RESUMO
Theories of moral development propose that empathy is transmitted across individuals. However, the mechanisms through which empathy is socially transmitted remain unclear. Here, we combine computational learning models and functional MRI to investigate whether, and if so, how empathic and non-empathic responses observed in others affect the empathy of female observers. The results of three independent studies showed that watching empathic or non-empathic responses generates a learning signal that respectively increases or decreases empathy ratings of the observer. A fourth study revealed that the learning-related transmission of empathy is stronger when observing human rather than computer demonstrators. Finally, we show that the social transmission of empathy alters empathy-related responses in the anterior insula, i.e., the same region that correlated with empathy baseline ratings, as well as its functional connectivity with the temporoparietal junction. Together, our findings provide a computational and neural mechanism for the social transmission of empathy that accounts for changes in individual empathic responses in empathic and non-empathic social environments.
Assuntos
Encéfalo , Empatia , Humanos , Feminino , Encéfalo/fisiologia , Aprendizagem , Reforço Psicológico , Meio SocialRESUMO
Foraging theory prescribes when optimal foragers should leave the current option for more rewarding alternatives. Actual foragers often exploit options longer than prescribed by the theory, but it is unclear how this foraging suboptimality arises. We investigated whether the upregulation of cholinergic, noradrenergic, and dopaminergic systems increases foraging optimality. In a double-blind, between-subject design, participants (N = 160) received placebo, the nicotinic acetylcholine receptor agonist nicotine, a noradrenaline reuptake inhibitor reboxetine, or a preferential dopamine reuptake inhibitor methylphenidate, and played the role of a farmer who collected milk from patches with different yield. Across all groups, participants on average overharvested. While methylphenidate had no effects on this bias, nicotine, and to some extent also reboxetine, significantly reduced deviation from foraging optimality, which resulted in better performance compared to placebo. Concurring with amplified goal-directedness and excluding heuristic explanations, nicotine independently also improved trial initiation and time perception. Our findings elucidate the neurochemical basis of behavioral flexibility and decision optimality and open unique perspectives on psychiatric disorders affecting these functions.
Assuntos
Acetilcolina , Metilfenidato , Humanos , Nicotina/farmacologia , Norepinefrina , Reboxetina , Método Duplo-CegoRESUMO
Representing the probability and uncertainty of outcomes facilitates adaptive behavior by allowing organisms to prepare in advance and devote attention to relevant events. Probability and uncertainty are often studied only for valenced (appetitive or aversive) outcomes, raising the question of whether the identified neural machinery also processes the probability and uncertainty of motivationally neutral outcomes. Here, we aimed to dissociate valenced from valence-independent (i.e., generic) probability (p; maximum at pâ =â 1) and uncertainty (maximum at p = 0.5) signals using human neuroimaging. In a Pavlovian task (n = 41; 19 females), different cues predicted appetitive, aversive, or neutral liquids with different probabilities (p = 0, p = 0.5, p = 1). Cue-elicited motor responses accelerated, and pupil sizes increased primarily for cues that predicted valenced liquids with higher probability. For neutral liquids, uncertainty rather than probability tended to accelerate cue-induced responding and decrease pupil size. At the neural level, generic uncertainty signals were limited to the occipital cortex, while generic probability also activated the anterior ventromedial prefrontal cortex. These generic probability and uncertainty signals contrasted with cue-induced responses that only encoded the probability and uncertainty of valenced liquids in medial prefrontal, insular, and occipital cortices. Our findings show a behavioral and neural dissociation of generic and valenced signals. Thus, some parts of the brain keep track of motivational charge while others do not, highlighting the need and usefulness of characterizing the exact nature of learned representations.
Assuntos
Sinais (Psicologia) , Humanos , Feminino , Masculino , Incerteza , Adulto , Adulto Jovem , Probabilidade , Imageamento por Ressonância Magnética , Pupila/fisiologia , Condicionamento Clássico/fisiologia , Motivação/fisiologia , Mapeamento Encefálico , Córtex Pré-Frontal/fisiologia , Córtex Pré-Frontal/diagnóstico por imagemRESUMO
From deciding which meal to prepare for our guests to trading off the proenvironmental effects of climate protection measures against their economic costs, we often must consider the consequences of our actions for the well-being of others (welfare). Vexingly, the tastes and views of others can vary widely. To maximize welfare according to the utilitarian philosophical tradition, decision-makers facing conflicting preferences of others should choose the option that maximizes the sum of the subjective value (utility) of the entire group. This notion requires comparing the intensities of preferences across individuals. However, it remains unclear whether such comparisons are possible at all and (if they are possible) how they might be implemented in the brain. Here, we show that female and male participants can both learn the preferences of others by observing their choices and represent these preferences on a common scale to make utilitarian welfare decisions. On the neural level, multivariate support vector regressions revealed that a distributed activity pattern in the ventromedial prefrontal cortex (VMPFC), a brain region previously associated with reward processing, represented the preference strength of others. Strikingly, also the utilitarian welfare of others was represented in the VMPFC and relied on the same neural code as the estimated preferences of others. Together, our findings reveal that humans can behave as if they maximized utilitarian welfare using a specific utility representation and that the brain enables such choices by repurposing neural machinery processing the reward others receive.
