Study summary · research use only
GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this human neuroblastoma (IMR-32) cell line study, researchers examined expression of 84 genes involved in GABAergic neurotransmission using qPCR, testing GABA, Selank, olanzapine, and combinations of Selank with GABA or olanzapine. The abstract reports no changes in mRNA levels of the studied genes with Selank alone, that combined GABA and Selank nearly completely suppressed the gene expression changes seen with GABA alone, and that Selank combined with olanzapine altered expression of more genes than olanzapine alone. The authors state Selank had no direct effect on mRNA levels of GABAergic system genes in IMR-32 cells, while the results partially support the idea that the peptide may affect GABA's interaction with GABAA receptors and that Selank may enhance olanzapine's effect on the genes studied.
Abstract
Clinical studies have shown that Selank had an anxiolytic effect comparable to that of classical benzodiazepine drugs, which can enhance the inhibitory effect of GABA by allosteric modulation of GABAA receptors. These data suggest that the molecular mechanism of the effect of Selank may also be related to its ability to affect the performance of the GABAergic system. To test this hypothesis, we studied the changes in expression of 84 genes involved in the functioning of the GABAergic system and in the processes of neurotransmission in the culture of neuroblastoma IMR-32 cells using qPCR method. As test substances, in addition to Selank, we selected the major GABAA receptor ligand, GABA, the atypical antipsychotic, olanzapine, and combinations of these compounds (Selank and GABA; Selank and olanzapine). We found no changes in the mRNA levels of the genes studied under the effect of Selank. The combined effect of GABA and Selank led to nearly complete suppression of changes in expression of genes in which mRNA levels changed under the effect of GABA. When Selank was used in conjunction with olanzapine, the expression alterations of more genes were observed compared with olanzapine alone. The data obtained indicate that Selank has no direct effect on the mRNA levels of the GABAergic system genes in neuroblastoma IMR-32 cells. At the same time, our results partially confirm the hypothesis that the peptide may affect the interaction of GABA with GABAA receptors. Our data also suggest that Selank may enhance the effect of olanzapine on the expression of the genes studied.
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