Ashokan et al vs Lehmann et al
Seminar in BioPsych
There was a stark difference in the delivery of these two papers. I found that Ashokan et al was rather dry (maybe due to the format of the journal — I’m not sure), although the finding was super interesting! Short term environmental enrichment is enough to lead to an inability to experience defeat! Not only is this true behaviorally (with regard to anxiety related and risk assessment behaviors), but they also found that there are distinct morphological changes (in spine density and dendritic morphology) as well as biochemical changes (in BDNF and corticosterone expression) in resilient states. Even still, the article sounded very little like a narrative, as I find scientific papers normally do, and more like a series of statistical findings.
Something interesting that I noted was that the statistical tests were very explicitly highlighted, which manifested that they conducted several statistical tests, of which some produced fruitful (statistically significant) results, while others did not. Why was this necessary? What’s a Sidak’s multiple comparisons test? And why is it important to conduct orthogonal planned comparisons along with ANOVAs? I think the density of statistical jargon clouded the message of the results section. Could this jargon have been shifted to the methods section? That’s where I go when I want to know the nitty gritty anyway.
Furthermore, I think it would’ve been interesting to know whether this short-term period of EE can lead to long-term resilience. Maybe the EE is just a distraction for a little while and once the transient euphoria of good experience fades, the dwindling road to depressive symptomatology ensues. It would have been an interesting question to probe.
Lehmann et al., on the other hand, addressed some really cool aspects of resilience — the induction of FosB as well as the role of the infralimbic cortex (ILCtx) in this phenomenon, a brain region largely implicated in limbic function. At first, they showed that EE indeed leads to a resilient behavioral state (as Ashokan et al. did). They then alluded to a really cool paper from 2010 by Vialou et al regarding the artificial induction of FosB and its antidepressant effects, as well as the physiological patterns of FosB induction after antidepressant administration (really cool paper). They found that environmental enrichment led to an increase in FosB, in line with the previously established role of FosB in resilience. However, they also found an opposite pattern of FosB expression in the HPA axis, which lends to a multifaceted role of FosB in different brain regions.
I found it interesting that they decided to address the question of whether ILCtx is crucial for resilience acquisition or for resilience expression, and more interesting that they found that its role lies in acquisition. FosB is known to degrade more slowly than many other proteins in the brain, and so it might make sense that gradual increase in FosB is concomitant with the gradual learning of resilience. Maybe if you selectively disabled FosB expression in the ILCtx during EE, resilience would not be able to be achieved. That would be a more targeted approach to answering the question of how FosB is important in resilience acquisition by the ILCtx. Furthermore, they showed that the ILCtx is necessary for resilience acquisition; however, it would have been interesting to see whether ILCtx activation is sufficient to enable a resilient phenotype. Considering how equivocal the data on ILCtx involvement in emotional regulation is, I imagine it’s more complicated than: increased ILCtx activity -> increased resilience. Perhaps, the opposite of the above proposed experiment (overexpressing FosB in the ILCtx instead of inactivating it) could provide some insight into the ILCtx’s involvement in the acquisition of a resilient phenotype.
Resilience is such an interesting phenomenon. I really wonder what allows some people to be more resilient to stress than others.