Assuntos
Recompensa , Humanos , Masculino , Feminino , Adulto , Adulto Jovem , Comportamento de Escolha/fisiologia , Córtex Pré-Frontal/fisiologia , Tomada de Decisões/fisiologia , Imageamento por Ressonância Magnética , Mapeamento EncefálicoRESUMO
Adaptive coding of reward is the process by which neurons adapt their response to the context of available compensations. Higher rewards lead to a stronger brain response, but the increase of the response depends on the range of available rewards. A steeper increase is observed in a narrow range and a more gradual slope in a wider range. In schizophrenia, adaptive coding appears to be affected in different domains, especially in the reward domain. Here, we tested adaptive coding of reward in a large group of patients with schizophrenia (n = 86) and control subjects (n = 66). We assessed: (i) the association between adaptive coding deficits and symptoms; (ii) the longitudinal stability of deficits (the same task was performed 3 months apart); and (iii) the stability of results between two experimental sites. We used functional MRI and the monetary incentive delay task to assess adaptation of participants to two different reward ranges: a narrow range and a wide range. We used a region-of-interest analysis to evaluate adaptation within striatal and visual regions. Patients and control subjects underwent a full demographic and clinical assessment. We found reduced adaptive coding in patients, with a decreased slope in the narrow reward range with respect to that of control participants, in striatal but not visual regions. This pattern was observed at both research sites. Upon retesting, patients increased their narrow-range slopes, showing improved adaptive coding, whereas control subjects slightly reduced them. At retesting, patients with overly steep slopes in the narrow range also showed higher levels of negative symptoms. Our data confirm deficits in reward adaptation in schizophrenia and reveal an effect of practice in patients, leading to improvement, with steeper slopes upon retesting. However, in some patients, an excessively steep slope may result in poor discriminability of larger rewards, owing to early saturation of the brain response. Together, the loss of precision of reward representation in new (first exposure, underadaptation) and more familiar (retest, overadaptation) situations might contribute to the multiple motivational symptoms in schizophrenia.
Assuntos
Apatia , Imageamento por Ressonância Magnética , Recompensa , Esquizofrenia , Humanos , Masculino , Feminino , Adulto , Esquizofrenia/fisiopatologia , Apatia/fisiologia , Pessoa de Meia-Idade , Psicologia do Esquizofrênico , Motivação/fisiologia , Adaptação Fisiológica/fisiologia , Encéfalo/fisiopatologia , Encéfalo/diagnóstico por imagem , Adaptação Psicológica/fisiologiaRESUMO
We and other animals learn because there is some aspect of the world about which we are uncertain. This uncertainty arises from initial ignorance, and from changes in the world that we do not perfectly know; the uncertainty often becomes evident when our predictions about the world are found to be erroneous. The Rescorla-Wagner learning rule, which specifies one way that prediction errors can occasion learning, has been hugely influential as a characterization of Pavlovian conditioning and, through its equivalence to the delta rule in engineering, in a much wider class of learning problems. Here, we review the embedding of the Rescorla-Wagner rule in a Bayesian context that is precise about the link between uncertainty and learning, and thereby discuss extensions to such suggestions as the Kalman filter, structure learning, and beyond, that collectively encompass a wider range of uncertainties and accommodate a wider assortment of phenomena in conditioning.
