Posts tagged Dopamine
Dopamine: prediction-error vs. incentive salience
Aug 21st
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The exact role that dopamine plays in learning remains controversial; some think it acts as a prediction error signal, while Berrdige et al believe that dopamine codes for incentive salience.
A recent paper throws some light on the issue. It uses a simple Pavlovian conditioning paradigm. To recap, US and CS are paired and after some time CS starts predicting the reward ; however the twist to usual Pavlovian conditioning is that when CS is presented before US; some rats become ‘sign trackers’ i.e. as soon as the CS comes start engaging with it; while other are ‘goal trackers’ i.e. as soon as CS comes start engaging with where the US would ultimately appear.
To elaborate, both types of rats are able to learn that CS predicts US , but only sign tracker s attach importance to CS in itself. Also if they are given an option to indulge in instrumental behavior to bring forth the CS (in absence of US) , it seems only the sign trackers are more willing to do work to get the CS and are thus motivated enough by Cs in itself. In other words, while both goal trackers and sign trackers endow CS with predictive capabilities; only sign trackers also endow it with incentive salience.
If all this seems confusing , consider the fact that we are all conditioned to like food/sex; but a secondary reinforcer like money which may predict that food will follow, might become a reward in itself and motivate some of us. while for some money may be as good as it is an indicator of food/sex to come; for other money may acquire an importance/ motivational value in itself.
After that crude analogy, lets return to our sign trackers; these rats are found in wild populations also, but a selectively bred rat breed that has been bred for Novelty preference (bHR) also displays these behaviors prominently. On the other hand those selectively bred not to show novelty preference are goal trackers by large. (bLR)
What the authors of this study showed was a dissociation between the necessity of dopamine for learning and performance in Pavlovian conditioning. they showed that while dopamine is not required for learning the prediction part (i.e. even in absence of dopamine both goal trackers and sign trackers could learn that CS predicts US) , it is indeed required for performance (i.e. in absence of dopamine neither goal trackers or sign trackers would perform the task whereby their learning of CS/US association resulted in overt behavior. ) . Further , it was found that for sign tracker dopamine was required for the sign tracking behavior.
To me, and to the authors too, the results seem to indicate that some individuals are more prone to associate incentive salience to CS and their primary mode of learning is via incentive salience mechanism of dopamine; these are also the one more susceptible to maladaptive behavior. However the learning that results in association of CS with US does not need dopamine; the association can happen without dopamine; but no behavior results if either CS/ US is not able to trigger dopamine release or able to tell the brain that this incentive/stimuli is salient.
To me this bodes victory for the Berridge et al camp of incentive salience theory of dopamine function, to whom I have always been more sympathetic ! do you agree?
Flagel, S., Clark, J., Robinson, T., Mayo, L., Czuj, A., Willuhn, I., Akers, C., Clinton, S., Phillips, P., & Akil, H. (2010). A selective role for dopamine in stimulus–reward learning Nature, 469 (7328), 53-57 DOI: 10.1038/nature09588
More brains and bonkers connection: thinking out of a broken box
May 24th
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We have covered many studies linking creativity with Psychosis and this new study by Manzano et al provides further corroborating evidence.
Dopamine has been linked with psychosis and is now also being increasingly being linked with creativity, especially divergent creativity and thinking style.
Divergent thinking is influenced by dopaminergic function. Reuter [6] found a correlation between divergent thinking (the Inventiveness battery of the Berliner Intelligenz Struktur Test) and polymorphisms of the dopamine D2 receptor gene–DRD2 TAQ IA. Higher creativity scores were observed in carriers of the A1 allele. This polymorphism is unrelated to general intelligence [7], [8], which suggests that it is more specifically related to Glr (“long-term storage and retrieval”). This finding is in line with functional imaging research showing the D2 system to be involved in attentional set shifting and response flexibility, which are important components of divergent thinking [9]. Furthermore, the finding indicates that divergent thinking is related to regional differences in D2 densities, since the DRD2 TAQ IA polymorphism has been shown to modulate D2 binding potential (D2BP) in both striatal [10] and extrastriatal regions [11].
