>Many target genes, upstream regulators and signalling pathways involved in the PFC response in our study could be linked to dendritic remodelling and spine atrophy, a well-described effect of chronic stress on the PFC. Based on the IPA pathway and upstream regulator analysis, glutamatergic and calcium signalling, as well as Htt and Bdnf-centred networks stood out as the most significantly involved. Indeed, repeated stress is known to cause suppressed glutamate receptor expression and signalling in the PFC, which is thought to be linked to dendritic atrophy (Yuen et al., 2012). Many recent studies have explored the antidepressant potential of ketamine in chronic stress animal models of depression, strengthening the glutamatergic theory of depression (Zhu et al., 2015; Sun, 2016). In addition, disruption of glutamatergic signalling has been previously linked to hyperactivity (Procaccini et al., 2011).

The animals in the study, as expected, showed depression-associated and hyperactivity behaviors. This study wasn't looking at any specific thing in a fine-grained sense, let alone trying to establish causation. But "no link" seems like quite a stretch.

Yes, of course they showed effects from the UCMS. But not one single sentence in that report said that those effects were from gene expression. YOU are the only one adding a link there. It's easy for someone like you to just say there's a link, but not even the study pretends to say there's a link between the results of trauma are because of gene expression.