Dissociation between Active and Observational Learning from Positive and Negative Feedback in Parkinsonism

Abstract

Feedback to both actively performed and observed behaviour allows adaptation of future actions. Positive feedback leads to increased activity of dopamine neurons in the substantia nigra, whereas dopamine neuron activity is decreased following negative feedback. Dopamine level reduction in unmedicated Parkinson’s Disease patients has been shown to lead to a negative learning bias, i.e. enhanced learning from negative feedback. Recent findings suggest that the neural mechanisms of active and observational learning from feedback might differ, with the striatum playing a less prominent role in observational learning. Therefore, it was hypothesized that unmedicated Parkinson’s Disease patients would show a negative learning bias only in active but not in observational learning. In a between-group design, 19 Parkinson’s Disease patients and 40 healthy controls engaged in either an active or an observational probabilistic feedback-learning task. For both tasks, transfer phases aimed to assess the bias to learn better from positive or negative feedback. As expected, actively learning patients showed a negative learning bias, whereas controls learned better from positive feedback. In contrast, no difference between patients and controls emerged for observational learning, with both groups showing better learning from positive feedback. These findings add to neural models of reinforcement-learning by suggesting that dopamine-modulated input to the striatum plays a minor role in observational learning from feedback. Future research will have to elucidate the specific neural underpinnings of observational learning.

The Inactivation of JAK2/STAT3 Signaling and Desensitization of M1 mAChR in Minimal Hepatic Encephalopathy (MHE) and the Protection of Naringin Against MHE

“…Some studies showed that learning and retention of memory, required for optimal response choice, are significantly reliant on dopamine in Alzheimer's Disease [29,30]. However, some studies found that dopamine impairs or have no effect on, stimulus-response learning and working memory in Parkinsonism or MHE [31,32,33], similarly in our present study we displayed that overproduction of DA is a feature for memory impairment in MHE. Brodskii VY et al reported that dopamine disorganizes the rhythm of protein synthesis in hepatocytes in vitro and in vivo [34,35], indicating the relationship of elevation of DA with liver cirrhosis on the other side.…”

Dopamine Burden Triggers Neurodegeneration via Production and Release of TNF-α from Astrocytes in Minimal Hepatic Encephalopathy

“…Therefore, although our findings in the present study must primarily be conceived as purely in vitro model data, they may also have some bearing in understanding liver cirrhosis complicated with MHE, when a disruption of the BBB is prone to occur. Numerous studies describe the specific effects of DA manipulations on learning and how low doses of DA facilitate cognitive abilities [25][26][27]; however, some studies (including our studies) show that overproduction of DA impairs learning and working memory [6][7][8][9]28]. Chronic HE patients exhibit abnormalities in their dopaminergic systems, including an increase in the brain content of DA metabolites [29] and increased turnover of DA [30].…”

Reward learning deficits in Parkinson's disease depend on depression

“…While some studies report performance to be unaltered in the OFF state compared with controls (Cools et al, 2006, Rutledge et al, 2009, Smittenaar et al, 2012, Moustafa et al, 2008, other studies report that reward-based learning is actually impaired relative to punishment (Bodi et al, 2009, Kobza et al, 2012, Frank et al, 2004, Palminteri et al, 2009. The pattern of impaired reward versus punishment learning in PD patients OFF medication resembles that described above in depressed individuals (non-PD) (Clark et al, 2009, Eshel andRoiser, 2010) and concurs generally with suggestions that striatal dopamine depletion contributes to depression in PD.…”