12/16/2023 0 Comments Hedonic glossMight contribute to the recent rise of obesity and eating disorders. As a corollary, dysfunction in reward circuits Generate “liking” and “wanting” for foods. What we eat, when and how much, all are influenced by brain reward mechanisms that DiFeliceantonio (2010) The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders. Neurobiology is not my field of expertise, but this paper seems relevant: But the basal ganglia, in general, are sometimes thought of as an action selection system (or "decision path" selection to use your words), so the ability of dopamine neurons to signal expectations is relevant. They also raise some tough questions about how exactly this dopamine signal interacts with other parts of the brain to mediate the learning suggested in the theory.Īs with basically all neurobiology theory, a full understanding of how this signal that we detect in individual neurons translates into a coherent behavioral response program is a long ways away. Importantly, they note that dopamine neurons suppress their activity in response to noxious stimuli (the pain aspect of your question). If a predicted reward does not occur, the neuron signals a negative error ("Aw shucks, guess that bell doesn't mean food after all.").Ī somewhat updated revision of the theory is outlined in a review by Redgrave and Gurney, 2006 ( PDF). If a predicted reward occurs, the neuron signals no error at the time of the reward ("shrug, I knew that was going to happen"). If an unpredicted reward occurs, the neuron signals a positive error ("Oops, that was a reward I should know about!"). So the theory goes that dopamine neurons are not simply saying whether a reward has occurred, but rather as a learning signal that adjusts predictions about rewards. Third, if the CS is presented and then the reward does not occur, the response to the CS occurs but the dopamine neuron depresses activity immediately after the reward should have happened. That is, the dopamine signal is now a predictive reward signal. Second, if a conditioned stimulus (CS) precedes the reward, the dopamine neuron fires in response to the CS but not the reward. First, an unexpected reward elicits a short activity increase in dopamine neurons. Some key experiments are outlined in Schultz, 1998 ( PDF). In this theory, dopamine neurons signal expectations about the outcome of particular stimuli. In particular, a leading theory of dopaminergic function is the predictive reward error or reinforcement learning hypothesis. I think part of the answer to your question is going to include the dopamine "reward" pathway in the basal ganglia. I am only concerned about the mechanism which can explain outwardly observable behavior - especially in simpler animals - such as the basic stimulus-response-reward/punishment learning that a mouse or bird can do.ĭo we understand the mechanism by which a pain signal causes the brain to suppress recently followed decision paths, and a pleasure signal causes the brain to reinforce them? Or is this still completely mysterious at this time? Obviously, the subjective "experience" of pleasure and pain gets more into philosophy of mind and that's not what I am asking about. This sort of thing is not that hard to replicate in computational models, so it is clearly nothing magical. Pain motivates the animal to stop whatever it was doing (possibly stopping the pain), and to avoid in the future repeating similar responses to those that preceded (and therefore were possibly causal toward) the incident that caused pain. as a part of learning and motivation system) then do we understand how this actually occurs at a neurobiological level? At least in "lower" animals, pain seems to simply cause an aversion response. If we are to view pleasure and pain as being essentially synonymous with the more mechanistic concept of reward and punishment (i.e.
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