The acute and chronic effects of combined antipsychotic–mood stabilizing treatment on the expression of cortical and striatal postsynaptic density genes

Protein expression of targets of the FMRP regulon is altered in brains of subjects with schizophrenia and mood disorders

“…Thus, in rat, haloperidol mostly increased mRNA for homer 1 in basal ganglia and other brain regions but not in prefrontal cortex (De Bartolomeis et al, 2002; Polese et al, 2002; Iasevoli et al, 2010a; Tomasetti et al, 2011) both acutely and chronically. Olanzapine increased mRNA in frontal cortex chronically (Fatemi et al, 2006) as well as in other brain regions (Iasevoli et al, 2010b).…”

Quetiapine and repetitive transcranial magnetic stimulation ameliorate depression-like behaviors and up-regulate the proliferation of hippocampal-derived neural stem cells in a rat model of depression: The involvement of the BDNF/ERK signal pathway

“…One study reported that the activation and expression of ERK1/2 MAP kinase is reduced in the post-mortem brains of depressed suicide subjects (Dwivedi et al, 2001). Several gene expression studies indicated that quetiapine up-regulates ERK1/2 expression (Tomasetti et al, 2011). And a recent study found that norquetiapine activates ERK/MAPK signaling to induce glial cell-derived neurotrophic factor release in C6 glioma cells (Di Benedetto et al, 2012), and this mechanism might contribute to the putative antidepressant action of QUE at the cellular level.…”

Modulation of neuronal plasticity following chronic concomitant administration of the novel antipsychotic lurasidone with the mood stabilizer valproic acid

“…While the efficacy of such combinations relies on receptor and synaptic mechanisms in order to control neurotransmitter/circuitry dysfunction underlying specific disease symptoms, it is important to consider that functional recovery may involve neuroadaptive modifications leading to structural and molecular changes in selected brain regions, which are set in motion by the interaction between different intracellular pathways (Krishnan and Nestler 2010). For example, we have previously shown that fluoxetine-olanzapine combination increases the expression of the neurotrophic molecule FGF2 in prefrontal cortex through the Akt pathway (Maragnoli et al 2004), whereas acute and chronic treatments with combined antipsychotic and mood stabilizers may alter the expression of synaptic proteins (Tomasetti et al 2011).…”