{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T17:15:42Z","timestamp":1789665342004,"version":"4.0.1"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2016,7,28]],"date-time":"2016-07-28T00:00:00Z","timestamp":1469664000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2016,9]]},"abstract":"Summary<\/jats:title>\n \n Objective<\/jats:title>\n \n Some antiseizure drugs (\n ASD<\/jats:styled-content>\n s) are associated with cognitive liability in patients with epilepsy, thus\n ASD<\/jats:styled-content>\n s without this risk would be preferred. Little comparative pharmacology exists with\n ASD<\/jats:styled-content>\n s in preclinical models of cognition. Few pharmacologic studies exist on the acute effects in rodents with chronic seizures. Predicting risk for cognitive impact with preclinical models may supply valuable\n ASD<\/jats:styled-content>\n differentiation data.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n ASD<\/jats:styled-content>\n s (phenytoin [\n PHT<\/jats:styled-content>\n ]; carbamazepine [\n CBZ<\/jats:styled-content>\n ]; valproic acid [\n VPA<\/jats:styled-content>\n ]; lamotrigine [\n LTG<\/jats:styled-content>\n ]; phenobarbital [\n PB<\/jats:styled-content>\n ]; tiagabine [\n TGB<\/jats:styled-content>\n ]; retigabine [\n RTG<\/jats:styled-content>\n ]; topiramate [\n TPM<\/jats:styled-content>\n ]; and levetiracetam [\n LEV<\/jats:styled-content>\n ]) were administered equivalent to maximal electroshock median effective dose ([\n ED<\/jats:styled-content>\n 50]; mice, rats), or median dose necessary to elicit minimal motor impairment (median toxic dose [\n TD<\/jats:styled-content>\n 50]; rats). Cognition models with naive adult rodents were novel object\/place recognition (\n NOPR<\/jats:styled-content>\n ) task with\n CF<\/jats:styled-content>\n \u20101 mice, and Morris water maze (\n MWM<\/jats:styled-content>\n ) with Sprague\u2010Dawley rats. Selected\n ASD<\/jats:styled-content>\n s were also administered to rats prior to testing in an open field. The effect of chronic seizures and\n ASD<\/jats:styled-content>\n administration on cognitive performance in\n NOPR<\/jats:styled-content>\n was also determined with corneal\u2010kindled mice. Mice that did not achieve kindling criterion (partially kindled) were included to examine the effect of electrical stimulation on cognitive performance. Sham\u2010kindled and age\u2010matched mice were also tested.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n No\n ASD<\/jats:styled-content>\n (\n ED<\/jats:styled-content>\n 50) affected latency to locate the\n MWM<\/jats:styled-content>\n platform;\n TD<\/jats:styled-content>\n 50 of\n PB<\/jats:styled-content>\n ,\n RTG<\/jats:styled-content>\n ,\n TPM<\/jats:styled-content>\n , and\n VPA<\/jats:styled-content>\n reduced this latency. In naive mice,\n CBZ<\/jats:styled-content>\n and\n VPA<\/jats:styled-content>\n (\n ED<\/jats:styled-content>\n 50) reduced time with the novel object. Of interest, no\n ASD<\/jats:styled-content>\n (\n ED<\/jats:styled-content>\n 50) affected performance of fully kindled mice in\n NOPR<\/jats:styled-content>\n , whereas\n CBZ<\/jats:styled-content>\n and\n LEV<\/jats:styled-content>\n improved cognitive performance of partially kindled mice.\n <\/jats:p>\n <\/jats:sec>\n \n Significance<\/jats:title>\n \n Standardized approaches to the preclinical evaluation of an\n ASD<\/jats:styled-content>\n 's potential cognitive impact are needed to inform drug development. This study demonstrated acute, dose\u2010 and model\u2010dependent effects of therapeutically relevant doses of\n ASD<\/jats:styled-content>\n s on cognitive performance of naive mice and rats, and corneal\u2010kindled mice. This study highlights the challenge of predicting clinical adverse effects with preclinical models.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/epi.13476","type":"journal-article","created":{"date-parts":[[2016,7,28]],"date-time":"2016-07-28T02:08:45Z","timestamp":1469671725000},"page":"1386-1397","source":"Crossref","is-referenced-by-count":46,"title":["Acute cognitive impact of antiseizure drugs in naive rodents and corneal\u2010kindled mice"],"prefix":"10.1111","volume":"57","author":[{"given":"Melissa L.","family":"Barker\u2010Haliski","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology Anticonvulsant Drug Development Program University of Utah Salt Lake City Utah U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabiola","family":"Vanegas","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology Anticonvulsant Drug Development Program University of Utah Salt Lake City Utah U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew J.","family":"Mau","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology Anticonvulsant Drug Development Program University of Utah Salt Lake City Utah U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tristan K.","family":"Underwood","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology Anticonvulsant Drug Development Program University of Utah Salt Lake City Utah U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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