P:// creativecommons.org/licenses/by-nc/3.0/13. 14. Goetz CG, Leurgans S, Pappert EJ, et al. Potential longitudinal assessment of hallucinations in Parkinson’s illness. Neurology 2001;57:2078?2. Williams DR, Lees AJ. Visual hallucinations within the diagnosis of idiopathic Parkinson’s illness: a retrospective autopsy study. Lancet Neurol 2005;four:605?0. Merims D, Shabtai H, Korczyn AD, et al. Antiparkinsonian medication just isn’t a risk factor for the improvement of hallucinations in Parkinson’s illness. J Neural Transm 2004;111:1447?three. Kawakami Y, Inoue A, Kawai T, et al. The rationale for E2020 as a potent acetylcholinesterase inhibitor. Bioorg Med Chem 1996;four:1429?six. Giacobini E, Zhu XD, Williams E, et al. The effect from the selective reversible acetylcholinesterase inhibitor E2020 on extracellular acetylcholine and biogenic amine levels in rat cortex. Neuropharmacology 1996;35:205?1. Nochi S, Asakawa N, Sato T. Kinetic study on the inhibition of acetylcholinesterase by 1-benzyl-4-[(five,6-dimethoxy-1-indanon)-2-yl] methylpiperidine hydrochloride (E2020). Biol Pharm Bull 1995;18:1145?. Kosasa T, Kuriya Y, Matsui K, et al. Effect of donepezil hydrochloride (E2020) on basal concentration of extracellular acetylcholine inside the hippocampus of rats. Eur J Pharmacol 1999;380:101?. Kosasa T, Kuriya Y, Yamanishi Y. Effect of donepezil hydrochloride (E2020) on extracellular acetylcholine concentration within the cerebral cortex of rats. Jpn J Pharmacol 1999;81:216?two. Manganelli F, Vitale C, Santangelo G, et al. Functional involvement of central cholinergic circuits and visual hallucinations in Parkinson’s illness. Brain 2009;132(Pt 9):2350?. Brandstaedter D, Spieker S, Ulm G, et al. Development and evaluation on the Parkinson Psychosis Questionnaire a screening-instrument for the early diagnosis of drug-induced psychosis in Parkinson’s illness. J Neurol 2005;252: 1060?. Daniel SE, Lees AJ. Parkinson’s Illness Society Brain Bank, London: overview and research. J Neural Transm 1993;39: 165?two.1255352-25-0 manufacturer
Psychopharmacology (2014) 231:3109?118 DOI 10.1007/s00213-014-3491-ORIGINAL INVESTIGATIONReactivation of cocaine reward memory engages the Akt/GSK3/mTOR signaling pathway and may be disrupted by GSK3 inhibitionXiangdang Shi Jonathan S. Miller Lauren J. Harper Rachel L. Poole Thomas J. Gould Ellen M. UnterwaldReceived: 26 September 2013 / Accepted: 4 February 2014 / Published on the web: 5 March 2014 # The Author(s) 2014.187039-57-2 uses This short article is published with open access at SpringerlinkAbstract Rational Memories return to a labile state following their retrieval and must undergo a course of action of reconsolidation to become maintained.PMID:35954127 As a result, disruption of cocaine reward memories by interference with reconsolidation could be therapeutically valuable within the remedy of cocaine addiction. Objective The objectives were to elucidate the signaling pathway involved in reconsolidation of cocaine reward memory and to test whether targeting this pathway could disrupt cocaine-associated contextual memory. Techniques Applying a mouse model of conditioned place preference, regulation on the activity of glycogen synthase kinase-3 (GSK3), mammalian target of Rapamycin complicated 1 (mTORC1), P70S6K, -catenin, and the upstream signaling molecule Akt, was studied in cortico-limbic-striatal circuitry following re-exposure to an atmosphere previously paired with cocaine. Result Levels of phosporylated Akt-Thr308, GSK3-Ser21, GSK3-Ser9, mTORC1, and P70S6K were decreased inside the nucleus accumbens and hippocampus 10 min a.