Divergent thinking is traditionally measured using alternate uses test, for eg., in which a familiar object like brick is provided and subjects asked to name novel use for that object. The responses are marked for creativity as per the follwoing criterion:
- Fluency–the number of valid responses;
- Originality–how frequent the participant’s responses were among the responses of the rest of the sample;
- Flexibility–the number of semantic categories produced;
- Switching–the number of shifts between semantic categories;
- and Elaboration–how extensive each response is (if the task involves producing more than single words)
The main findings of the study was that dopamine D2 binding potential (D2BP) receptor density in thalamus correlated negatively with divergent thinking and creativity scores. Here is how the authors interpret the results:
Based on the current findings, we suggest that a lower D2BP in the thalamus may be one factor that facilitates performance on divergent thinking tasks. The thalamus contains the highest levels of dopamine D2 receptors out of all extrastriatal brain regions [33], [45]. Decreased D2BP in the thalamus has been suggested, firstly, to lower thalamic gating thresholds, resulting in decreased filtering and autoregulation of information flow [31] and, secondly, to increase excitation of cortical regions through decreased inhibition of prefrontal pyramidal neurons [46], [47], [48]. The decreased prefrontal signal-to-noise ratio may place networks of cortical neurons in a more labile state, allowing them to more easily switch between representations and process multiple stimuli across a wider association range [49]. This state, which we hereforth will refer to as the “creative bias”, could benefit performance on tasks that involve continuous generation and (re-)combination of mental representations and switching between mind-sets. The creative bias could also explain why the different measures of divergent task performance correlate: A decreased signal-to-noise ratio in thalamus would decrease information gating and possibly increase fluency; decreased signal-to-noise ratio in cortical regions should better enable flexibility and switching between representations; similarly, the associative range should be widened and selectivity should be decreased which might spur originality and elaboration.
Besides carrying benefits related to fluency and switching, the decreased signal-to-noise ratio associated with the creative bias should be disadvantageous in relation to tasks that require high levels of selective attention. Some support for this prediction can be taken from Dorfman [50] who showed that the greater a person’s divergent thinking scores, the slower his or her reaction times were on a negative priming task requiring the inhibition of interfering information. Furthermore, the creative bias may also bring a risk of excessive excitatory signals from the thalamus overwhelming cortical neurotransmission, with ensuing cognitive disorganization and positive symptoms [30]. It is thus tempting to suggest that dopaminergic modulation of neurotransmission mediated through dopamine D2-receptors could be one of the mechanisms which associate creativity with positive psychotic symptoms. Interestingly, positive symptoms are not necessarily related to problems in executive function, at least not to the same extent as negative symptoms [51], which indicates that in the creative individual “blind variation” might be affected without a concomitant decline in “selective retention”. It can be speculated that aberrant thalamic function may promote unusual associations, as well as improved performance on divergent thinking tests in healthy individuals, in the absence of the detrimental effects typically associated with psychiatric disorders. In other words, thinking outside the box might be facilitated by having a somewhat less intact box.
In plain English speak, the same decreased signal-to-noise ratio in perfrontal regions that gives rise to creativity also gives rise to proneness to psychosis. The more the noise that is introduced the greater the chances that the ideas generated by ‘blind variation’ are more creative; if the ‘selective retention’ procedure is also defective or loosened to an extent, it may result in psychopathology and psychosis, while if intact it leads to creativity. Thus while one factor , that of loosening of associations, flexibility and set switching is common to both psychosis and creativity, the defects in selective retention may be the crucial factor that distinguishes brains from bonkers.
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de Manzano, ?., Cervenka, S., Karabanov, A., Farde, L., & Ullén, F. (2010). Thinking Outside a Less Intact Box: Thalamic Dopamine D2 Receptor Densities Are Negatively Related to Psychometric Creativity in Healthy Individuals PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010670
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The Creativity-dopamine (b)linkage: more brains and bonkers connections
Apr 14th
- Image by jef safi via Flickr
Creativity is certainly different from intelligence; it is usually gauged as the ability to make novel and useful unique contributions to a field. Creativity itself is not a unified construct but can be broken into convergent creativity (involving more focused approach) and divergent creativity (involving more widening and loosening of associations).
