. Amyloid β (Aβ) oligomers promote Ca&lt;sup>2+&lt;/sup> influx, mitochondrial Ca&lt;sup>2+&lt;/sup> overload and apoptosis in hippocampal neurons in vivo and in vitro, but the primary Ca&lt;sup>2+&lt;/sup> entry pathways are unclear. We studied Ca&lt;sup>2+&lt;/sup> entry pathways induced by Aβ oligomers in rat hippocampal and cerebellar neurons. Aβ oligomers induce Ca&lt;sup>2+&lt;/sup> entry in neurons. Ca&lt;sup>2+&lt;/sup> responses to Aβ oligomers are large after synaptic networking and prevented by blockers of synaptic transmission. In contrast, in neurons devoid of synaptic connections, Ca&lt;sup>2+&lt;/sup> responses to Aβ oligomers are small and prevented only by blockers of amyloid channels (NA7) and NMDA receptors (MK801). A combin</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2025-04-21T17:32:32.489Z</modification><creation>2025-04-05T16:40:23.722Z</creation></dates><accession>S-EPMC9138537</accession><cross_references><pubmed>35625890</pubmed><doi>10.3390/biomedicines10051153</doi></cross_references></HashMap>