{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T07:53:35Z","timestamp":1789372415633,"version":"build-2803163510"},"reference-count":49,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":3134,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2000,7]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Prisms of adult rat cortex were maintained <jats:italic>in vitro<\/jats:italic> in either aerobic conditions (control) or conditions simulating an acute ischaemic challenge (hypoxia with no added glucose).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Endogenous glutamate efflux increased with time in ischaemic conditions, being 2.7 fold higher than control efflux at 45\u2003min. Returning prisms to control solution after 20\u2003min of simulated ischaemia resulted in glutamate efflux returning to near\u2010control values. Endogenous GABA efflux in ischaemic conditions also increased, being 4.5 fold higher than control efflux at 45\u2003min.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Ischaemia\u2010induced glutamate efflux was not accompanied by increased lactate dehydrogenase efflux and was unaltered by omitting calcium from the extra\u2010cellular solution and adding EGTA (0.1\u2003m<jats:sc>M<\/jats:sc>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Both GABA and the GABA\u2010mimetic clomethiazole inhibited ischaemia\u2010induced glutamate efflux, with IC<jats:sub>50<\/jats:sub> values of 26 and 24\u2003\u03bc<jats:sc>M<\/jats:sc> respectively. The maximum inhibition by either drug was 60\u201370%. Bicuculline (10\u2003\u03bc<jats:sc>M<\/jats:sc>) abolished the inhibitory effect of GABA (100\u2003\u03bc<jats:sc>M<\/jats:sc>) but not clomethiazole (100\u2003\u03bc<jats:sc>M<\/jats:sc>). Picrotoxin (100\u2003\u03bc<jats:sc>M<\/jats:sc>) abolished the action of both GABA and clomethiazole.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Pentobarbitone inhibited glutamate efflux at 100\u2013300\u2003\u03bc<jats:sc>M<\/jats:sc> (maximal inhibition: 39%). Bicuculline (10\u2003\u03bc<jats:sc>M<\/jats:sc>) abolished this effect.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These data suggest that ischaemia\u2010induced glutamate efflux from rat cerebral cortex is calcium\u2010independent and not due to cell damage up to 45\u2003min. The inhibitory effect of GABA, clomethiazole and pentobarbitone on ischaemia\u2010induced glutamate efflux appears to be mediated by GABA<jats:sub>A<\/jats:sub> receptors. The results suggest that clomethiazole, unlike pentobarbitone, is able to activate the GABAA receptor\u2010linked chloride channel directly and not merely potentiate the effect of endogenous GABA.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p> <jats:italic>British Journal of Pharmacology<\/jats:italic> (2000) <jats:bold>130<\/jats:bold>, 1124\u20131130; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0703398\">10.1038\/sj.bjp.0703398<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0703398","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T21:15:45Z","timestamp":1106946945000},"page":"1124-1130","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["On the regulation of ischaemia\u2010induced glutamate efflux from rat cortex by GABA; <i>in vitro<\/i> studies with GABA, clomethiazole and pentobarbitone"],"prefix":"10.1111","volume":"130","author":[{"given":"R M","family":"Nelson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A R","family":"Green","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D G","family":"Lambert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A H","family":"Hainsworth","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0028-3908(93)90169-4"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1994.tb13050.x"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1984.tb05396.x"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1991.tb12443.x"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1995.tb14949.x"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1989.tb16893.x"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(99)01463-0"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0166-2236(99)01401-0"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.20.12.1627"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7742(08)60716-3"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0163-7258(98)00024-2"},{"key":"e_1_2_7_13_1","unstructured":"GREEN A.R.&CROSS A.J.(1997a).Neuroprotective agents and cerebral ischaemiapp373.London: Academic Press."},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7742(08)60715-1"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(92)90491-O"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(99)00233-6"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0028-3908(96)00060-3"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703042"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(92)90410-6"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1983.tb10045.x"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF01411367"},{"key":"e_1_2_7_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-6147(00)88999-3"},{"key":"e_1_2_7_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/0168-0102(88)90007-7"},{"key":"e_1_2_7_24_1","doi-asserted-by":"publisher","DOI":"10.1034\/j.1399-6576.1999.430206.x"},{"key":"e_1_2_7_25_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1993.tb09803.x"},{"key":"e_1_2_7_26_1","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(88)90228-X"},{"key":"e_1_2_7_27_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.29.3.705"},{"key":"e_1_2_7_28_1","doi-asserted-by":"crossref","first-page":"A7","DOI":"10.1038\/399a007","article-title":"The changing landscape of ischaemic brain injury mechanisms","volume":"399","author":"LEE J\u2010M.","year":"1999","journal-title":"Nature"},{"key":"e_1_2_7_29_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0074-7742(08)60722-9"},{"key":"e_1_2_7_30_1","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.1998.6994"},{"key":"e_1_2_7_31_1","first-page":"27","article-title":"Protection against ischaemic neuronal damage by drugs acting on excitatory neurotransmission","volume":"2","author":"MELDRUM B.","year":"1990","journal-title":"Cerebrovasc. 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