{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:43:39Z","timestamp":1773150219135,"version":"3.50.1"},"reference-count":84,"publisher":"Society for Neuroscience","issue":"26","license":[{"start":{"date-parts":[[2004,12,30]],"date-time":"2004-12-30T00:00:00Z","timestamp":1104364800000},"content-version":"vor","delay-in-days":183,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2004,6,30]]},"abstract":"<jats:p>Extracellular signal-regulated kinase (ERK) 1\/2, a well known regulator of gene expression, is likely to contribute to signaling events underlying enduring neural adaptations. Phosphorylated (phospho)-ERK was examined immunohistochemically after both single and repeated (i.e., sensitizing) doses of the partial D<jats:sub>1<\/jats:sub>-dopamine (DA) receptor agonist SKF-38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benazepine HCl) to adult rats lesioned as neonates (neonate lesioned) with 6-hydroxydopamine. Remarkably, prolonged phospho-ERK accumulated primarily in layers II-III of medial prefrontal cortex (MPC), where it declined gradually yet remained significantly elevated for at least 36 d after repeated doses of SKF-38393. Sustained (\u22657 d) phospho-ERK was observed for shorter periods in various other cortical regions but was not detectable in striatum or nucleus accumbens. At 36 d, an additional injection of SKF-38393 to sensitized rats restored phospho-ERK to maximal levels only in MPC when examined 7 d later. Phosphorylated cAMP response element-binding protein (CREB), examined 7 d after the sensitizing regimen, was observed exclusively in MPC, where it was abundant throughout all layers. Systemic injections of SL327 (\u03b1-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile), an inhibitor of the upstream ERK activator mitogen ERK kinase, attenuated both ERK and CREB phosphorylation in layers II-III of MPC. Pretreatment with the D<jats:sub>1<\/jats:sub>antagonist SCH-23390 ((<jats:italic>R<\/jats:italic>)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-OL maleate) inhibited the prolonged increase in MPC phospho-ERK, whereas the 5-HT<jats:sub>2<\/jats:sub>receptor antagonist ketanserin (3-[2-[4-(4-fluorobenzoyl)-1-piperidinyl]ethyl]-2,4(1H,3H)-quinazolinedione tartrate) was ineffective. Competitive and noncompetitive NMDA receptor antagonists also blocked sustained ERK phosphorylation. Collectively, the present results demonstrate coupling of D<jats:sub>1<\/jats:sub>and NMDA receptor function reflected in sustained activation of the ERK signaling pathway in MPC of SKF-38393-sensitized neonate-lesioned rats. Ultimately, long-lasting phosphorylation of ERK and CREB in MPC may play a pivotal role in any permanent adaptive change(s) in these animals.<\/jats:p>","DOI":"10.1523\/jneurosci.0528-04.2004","type":"journal-article","created":{"date-parts":[[2004,6,30]],"date-time":"2004-06-30T16:23:28Z","timestamp":1088612608000},"page":"5863-5876","source":"Crossref","is-referenced-by-count":38,"title":["Sustained Extracellular Signal-Regulated Kinase 1\/2 Phosphorylation in Neonate 6-Hydroxydopamine-Lesioned Rats after Repeated D<sub>1<\/sub>-Dopamine Receptor Agonist Administration: Implications for NMDA Receptor Involvement"],"prefix":"10.1523","volume":"24","author":[{"given":"Sophia T.","family":"Papadeas","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bonita L.","family":"Blake","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darin J.","family":"Knapp","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George R.","family":"Breese","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"393","published-online":{"date-parts":[[2004,6,30]]},"reference":[{"key":"2023041303072007000_24.26.5863.1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.42.082701.145401"},{"key":"2023041303072007000_24.26.5863.2","doi-asserted-by":"publisher","DOI":"10.1007\/s002210050544"},{"key":"2023041303072007000_24.26.5863.3","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(97)00842-1"},{"key":"2023041303072007000_24.26.5863.4","doi-asserted-by":"publisher","DOI":"10.1038\/2836"},{"key":"2023041303072007000_24.26.5863.5","doi-asserted-by":"publisher","DOI":"10.1126\/science.1715095"},{"key":"2023041303072007000_24.26.5863.6","doi-asserted-by":"publisher","DOI":"10.1007\/BF02245123"},{"key":"2023041303072007000_24.26.5863.7","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(03)00012-5"},{"key":"2023041303072007000_24.26.5863.8","doi-asserted-by":"crossref","first-page":"107","DOI":"10.3109\/10799898809048981","volume":"8","year":"1988","journal-title":"J Recept Res"},{"key":"2023041303072007000_24.26.5863.9","doi-asserted-by":"crossref","unstructured":"Bishop C, Tessmer JL, Ullrich T, Rice KC, Walker PD (2004) Serotonin 5-HT2A receptors underlie increased motor behaviors induced in dopamine-depleted rats by intrastriatal 5-HT2A\/2C agonism. 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