{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T13:50:03Z","timestamp":1768917003771,"version":"3.49.0"},"reference-count":52,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2024,1,18]],"date-time":"2024-01-18T00:00:00Z","timestamp":1705536000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000780","name":"European Commission","doi-asserted-by":"publisher","award":["101078981"],"award-info":[{"award-number":["101078981"]}],"id":[{"id":"10.13039\/501100000780","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia Open"],"published-print":{"date-parts":[[2024,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>The objective of the study was to propose a candidate animal model of absence status epilepticus induced by specific alpha\u20102a adrenergic receptor (\u03b12AR) activation. We also aim to investigate the responsiveness of this model to classical anti\u2010status or anti\u2010absence medications.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>An \u03b12AR agonist, dexmedetomidine (DEX), was injected intracerebroventricularly into adult rats with genetic absence epilepsy, and their electroencephalography (EEG) was recorded. The total duration, number, and mean duration of each spike\u2010and\u2010wave discharges (SWDs) were evaluated. The blocks of absence status events were classified as the initial and second sets of absence statuses. Ethosuximide (ETX) was administered as a pretreatment to another group of rats and later injected with 2.5\u2009\u03bcg DEX. In addition, ETX, valproic acid (VPA), diazepam (DIAZ), and atipamezole (ATI) were administered after induced status\u2010like events following DEX administration. Power spectral characteristics and coherence analysis were performed on the EEG to assess the absence status events and sleep.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The 2.5\u2009\u03bcg dose of DEX increased the total SWD duration and induced continuous SWDs up to 26\u2009min. Following the initial absence status event, sleep was induced; then, the second period of absence status\u2010like activities were initiated. ETX pretreatment blocked the occurrence of absence status\u2010like activities. Power spectral density analyses revealed that DEX\u2010induced post\u2010sleep activities had higher power in delta frequency band (1\u20134\u2009Hz) and attenuated power of 7\u2009Hz harmonics (14 and 21\u2009Hz) than the pre\u2010injection seizure. The mean duration of SWDs were decreased in all the groups, but occasional prolonged activities were seen in ETX or VPA\u2010injected rats but not with DIAZ or ATI.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>This study presents an absence status epilepticus animal model that is activated by \u03b12AR activation to investigate the pathophysiological role of absence status. Unlike other agents ATI switched off the second set of absence statuses to normal SWDs, without sedation or lethargy, can show it may preferentially block absence status\u2010like activity.<\/jats:p><\/jats:sec><jats:sec><jats:title>The Plain Language Summary<\/jats:title><jats:p>This study proposes a rat model for prolonged seizures, resembling absence status epilepticus. Activating the brain\u2019s alpha\u20102a adrenergic receptor with dexmedetomidine induced seizures lasting up to 26 minutes. Ethosuximide pretreatment and post\u2010treatment with valproic acid, diazepam, and atipamezole decreased induced seizures. The findings suggest this model is valuable for studying absence status epilepticus. In addition, atipamezole normalized abnormal seizures without sedation, hinting at its potential for targeted treatment and further research.<\/jats:p><\/jats:sec>","DOI":"10.1002\/epi4.12879","type":"journal-article","created":{"date-parts":[[2023,12,10]],"date-time":"2023-12-10T04:05:20Z","timestamp":1702181120000},"page":"534-547","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Alpha\u20102a adrenergic receptor activation in genetic absence epilepsy: An absence status model?"],"prefix":"10.1002","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1250-9755","authenticated-orcid":false,"given":"Melis","family":"Yavuz","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Faculty of Pharmacy Acibadem Mehmet Ali Aydinlar University University  Istanbul 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