It has been evident for quite some time that there is a connection between insanity (especially bipolar/schizophrenia spectrum) and creativity , especially as evidenced by the creative bent of schizotypal people. See for example this article covering a recent study that looks at exactly the same issue. However, most of these studies rely on a unitary construct of creativity that does not do full justice to the correlations that could be found if convergent and divergent creativity was distinguished and effect of intelligence was factored out. The new study by Hommel, B. does just that.
Schizophrenia/psychosis as many will know from their elementary neuroscience knowledge is associated with dopamine dysfunction; specifically it is believed that high baseline dopamine levels are there in schizophrenics/psychotics. So it was not unreasonable for Hommel et al to hypothesize that dopamine should have some relation with creativity possible higher dopamine associated with high creativity. However, dopamine has shown an inverse U relation for many other factors and thus they were cautious and tried to fit both linear and quadratic graphs to their data. But we are moving ahead of ourselves. Before they could find the underlying relation between dopamine and creativity, they had to measure these things accurately.
They measured dopamine using Eye Blink Rate (EBR): that is how many time you blink in a minute. For creativity , they measured Convergent Creativity using a remote association task (don’t go by the name …the task has only one answer and measures convergent thinking) . for eg. a subject is given three words (say time, hair, stretch) and have to come up with a word that is commonly related to all three (answer: long) . this reliably measures creativity but of he convergent type. For Divergent thinking , they administered the Alternate Uses task (AUT),a task that requires one tocome up with novel uses of everyday objects like brick, toothpaste etc. The responses to AUT were further coded for fluency (how easily one could come up with alternatives measured by total no. of responses) , flexibility(the number of different categories used or how remote the mind wandered) and elaboration (the level of detail surrounding the use). They also measured fluid intelligence using Raven’s progressive matrices.
They then conducted experiments (administered the tests to subjects) , collected data and analyzed the results. The main findings of interest to us is that they found a inverse u shaped relation between dopamine (EBR) and flexibility dimension fo divergent thinking. This effect was present even when the effect of intelligence was factored out. thus both low dopamine, as well as too much dopamine is detrimental to flexible divergent thinking/creativity and schizotypals , placed precariously between normals and psychotics are best placed to be the most creative as they presumably have the optimum dopamine levels. the authors also argue that schizophrenics dopamine levels should not be brought down indiscreetly by using anti-psychotics (which reduce dopamine levels) but they should be brought in the optimum range of dopamine functioning. this obviously has immense importance and treatment implications. No wonder creative people feel stiffed when on anti-psychotics- their dopamine levels are being brought down way too much.
The other interesting finding was that dopamine (EBR) was negatively ad linearly related to convergent thinking. Thus, it is evident that convergent creativity and divergent creativity are different constructs and while dopamine has a complex quadratic relationship with divergent thinking, that with convergent thinking is linear though not very comforting. It seems that as dopamine levels increase the ability to narrow focus diminishes and this would be concordant with other studies linking dopamine to ADHD for example.
Overall, a view of how brains and bonkers are two sides of the same coin is emerging and it is exciting to note that many previous inconsistencies in literature around this issue may have to do with not differentiating and decomposing creativity into its many components and not looking for inverse u shaped effects.
Chermahini SA, & Hommel B (2010). The (b)link between creativity and dopamine: Spontaneous eye blink rates predict and dissociate divergent and convergent thinking. Cognition PMID: 20334856
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Dopamine and theory of mind: another autism/schizophrenia dichotomy
Mar 17th
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There is an article in press in Neuropsyhcologia by Lackner et al that related Dopamine (DA) levels as measured by Eye Blink Rate (EBR) to preschoolers (3-5 yrs old) Representational theory of Mind (RTM).
The authors hypothesized that as one of the neural correlates of RTM is dMPFC, and as dMPFC has dopamine receptors and is innervated by dopmainergic projections along the dopamine mesocortical pathways , hence perhaps it is the dopamine’s tonic and phasic levels that may be correlated with and have a causal role in the preschoolers’ developing RTM abilities.