Assuntos
Teorema de Bayes , Condicionamento Clássico , Reforço Psicológico , Humanos , Condicionamento Clássico/fisiologia , Aprendizagem/fisiologia , Modelos Psicológicos , IncertezaRESUMO
Recent evidence has linked testosterone, a major sex hormone, to selfishness in economic decision-making. Here, we aimed to investigate the neural mechanisms through which testosterone reduces generosity by combining functional MRI with pharmacological manipulation among healthy young males in a double-blind, placebo-controlled, between-subject design. After testosterone or placebo gel administration, participants performed a social discounting task in which they chose between selfish options (benefiting only the participant) and generous options (providing also some benefit to another person at a particular social distance). At the behavioral level, testosterone reduced generosity compared to the placebo. At the neural level (n = 60), the temporoparietal junction (TPJ) encoded the other-regarding value of the generous option during generous choices, and this effect was attenuated by testosterone, suggesting that testosterone reduced the consideration of other's welfare as underpinned by TPJ activity. Moreover, TPJ activity more strongly reflected individual differences in generosity in the placebo than the testosterone group. Furthermore, testosterone weakened the relation between the other-regarding value of generous decisions and connectivity between the TPJ and a region extending from the insula into the striatum. Together, these findings suggest that a network encompassing both cortical and subcortical components underpins the effects of testosterone on social preferences.
Assuntos
Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/fisiologia , Personalidade/efeitos dos fármacos , Testosterona/farmacologia , Mapeamento Encefálico , Estudos de Casos e Controles , Córtex Cerebral/diagnóstico por imagem , Tomada de Decisões , Humanos , Imageamento por Ressonância Magnética , Masculino , Comportamento SocialRESUMO
Decisions are based on the subjective values of choice options. However, subjective value is a theoretical construct and not directly observable. Strikingly, distinct theoretical models competing to explain how subjective values are assigned to choice options often make very similar behavioral predictions, which poses a major difficulty for establishing a mechanistic, biologically plausible explanation of decision-making based on behavior alone. Here, we demonstrate that model comparison at the neural level provides insights into model implementation during subjective value computation even though the distinct models parametrically identify common brain regions as computing subjective value. We show that frontal cortical regions implement a model based on the statistical distributions of available rewards, whereas intraparietal cortex and striatum compute subjective value signals according to a model based on distortions in the representations of probabilities. Thus, better mechanistic understanding of how cognitive processes are implemented arises from model comparisons at the neural level, over and above the traditional approach of comparing models at the behavioral level alone.
Assuntos
Encéfalo/fisiologia , Comportamento de Escolha/fisiologia , Adulto , Teorema de Bayes , Encéfalo/diagnóstico por imagem , Mapeamento Encefálico , Tomada de Decisões/fisiologia , Feminino , Humanos , Masculino , Modelos Neurológicos , Modelos Psicológicos , Mascaramento Perceptivo/fisiologia , Córtex Pré-Frontal/diagnóstico por imagem , Córtex Pré-Frontal/fisiologia , Adulto JovemRESUMO
Humans form impressions toward individuals of their own social groups (ingroup members) and of different social groups (outgroup members). Outgroup-focused theories predict that intergroup impressions are mainly shaped by experiences with outgroup individuals, while ingroup-focused theories predict that ingroup experiences play a dominant role. Here we test predictions from these two psychological theories by estimating how intergroup impressions are dynamically shaped when people learn from both ingroup and outgroup experiences. While undergoing fMRI, male participants had identical experiences with different ingroup or outgroup members and rated their social closeness and impressions toward the ingroup and the outgroup. Behavioral results showed an initial ingroup bias in impression ratings which was significantly reduced over the course of learning, with larger effects in individuals with stronger ingroup identification. Computational learning models revealed that these changes in intergroup impressions were predicted by the weight given to ingroup prediction errors. Neurally, the individual weight for ingroup prediction errors was related to the coupling between the left inferior parietal lobule and the left anterior insula, which, in turn, predicted learning-related changes in intergroup impressions. Our findings provide computational and neural evidence for ingroup-focused theories, highlighting the importance of ingroup experiences in shaping social impressions in intergroup settings.Significance Statement:Living in multicultural societies, humans interact with individuals of their own social groups (ingroup members) and of different social groups (outgroup members). However, little is known about how people learn from the mixture of ingroup and outgroup interactions, the most natural experiences in current societies. Here, participants had identical, intermixed experiences with different ingroup and outgroup individuals and rated their closeness and impressions toward the ingroup and the outgroup. Combining computational models and fMRI, we find that the weight given to ingroup experiences (ingroup prediction errors) is the main source of intergroup impression change, captured by changes in connectivity between the parietal lobe and insula. These findings highlight the importance of ingroup experiences in shaping intergroup impressions in complex social environments.
