Why we put off things we enjoy doing.

Interesting perspective from Hagen and Brien: 

Abstract

People commonly experience long gaps of time between getting to do things they love to do. In principle, the longer it has been since people last enjoyed something, the quicker they should jump at the chance to enjoy it again. In practice, five experiments reveal a case of the opposite: The longer since people's last enjoyable experience, the more they postpone returning—in part because they demand their return be “extra special” to offset the wait. This effect emerged across many controlled parameters. For example, participants chose to avoid contacting close friends after large vs. small gaps in contact, all else equal—a choice that undermined their immediate happiness. This effect further extended to COVID-19 contexts, regarding people's returns from lengthy shutdowns: Somewhat nonobviously, we found that participants delayed returning to everyday activities even longer (as opposed to jumping back at their first sufficiently good chance) if it meant that they could better mark the occasion. Finally, this effect was uniquely attenuated by helping participants reconstrue any chance to return as “extra special.” Together, these findings suggest that time delays create psychological barriers to returning, which people self-impose. People may increasingly avoid contacting loved ones, getting back into rewarding hobbies, and so on, the longer it has been since last time, promoting vicious cycles of deferment. Motivating people to return to experiences that would enhance their immediate happiness—experiences they still want to have and are now theirs to take—may be surprisingly difficult.

 

The optimistic brain - fMRI reveals shared thought patterns.

From Yanagisawa et al.:  

Significance

Optimism, defined as maintaining positive expectations for the future, is a crucial psychological resource correlated with enhanced well-being and physical health. Recent research suggests that neural processing of cognitive function is similar among individuals with positive traits but more dissimilar among those with negative traits. Applying the cross-subject neural representational analytical approach, we found that optimistic individuals display similar neural processing when imagining the future, whereas less optimistic individuals show idiosyncratic differences. Additionally, we found that optimistic individuals imagined positive events as more distinct from negative events than less optimistic individuals. These results have both theoretical and methodological implications for our understanding of the adaptive nature of optimism.

Abstract

Optimism is a critical personality trait that influences future-oriented cognition by emphasizing positive future outcomes and deemphasizing negative outcomes. How does the brain represent idiosyncratic differences in episodic future thinking that are modulated by optimism? In two functional MRI (fMRI) studies, participants were scanned during an episodic future thinking task in which they were presented with a series of episodic scenarios with different emotional valence and prompted to imagine themself (or their partner) in the situation. Intersubject representational similarity analysis revealed that more optimistic individuals had similar neural representations in the medial prefrontal cortex (MPFC), while less optimistic individuals exhibited more idiosyncratic neural representations in the MPFC. Additionally, individual difference multidimensional scaling of MPFC activity revealed that the referential target and emotional valence of imagined events were clearly mapped onto different dimensions. Notably, the weights along the emotional dimension were closely linked to the optimism scores of participants, suggesting that optimistic individuals imagine positive events as more distinct from negative events. These results suggest that shared neural processing of the MPFC among optimistic individuals supports episodic future thinking that facilitates psychological differentiation between positive and negative future events.

 

 

How ketamine breaks through anhedonia - reigniting desire

When chronic depression has not been relieved by behavioral therapies such as meditation or cognitive therapy ketamine is sometimes found to provide relief. Lucan at all probe brain changes in mice given a single expose to ketamine that rescues then from chronic stress inducted anhedonia.  Here is their summary of the paper:

Ketamine is recognized as a rapid and sustained antidepressant, particularly for major depression unresponsive to conventional treatments. Anhedonia is a common symptom of depression for which ketamine is highly efficacious, but the underlying circuits and synaptic changes are not well understood. Here, we show that the nucleus accumbens (NAc) is essential for ketamine’s effect in rescuing anhedonia in mice subjected to chronic stress. Specifically, a single exposure to ketamine rescues stress-induced decreased strength of excitatory synapses on NAc-D1 dopamine receptor-expressing medium spiny neurons (D1-MSNs). Using a cell-specific pharmacology method, we establish the necessity of this synaptic restoration for the sustained therapeutic effects of ketamine on anhedonia. Examining causal sufficiency, artificially increasing excitatory synaptic strength onto D1-MSNs recapitulates the behavioral amelioration induced by ketamine. Finally, we used opto- and chemogenetic approaches to determine the presynaptic origin of the relevant synapses, implicating monosynaptic inputs from the medial prefrontal cortex and ventral hippocampus.