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Age\u2010related deficit of the dopaminergic system may contribute to impairment of <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>1 <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>. Here we assessed how the modulation of <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>1 <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> by dopamine is affected by aging and how it is dependent on the Ca<jats:sup>2+<\/jats:sup> source. In slices from adult mice, the initial slope of the field potential showed strong <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>, but in slices from aged mice <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> was impaired. Dopamine did not affect <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in adult slices, but enhanced <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices. The dopamine D1\/D5 receptor (D1R\/D5R) agonist <jats:styled-content style=\"fixed-case\">SKF<\/jats:styled-content>\u201081297 did not affect <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in adult but caused a relative small increase in <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices; however, although there was no difference in dopamine D4 receptor (D4R) expression, the D4R agonist <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>168077 increased <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices to a magnitude similar to that in adult slices. The <jats:italic>N<\/jats:italic>\u2010Methyl\u2010D\u2010aspartate receptor antagonist D\u2010<jats:styled-content style=\"fixed-case\">AP<\/jats:styled-content>5 reduced <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in adult slices, but not in aged slices. However, in the presence of D\u2010<jats:styled-content style=\"fixed-case\">AP<\/jats:styled-content>5, <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>168077 completely blocked <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices. The voltage\u2010dependent calcium channel (<jats:styled-content style=\"fixed-case\">VDCC<\/jats:styled-content>) blocker nifedipine reduced <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in adult slices, but surprisingly enhanced <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices. Furthermore, in the presence of nifedipine, <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>168077 caused a strong enhancement of <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aged slices to a magnitude exceeding <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in adult slices. Our results indicate that the full rescue of impaired <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> in aging by the selective D4R activation and that a large potentiation role on <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content> by co\u2010application of D4R agonist and <jats:styled-content style=\"fixed-case\">VDCC<\/jats:styled-content> blocker may provide novel strategies for the intervention of cognitive decline of aging and age\u2010related diseases.<\/jats:p>","DOI":"10.1111\/acel.12666","type":"journal-article","created":{"date-parts":[[2017,10,4]],"date-time":"2017-10-04T04:10:38Z","timestamp":1507090238000},"page":"1323-1333","source":"Crossref","is-referenced-by-count":22,"title":["Dopamine D4 receptor activation restores <scp>CA<\/scp>1 <scp>LTP<\/scp> in hippocampal slices from aged mice"],"prefix":"10.1111","volume":"16","author":[{"given":"Fangli","family":"Guo","sequence":"first","affiliation":[{"name":"Key Lab of Brain Research 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