RESUMO
Deficits in neural processing of reward have been described in both bipolar disorder (BD) and schizophrenia (SZ), but it remains unclear to what extent these deficits are caused by similar mechanisms. Efficient reward processing relies on adaptive coding which allows representing large input spans by limited neuronal encoding ranges. Deficits in adaptive coding of reward have previously been observed across the SZ spectrum and correlated with total symptom severity. In the present work, we sought to establish whether adaptive coding is similarly affected in patients with BD. Twenty-five patients with BD, 27 patients with SZ and 25 healthy controls performed a variant of the Monetary Incentive Delay task during functional magnetic resonance imaging in two reward range conditions. Adaptive coding was impaired in the posterior part of the right caudate in BD and SZ (trend level). In contrast, BD did not show impaired adaptive coding in the anterior caudate and right precentral gyrus/insula, where SZ showed deficits compared to healthy controls. BD patients show adaptive coding deficits that are similar to those observed in SZ in the right posterior caudate. Adaptive coding in BD appeared more preserved as compared to SZ participants especially in the more anterior part of the right caudate and to a lesser extent also in the right precentral gyrus. Thus, dysfunctional adaptive coding could constitute a fundamental deficit in severe mental illnesses that extends beyond the SZ spectrum.
Assuntos
Transtorno Bipolar , Esquizofrenia , Humanos , Transtorno Bipolar/diagnóstico por imagem , Transtorno Bipolar/patologia , Imageamento por Ressonância Magnética , Motivação , RecompensaRESUMO
Studies of neural processes underlying delay of gratification usually focus on prefrontal networks related to curbing affective impulses. Here, we provide evidence for an alternative mechanism that facilitates delaying gratification by mental orientation towards the future. Combining continuous theta-burst stimulation (cTBS) with functional neuroimaging, we tested how the right temporoparietal junction (rTPJ) facilitates processing of future events and thereby promotes delay of gratification. Participants performed an intertemporal decision task and a mental time-travel task in the MRI scanner before and after receiving cTBS over the rTPJ or the vertex (control site). rTPJ cTBS led to both stronger temporal discounting for longer delays and reduced processing of future relative to past events in the mental time-travel task. This finding suggests that the rTPJ contributes to the ability to delay gratification by facilitating mental representation of outcomes in the future. On the neural level, rTPJ cTBS led to a reduction in the extent to which connectivity of rTPJ with striatum reflected the value of delayed rewards, indicating a role of rTPJ-striatum connectivity in constructing neural representations of future rewards. Together, our findings provide evidence that the rTPJ is an integral part of a brain network that promotes delay of gratification by facilitating mental orientation to future rewards.
Assuntos
Corpo Estriado/fisiologia , Tomada de Decisões/fisiologia , Desvalorização pelo Atraso/fisiologia , Rede Nervosa/fisiologia , Lobo Parietal/fisiologia , Lobo Temporal/fisiologia , Adulto , Mapeamento Encefálico , Corpo Estriado/anatomia & histologia , Corpo Estriado/diagnóstico por imagem , Feminino , Neuroimagem Funcional , Humanos , Comportamento Impulsivo/fisiologia , Masculino , Rede Nervosa/anatomia & histologia , Rede Nervosa/diagnóstico por imagem , Lobo Parietal/anatomia & histologia , Lobo Parietal/diagnóstico por imagem , Recompensa , Lobo Temporal/anatomia & histologia , Lobo Temporal/diagnóstico por imagem , Estimulação Magnética TranscranianaRESUMO
Humans are less likely to learn from individuals belonging to a different group (outgroup) than from individuals of their own group (ingroup), yet the source of this societally relevant deficit has remained unclear. Here we used neuroimaging and computational modeling to investigate how people learn from observing the actions and outcomes of ingroup and outgroup demonstrators. Politically left-wing male and female participants performed worse when observing computer-simulated actions they believed were from a right-wing outgroup member compared with those from a left-wing ingroup member. A control experiment in which participants observed choices from a nonhuman agent confirmed that this performance difference reflected an outgroup deficit, rather than an ingroup gain. Accounting for the outgroup deficit, a computational model showed that participants relied less on information from outgroup actions compared with ingroup actions, while learning from outgroup outcomes was not impaired. At the neural level, the differences in observational ingroup versus outgroup learning were reflected in lateral prefrontal activity. The stronger the activity in this region, the more strongly participants weighed ingroup compared with outgroup learning signals (action prediction errors), which formally captured deficits in outgroup learning. Together, our work provides a computational and neural account of why people learn less from observing outgroups.SIGNIFICANCE STATEMENT Learning from observing others is an efficient way to acquire knowledge. In our globalized world, "the others" often are people from a different social group (outgroup). There is evidence that people learn less from observing outgroup individuals compared with individuals from their own group (ingroup). However, the source of this outgroup deficit in observational learning remained unknown, which limits our chances to improve intergroup learning. Our results showed that participants rely less on observed outgroup actions compared with ingroup actions, while learning from outgroup outcomes is not impaired. On the neural level, this outgroup deficit was reflected in the activation of the inferior frontal gyrus. These findings imply that intergroup learning should rely on observing outcomes, rather than actions.
