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Addiction Pathways

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This week’s papers, Venniro et al. 2018 and deGuglielmo et al. 2019, dive deeply into secondary neural systems involved in perpetuating addiction. Most common knowledge implicates reward pathways and decision-making in driving an animal do pursue chronic drug use as a salient reward. But, these papers implicate social interaction dependent pathways as well as CRF reception in the amygdala respectively as other effectors in which can modulate rats’ addictive response to drug self-administration. In proving so, these papers back up the fact that addiction truly isn’t a homogeneous condition, therefore many other realms should be studied in order to understand the true complexity. 
            Venniro et al. 2018 presents an interesting look at how the choice of social interaction can overwhelm the choice of drug intake in rats regardless of certain predispositions in forming addiction. In the discussion of this paper, the translational value of this information and model is spoken about, asking if social interaction in humans may have a similar affect. I think that this presents an interesting debate as some social interaction in humans can influence drug use and further addiction. Therefore, I think the valence of the social interaction comes into play. It could’ve been interesting look at not just the operant choice of social interaction but how forced social interaction with different valences and groups can affect addiction. For example, if a mouse who had developed a methamphetamine or heroin addiction was placed in a group of mice, would this reduce the addictive habits or does primary exposure to group social interaction decrease the likelihood of addiction prior to or during usage. In humans, a common protective factor to reducing relapse and reinstatement of usage are focus groups in which social interaction is mostly forced. Therefore, I think this could be a very interesting future direction for the research done here. 
            deGuglielmo et al. 2019 investigates a different avenue in alcohol addiction in which CRF receptor expression is shown to be profound in the central amygdala and can decrease alcohol consumption as well as withdrawal in rats. Their data is pretty convincing and show the underpinnings of the CeA-BNST CRF dependent circuit in modulating alcohol dependency. What is interesting to consider is how stress would relate to CRF levels in the ISF and how transient a HPA axis-mediated response would be in affecting alcohol usage. Therefore, there could be a further link here in how stress responses might affect addiction pathways indirectly, especially due to the involvement of the amygdala. 
            In conclusion, both papers implicate the amygdala’s central role in mediating effectors of addiction that contribute to its complex heterogeneous nature. Therefore, it is very exciting to see other paradigms and biological basis being involved in the discussions surrounding how addiction manifests in the brain.

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