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Together, these findings suggest that the aberrant astrocytic GABA in PTSD is possibly driven by enhanced synthesis via MAOB and reduced degradation via ABAT in reactive astrocytes, contributing to the excessive inhibitory tone observed in PTSD

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Specific numbers from animal studies include: reported upregulation of growth hormone receptor expression in tendon fibroblasts, effects on VEGF-mediated tube formation in endothelial cell assays, and dose-dependent reductions in gastric ulcer area in rat models at doses ranging from 10 micrograms per kilogram to higher concentrations