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We tested the hypothesis that a single episode of neonatal seizures (sNS) on rat postnatal day (P) 7 permanently impairs hippocampal\u2010dependent function in mature (P60) rats because of long\u2010lasting changes at the synaptic level.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>sNS was induced with subcutaneously injected kainate on P7. Learning, memory, mossy fiber sprouting, spine density, hippocampal synaptic plasticity, and glutamate receptor expression and subcellular distribution were measured at P60.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      sNS selectively impaired working memory in a hippocampal\u2010dependent radial arm water\u2010maze task without inducing mossy fiber sprouting or altering spine density. sNS impaired CA1 hippocampal long\u2010term potentiation and enhanced long\u2010term depression. Subcellular fractionation and cross\u2010linking, used to determine whether glutamate receptor trafficking underlies the alterations of memory and synaptic plasticity, demonstrated that sNS induced a selective reduction in the membrane pool of glutamate receptor 1 subunits. sNS induced a decrease in the total amount of\n                      <jats:italic>N<\/jats:italic>\n                      \u2010methyl\u2010\n                      <jats:sc>D<\/jats:sc>\n                      \u2010aspartate receptor 2A and an increase in the primary subsynaptic scaffold, PSD\u201095.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>These molecular consequences are consistent with the alterations in plasticity and memory caused by sNS at the synaptic level. Our data demonstrate the cognitive impact of sNS and associate memory deficits with specific alterations in glutamatergic synaptic function. Ann Neurol 2007<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.21071","type":"journal-article","created":{"date-parts":[[2007,2,23]],"date-time":"2007-02-23T15:26:02Z","timestamp":1172244362000},"page":"411-426","source":"Crossref","is-referenced-by-count":127,"title":["A single episode of neonatal seizures permanently alters glutamatergic synapses"],"prefix":"10.1002","volume":"61","author":[{"given":"Brandon J.","family":"Cornejo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael H.","family":"Mesches","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Coultrap","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael D.","family":"Browning","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy A.","family":"Benke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2007,2,23]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1157.1999.tb00878.x"},{"key":"e_1_2_6_3_2","first-page":"191","volume-title":"Neonatal seizures. 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