In one of my recent posts on the role of basal ganglia in reinforcement learning, I highlighted research that showed that having high dopamine levels in basal ganglia causes an inability to learn form negative reinforcements, because of the low activity of the proposed NoGo system. Conversely a low dopamine level is associated with more effective negative reinforcement learning. To quote form the earlier article:

We found a striking effect of the different dopamine medications on this positive versus negative learning bias, consistent with predictions from our computer model of the learning process. While on placebo, participants performed equally well at choose-A and avoid-B test choices. But when their dopamine levels were increased, they were more successful at choosing the most positive symbol A and less successful at avoiding B. Conversely, lowered dopamine levels were associated with the opposite pattern: worse choose-A performance but more-reliable avoid-B choices. Thus the dopamine medications caused participants to learn more or less from positive versus negative outcomes of their decisions.

A similar result has been obtained for those who have an A1 allele for dopamine receptor D2. This allele causes fewer dopamine D2 receptor density, though as the paper is behind a subscription firewall, I could not ascertain if the decreased density is both in the Go as well as NoGo pathway. Anyway, it might be hypothesized that to compensate for the low receptor density more dopamine needs to be produced. this paradoxically leads to the situation where there is more baseline dopamine in the basal ganglia Go and NoGO pathways, thus leading to easy excitation of Go Pathway , but to lesser inhibition due to NoGo pathway. As a result, those who have A1 Allele would end up being unable to learn from negative reinforcement, and this is exactly what the authors have found. Here is the abstract of the paper:

The role of dopamine in monitoring negative action outcomes and feedback-based learning was tested in a neuroimaging study in humans grouped according to the dopamine D2 receptor gene polymorphism DRD2-TAQ-IA. In a probabilistic learning task, A1-allele carriers with reduced dopamine D2 receptor densities learned to avoid actions with negative consequences less efficiently. Their posterior medial frontal cortex (pMFC), involved in feedback monitoring, responded less to negative feedback than others’ did. Dynamically changing interactions between pMFC and hippocampus found to underlie feedback-based learning were reduced in A1-allele carriers. This demonstrates that learning from errors requires dopaminergic signaling. Dopamine D2 receptor reduction seems to decrease sensitivity to negative action consequences, which may explain an increased risk of developing addictive behaviors in A1-allele carriers.

I came to know this via the Action Potential blog. Though the AP blog is dismissive of this study, it provided a much more detailed description of the actual study.

Staying on the genetics theme, a recent Science article suggests that a particular variant of the dopamine receptor (D2) causes some people to poorly learn via negative reinforcement. The A1 allele, as this variant is known, has previously been linked to increased vulnerability of addiction.

The researchers recruited volunteers, who performed a learning task while lying in an fMRI machine. Individuals with the A1 allele (at least one copy) were equally successful at selecting a targeted “good” symbol reinforced with positive feedback (the display of a “smiley face”) as those individuals completely lacking the A1 allele. However, when the task was changed such that negative reinforcement drove the learning (subjects were asked to avoid the “bad symbol”), those individuals with the A1 allele failed to perform as well as their A1-lacking colleagues.

Examining the fMRI data, those with the A1 allele had less activity in the frontal cortex and hippocampus, two areas normally responsive during tasks involving negative reinforcement and memory. This reduction was thought to be because possessing the A1 allele can cause up to a 30% reduction in D2 receptor density in individuals, presumably affecting the neural circuitry, and likely influencing the activity within the reward signaling pathways.

The AP blog may dismiss this on methodological grounds, and I because I have not read the original paper , would not comment much on that; but if I have understood the study method correctly, it seems to be the same as described in my earlier post on basal ganglia and seems a valid study paradigm. I am excited by this research and this definitely adds to our understanding of the dopamine pathways involved.

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