Assuntos
Processos Grupais , Aprendizagem/fisiologia , Observação , Identificação Social , Atitude , Simulação por Computador , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Neuroimagem , Política , Desempenho Psicomotor/fisiologia , Percepção Social , Adulto JovemRESUMO
In today's world, mass-media and online social networks present us with unprecedented exposure to second-hand, vicarious experiences and thereby the chance of forming associations between previously innocuous events (e.g., being in a subway station) and aversive outcomes (e.g., footage or verbal reports from a violent terrorist attack) without direct experience. Such social threat, or fear, learning can have dramatic consequences, as manifested in acute stress symptoms and maladaptive fears. However, most research has so far focused on socially acquired threat responses that are expressed as increased arousal rather than active behavior. In three experiments (n = 120), we examined the effect of indirect experiences on behaviors by establishing a link between social threat learning and instrumental decision making. We contrasted learning from direct experience (i.e., Pavlovian conditioning) (experiment 1) against two common forms of social threat learning-social observation (experiment 2) and verbal instruction (experiment 3)-and how this learning transferred to subsequent instrumental decision making using behavioral experiments and computational modeling. We found that both types of social threat learning transfer to decision making in a strong and surprisingly inflexible manner. Notably, computational modeling indicated that the transfer of observational and instructed threat learning involved different computational mechanisms. Our results demonstrate the strong influence of others' expressions of fear on one's own decisions and have important implications for understanding both healthy and pathological human behaviors resulting from the indirect exposure to threatening events.
Assuntos
Tomada de Decisões , Aprendizado Social , Adulto , Nível de Alerta , Condicionamento Clássico , Medo , Feminino , Humanos , Masculino , Adulto JovemRESUMO
The value of rewards arises from multiple hedonic and motivational dimensions. Reward-encoding brain regions such as the ventral striatum (VS) are known to process these dimensions. However, the mechanism whereby distinct reward dimensions are selected for neural processing and guiding behavior remains unclear. Here, we used functional imaging to investigate how human individuals make either hedonic (liking) or motivational (wanting) evaluations of everyday items. We found that the two types of evaluations were differently modulated depending on whether participants won or lost these items. Neural activity in the VS encoded both hedonic and motivational dimensions of reward, whereas ventromedial prefrontal activity encoded primarily motivational evaluations and central orbitofrontal activity encoded predominantly hedonic evaluations. These distinct prefrontal representations arose regardless of which judgment was currently relevant for behavior. Critically, the VS preferentially processed the reward dimension currently being evaluated and showed judgment-specific functional connectivity with the dimension-specific prefrontal areas. Thus, our data are in line with a gating mechanism by which prefrontal cortex (PFC)-VS pathways flexibly encode reward dimensions depending on their behavioral relevance. These findings provide a prototype for a generalized information selection mechanism through content-tailored frontostriatal communication.
Assuntos
Encéfalo/fisiologia , Tomada de Decisões/fisiologia , Filtro Sensorial/fisiologia , Adulto , Encéfalo/anatomia & histologia , Mapeamento Encefálico/métodos , Comportamento de Escolha/fisiologia , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Motivação , Córtex Pré-Frontal/fisiologia , Recompensa , Estriado Ventral/diagnóstico por imagem , Adulto JovemRESUMO
Dorsolateral prefrontal cortex (DLPFC) is well-known for its role in exerting mental work, however the contribution of DLPFC for deciding whether or not to engage in effort remains unknown. Here, we assessed the causal role of DLPFC in effort-based decision making. We disrupted functioning of DLPFC with noninvasive brain stimulation before participants repeatedly decided whether to exert mental effort in a working memory task. We found the same DLPFC subregion involved in mental effort exertion to influence also effort-based decisions: First, it enhanced effort discounting, suggesting that DLPFC may signal the capacity to successfully deal with effort demands. Second, a novel computational model integrating the costs of enduring effort into the effort-based decision process revealed that DLPFC disruption reduced fatigue after accumulated effort exertion, linking DLPFC activation with fatigue. Together, our findings indicate that in effort-based decisions DLPFC represents the capacity to exert mental effort and the updating of this information with enduring time-on-task, informing theoretical accounts on the role of DLPFC in the motivation to exert mental effort and the fatigue arising from it.
