Answer:
xxxxxxxxx, arising from xxxxxxxxxxxxxxxxxx nuclei, is intimately involved in the treatment of xxxxxxxxxxxxxxxxx and anxiety xxxxxxxxxxxx. Serotonin selective reuptake xxxxxxxxxxxxxxx (SSRIs) are xxxxxxxxxxxxtherapy for both of these conditions, and have well-described behavioral effects in animal models of emotional behavior. Yet, administration of SSRIs during xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx an opposing xxxxxxxxxxxx, including increased anxiety- xxxxxxxxxxxxxxxxxxxx depression-like and reduced social behaviors.xxxxxxxxxxxxxxxxxxxxx, the target of these drugs, is expressed xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx, I sought to identify xxxxxxxxxxxxxxxxxxxxxxxxxx for behavioral xxxxxxxxxxxxxxxxxxxxx and postnatal SSRI treatment in this cell xxxxxxxxxxxxxxxxxxxx. Initially, we compared the transcriptome of serotonergic neurons to whole brain homogenate, in order to xxxxxxxxxxxxxxxxxxxxxx the experimental xxxxxxxxxxxxxx, and to provide a xxxxxxxxxxxxxxxxx analysis of gene expression in this xxxxxxxxxxxxxxxx. Many xxxxxxxxxxxxxxxxxxx were enriched in raphé xxxxxxxxx, including both known xxxxxxxxxxxxxxx of serotonergic xxxxxxxxxxxxx, and xxxxxxxxxxxxxxxx genes, most of which could be xxxxxxxxxxxxxxxxx from by in situ hybridization xxxxxxxxxxx from the xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx.
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx mice, xxxxxxxxxxxxxxxxxx expression profiling xxxxxxxxxxxxxxxxxxxxxxx of differentially xxxxxxxxxxxxxxxx transcripts. We further used postnatal fluoxetine treatment as a model of treatment resistance, investigating the transcriptional xxxxxxxxxxxxxxxx fluoxetine treatment in xxxxxxxxxxxxxxx- vs. saline-treated xxxxxxxxxxxxx, in order to identify transcripts xxxxxxxxxxxxxxwith behavior. We found xxxxxxxxxxxxof a number of promising candidate genes, including vesicular glutamate transporter xxxxxxxx, histamine receptor xxxxxxxx, and the xxxxxxxxxxxxxx processing enzyme xxxxxxxxxxxxxxx.
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