کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
333408 | 545917 | 2015 | 7 صفحه PDF | دانلود رایگان |
• Immobilization stress reduces p-GSK-3β and β-catenin levels in the frontal cortex.
• This stress decreases the levels of BDNF, PSD-95, and synaptophysin.
• Atypical antipsychotics reversed stress-induced decrease in these proteins levels.
• However, typical antipsychotic drug haloperidol had no such effects.
• Atypical antipsychotics may improve the impaired synaptic plasticity.
The present study examined the effects of antipsychotic drugs on the expression of synapse-associated proteins in the frontal cortex of rats with and without immobilization stress. Rats were subjected to immobilization stress 6 h/day for 3 weeks. The effects of atypical antipsychotic drugs, olanzapine and aripiprazole, on expression of serine9-phosphorylated GSK-3β, β-catenin, BDNF, PSD-95, and synaptophysin were determined by Western blotting. A typical antipsychotic drug, haloperidol, was used for comparison. Immobilization stress significantly decreased the expression of these proteins in the frontal cortex. Chronic administration of olanzapine and aripiprazole significantly attenuated the immobilization stress-induced decrease in the levels of these proteins, whereas haloperidol had no such effect. Additionally, olanzapine and aripiprazole significantly increased levels of phosphorylated GSK-3β under normal conditions without stress, and aripiprazole also increased BDNF levels under this condition. These results indicate that olanzapine and aripiprazole, and, haloperidol, differentially regulate the levels of synapse-associated proteins in the rat frontal cortex. These findings may contribute to explain the neurobiological basis of how olanzapine and aripiprazole up-regulated synapse-associated proteins.
Journal: Psychiatry Research - Volume 229, Issue 3, 30 October 2015, Pages 968–974