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Prevention of<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\u03b2\u2010induced synaptic failure remains an unsolved problem for the treatment of<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>. Here, the effects of 2\u2010aminoethoxydiphenyl borate (2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>), a non\u2010specific, but moderately potent<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>channel inhibitor, on<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\u03b2\u2010induced deficit of synaptic long\u2010term potentiation (<jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>) and the underlying molecular mechanisms were explored.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>We used hippocampal slices and primary cultures of hippocampal neurons from<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice. Methods applied in our study included electrophysiological recording, membrane protein extraction,<jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>estern blot assay and<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>imaging.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>at 10\u2009<jats:styled-content style=\"fixed-case\">\u03bcM<\/jats:styled-content>effectively reversed suppression by oligomeric<jats:styled-content style=\"fixed-case\">A\u03b2<\/jats:styled-content><jats:sub>1\u201342<\/jats:sub>(500\u2009<jats:styled-content style=\"fixed-case\">nM<\/jats:styled-content>) of<jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>in hippocampal slices. 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>also restored phosphorylation and trafficking of the glutamate receptor subunit<jats:styled-content style=\"fixed-case\">GluA1<\/jats:styled-content>in<jats:styled-content style=\"fixed-case\">A\u03b2<\/jats:styled-content>\u2010treated hippocampal slices, supporting its protective action on synaptic function.<jats:styled-content style=\"fixed-case\">A\u03b2<\/jats:styled-content>\u2010mediated abnormal neuronal [<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>]<jats:styled-content style=\"fixed-case\"><jats:sub>i<\/jats:sub><\/jats:styled-content>elevation and hyperactivation of the mitochondrial apoptotic proteins<jats:styled-content style=\"fixed-case\">BAX<\/jats:styled-content>, caspase\u20103, and glycogen synthase kinase\u20103\u03b2, were blocked by 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>pretreatment. Moreover, the defict in long term potentiation deficit in hippocampal slices from<jats:styled-content style=\"fixed-case\">APP<jats:sub>swe<\/jats:sub><\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PS<\/jats:styled-content>1<jats:styled-content style=\"fixed-case\"><jats:sub>\u0394E<\/jats:sub><\/jats:styled-content><jats:sub>9<\/jats:sub>gene mutant mice was rescued by 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>at 10\u2009<jats:styled-content style=\"fixed-case\">\u03bcM<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implication<\/jats:title><jats:p>These data demonstrate that 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>is a potentially useful chemical to protect synaptic plasticity against neurotoxic effects of<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\u03b2 in<jats:styled-content 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