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http://dx.doi.org/10.1176/ajp.143.5.681 | DOI Listing |
World J Biol Psychiatry
December 2020
Centre for Molecular and Medical Research, School of Medicine, Deakin University, Geelong, Australia.
To create a gene expression signature (GES) to represent the biological effects of a combination of known drugs for bipolar disorder (BD) on cultured human neuronal cells (NT2-N) and rat brains, which also has evidence of differential expression in individuals with BD. To use the GES to identify new drugs for BD using Connectivity Map (CMap). NT2-N ( = 20) cells and rats ( = 8) were treated with a BD drug combination (lithium, valproate, quetiapine and lamotrigine) or vehicle for 24 and 6 h, respectively.
View Article and Find Full Text PDFPharmacopsychiatry
March 2002
Department of General Psychiatry, University of Vienna, Austria.
Recurrent Brief Depression (RBD) is a prevalent condition among the depressive illnesses, and is characterized by depressive episodes of a few days' duration occurring almost every month that are unrelated to the menstruation cycle. So far, RBD has not been shown to respond to antidepressive treatment in controlled clinical trials with citalopram, fluoxetine, flupenthixol, paroxetine, or mianserin using a "classical" parallel group design. However, successful RBD treatment on about sixty patients has so far been reported in one open trial with fluoxetine and in several cases with lithium, mirtazapine, and tranylcypromine.
View Article and Find Full Text PDFBehav Brain Res
February 2002
Department of Anatomy and Cell Biology, Neurobiology Research Group, University of Toronto, Medical Sciences Building, Toronto, Ont., Canada.
We have previously reported that mesolimbic dopamine (DA) substrates are critically involved in the rewarding effects of opiates only during states of opiate-dependence and withdrawal. However, in previously drug-naive animals, opiate reward is mediated through a DA-independent neural system. In the present study, we report that bilateral microinjections of a DA receptor antagonist, alpha-flupenthixol (0.
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