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A 10\u00a0min application of 5-100\u00a0\u03bcM DA decreases LP I<jats:sub>A<\/jats:sub> by producing a decrease in I<jats:sub>A<\/jats:sub> maximal conductance (G<jats:sub>max<\/jats:sub>) and a depolarizing shift in I<jats:sub>A<\/jats:sub> voltage dependence through a cAMP-Protein kinase A (PKA) dependent mechanism. Alternatively, a 1\u00a0hr application of DA (\u22655 nM) generates a persistent (measured 4\u00a0hr after DA washout) increase in I<jats:sub>A<\/jats:sub> G<jats:sub>max<\/jats:sub> in the same neuron, through a mechanistic target of rapamycin (mTOR) dependent translational mechanism. We examined the dose, time and protein dependencies of the persistent DA effect.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>We found that disrupting normal modulatory tone decreased LP I<jats:sub>A<\/jats:sub>. Addition of 500 pM-5 nM DA to the saline for 1\u00a0hr prevented this decrease, and in the case of a 5 nM DA application, the effect was sustained for &gt;4\u00a0hrs after DA removal. To determine if increased cAMP mediated the persistent effect of 5nM DA, we applied the cAMP analog, 8-bromo-cAMP alone or with rapamycin for 1\u00a0hr, followed by wash and TEVC. 8-bromo-cAMP induced an increase in I<jats:sub>A<\/jats:sub> G<jats:sub>max<\/jats:sub>, which was blocked by rapamycin. Next we tested the roles of PKA and guanine exchange factor protein activated by cAMP (ePACs) in the DA-induced persistent change in I<jats:sub>A<\/jats:sub> using the PKA specific antagonist Rp-cAMP and the ePAC specific agonist 8-pCPT-2\u2032-O-Me-cAMP. The PKA antagonist blocked the DA induced increases in LP I<jats:sub>A<\/jats:sub> G<jats:sub>max<\/jats:sub>, whereas the ePAC agonist did not induce an increase in LP I<jats:sub>A<\/jats:sub> G<jats:sub>max<\/jats:sub>. Finally we tested whether extracellular signal regulated kinase (Erk) activity was necessary for the persistent effect by co-application of Erk antagonists PD98059 or U0126 with DA. Erk antagonism blocked the DA induced persistent increase in LP I<jats:sub>A<\/jats:sub>.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>These data suggest that dopaminergic tone regulates ion channel density in a concentration and time dependent manner. The D1R- PKA axis, along with Erk and mTOR are necessary for the persistent increase in LP I<jats:sub>A<\/jats:sub> induced by high affinity D1Rs.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2202-14-143","type":"journal-article","created":{"date-parts":[[2013,11,13]],"date-time":"2013-11-13T12:02:07Z","timestamp":1384344127000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Dopaminergic tone regulates transient potassium current maximal conductance through a translational mechanism requiring D1Rs, cAMP\/PKA, Erk and mTOR"],"prefix":"10.1186","volume":"14","author":[{"given":"Edmund W","family":"Rodgers","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wulf-Dieter","family":"Krenz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyue","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingjun","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah J","family":"Baro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2013,11,13]]},"reference":[{"issue":"2","key":"3441_CR1","doi-asserted-by":"publisher","first-page":"241","DOI":"10.1016\/S0896-6273(02)00967-4","volume":"36","author":"W Schultz","year":"2002","unstructured":"Schultz W: Getting formal with dopamine and reward. 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