3-5 years is a critical period in which the RTM abilities are developing in a normal kid and are first found to be deficient in autistic kids. another linkage the authors seem relevant, but which I don’t agree to much, is the error -prediction theory of dopamine. They believe that ToM/RTM abilities develop when one takes into account the behavior of others and finds discrepancies in ones own knowledge and why they act based on certain different assumptions and by realizing this error of prediction modifies ones understanding of others and starts attributing a mind to them. The authors believe that phasic dopamine which has error prediction functions may be affecting RTM via this pathway too; I find that not very convincing.
However, their basic premise that tonic or baseline dopamine affects RTM abilite seems to be on firm ground and they found support for this hypothesis. They did not measure DA levels directly , but instead relied on Eye Bink Rate (EBR) which is a robuts predictor of overall dopamine in the mesolimbic pathways via the caudate nucleus dopamine levels. They also did not measure EBR directly but measured it using EEG waveforms of relevant brain regions above the eyes.
The RTM tasks they used and the Response -conflict executive function (RC-EF) tasks they used are very simple and intuitive and I refer the reader to methods section to pursue them in detail. For our purpose it is sufficient to mention that RTM did not include the famous anne-sally false belief task but had other variants like false belief location task etc.
Their findings were unequivocal. They found that DA levels as gauged from EBR were a significant predictors of RTM abilities and the effect was not mediated by a possible confound- that of RTM and RC-EF linkages and correlations.
For our purposes what is most important is the direction of the effect . More DA levels were associated with better RTM ; while lower DA was associated with lower RTM performance. This is consistent with the DA relation of Schizophrenia/Autism one of which has higher DA levels and better ToM; while the other both poorer ToM and lower baseline DA. To quote:
These findings dovetail with other research connecting dopamine and representational theory of mind in autistic and schizophrenic populations. Both autism and schizophrenia have been associated with RTM impairment (Pickup, 2008; Sabbagh,2004; Savina & Beninger, 2007) and dysregulation of DA (Braver, Barch, & Cohen, 1999; Lam, Aman, & Arnold, 2006). For instance, in the case of schizophrenia there is some evidence that increased levels of frontal dopamine, as a consequence of the pharmacological activity of some atypical antipsychotics, leads to increased performance on RTM tasks (Savina & Beninger, 2007). The present study added to this body of literature by demonstrating associations between RTM and DA in typically developing children. Considered together, this further supports the hypothesis that dopaminergic functioning plays a role in RTM development.
As always, I am excited by more support for Autism and Psychosis as opposites theory and belive this further cements the case and shows possible neurochemichal mechanisms underlying the difference.
Lackner, C., Bowman, L., & Sabbagh, M. (2010). Dopaminergic functioning and preschoolers’ theory of mind Neuropsychologia DOI: 10.1016/j.neuropsychologia.2010.02.027
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Dopamine mediated ‘sign’ based learning
Oct 25th
There is an interesting must watch Video of Paul Phillips discussing dopamine based learning and I have embedded the video below. Please do have a look. Original video with some other relevant information can be found here.
Paul discusses the dopamine surge at the Unconditioned Stimulus/reward (US) before the training being replaced by a dopamine surge at Conditioned stimulus(CS) after the learning and how this has led to the reward prediction theory (Schultz) of dopamine function. He also discusses the Cambridge(UK) or Ken Berridge group of objections to this and their discovery that different regions of the brain react differently (ventral and dorsal striatum have different dopamine surges associated with the same stimulus/reward pair in the same animal). He uses electrochemical methods (suing electrodes implanted in the rats brains) to measure tonic dopamine release and there are interesting and informative graphics as well as videso of rats indulging in approach behavior as soon as CS is presented (after conditioning).
He also discusses model-free and model-based reinforcement learning paradigms and discusses how dopamine is only necessary for model-free (simple value association) learning and is not necessarily involved in model-based learning. this he demonstrates beautifully with videos and graphs of selectively bred mice (bred for locomotion), in which high locomotors follow a different (sign-based or model-free) while the low locomotors display goal based or model-based learning. By dopamine manipulations (giving a dopamine antagonist) he is able to show that dopamine is not really necessary for model-based learning.
All in all a very engaging and informative video. A must, must watch that is very highly recommended for anybody who has given a minor thought also to dopamine and what it does in the brain.
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