Assuntos
Tomada de Decisões/fisiologia , Córtex Pré-Frontal Dorsolateral/fisiologia , Fadiga/fisiopatologia , Memória de Curto Prazo/fisiologia , Motivação/fisiologia , Desempenho Psicomotor/fisiologia , Estimulação Magnética Transcraniana , Adulto , Anedonia/fisiologia , Feminino , Humanos , Masculino , Modelos Teóricos , Recompensa , Adulto JovemRESUMO
BACKGROUND: Bipolar disorder I (BD-I) is defined by episodes of mania, depression and euthymic states. These episodes are among other symptoms characterized by altered reward processing and negative symptoms (NS), in particular apathy. However, the neural correlates of these deficits are not well understood. METHODS: We first assessed the severity of NS in 25 euthymic BD-I patients compared with 25 healthy controls (HC) and 27 patients with schizophrenia (SZ). Then, we investigated ventral (VS) and dorsal striatal (DS) activation during reward anticipation in a Monetary Incentive Delayed Task and its association with NS. RESULTS: In BD-I patients NS were clearly present and the severity of apathy was comparable to SZ patients. Apathy scores in the BD-I group but not in the SZ group correlated with sub-syndromal depression scores. At the neural level, we found significant VS and DS activation in BD-I patients and no group differences with HC or SZ patients. In contrast to patients with SZ, apathy did not correlate with striatal activation during reward anticipation. Explorative whole-brain analyses revealed reduced extra-striatal activation in BD-I patients compared with HC and an association between reduced activation of the inferior frontal gyrus and apathy. CONCLUSION: This study found that in BD-I patients apathy is present to an extent comparable to SZ, but is more strongly related to sub-syndromal depressive symptoms. The findings support the view of different pathophysiological mechanisms underlying apathy in the two disorders and suggest that extra-striatal dysfunction may contribute to impaired reward processing and apathy in BD-I.
Assuntos
Apatia/fisiologia , Transtorno Bipolar/fisiopatologia , Transtornos Dissociativos/fisiopatologia , Recompensa , Esquizofrenia/fisiopatologia , Adulto , Transtorno Bipolar/diagnóstico por imagem , Encéfalo/fisiopatologia , Mapeamento Encefálico , Transtornos Dissociativos/diagnóstico por imagem , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Motivação , Neostriado/diagnóstico por imagem , Neostriado/fisiopatologia , Córtex Pré-Frontal/fisiopatologia , Esquizofrenia/diagnóstico por imagem , Psicologia do Esquizofrênico , Estriado Ventral/diagnóstico por imagem , Estriado Ventral/fisiopatologia , Adulto JovemRESUMO
BACKGROUND: Striatal dysfunction has been proposed as a pathomechanism for negative symptoms in schizophrenia. There is consensus that negative symptoms can be grouped into 2 dimensions: apathy and diminished expression. Recent studies suggest that different neural mechanisms underlie these dimensions, but the relationship between regional resting-state cerebral blood flow (rCBF) and negative symptom dimensions has not been investigated. METHODS: This study included 29 patients with schizophrenia and 20 healthy controls. We measured rCBF in the striatum using arterial spin labelling (ASL) MRI. We assessed negative symptoms using the Brief Negative Symptom Scale. RESULTS: In the ventral and dorsal striatum, rCBF was not different between patients with schizophrenia and controls. However, we did find a positive association between the severity of apathy and increased rCBF in the ventral and dorsal striatum in patients with schizophrenia. This effect was not present for diminished expression. LIMITATIONS: All patients were taking atypical antipsychotics, so an effect of antipsychotic medication on rCBF could not be excluded, although we did not find a significant association between rCBF and chlorpromazine equivalents. CONCLUSION: The main finding of this study was a specific association between increased striatal rCBF and the negative symptom dimension of apathy. Our results further support the separate assessment of apathy and diminished expression when investigating the neural basis of negative symptoms. The ASL technique can provide a direct and quantitative approach to investigating the role of rCBF changes in the pathophysiology of negative symptoms.
Assuntos
Apatia/fisiologia , Circulação Cerebrovascular/fisiologia , Corpo Estriado/fisiopatologia , Esquizofrenia/fisiopatologia , Adulto , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Esquizofrenia/diagnóstico por imagem , Adulto JovemRESUMO
Adaptive coding of information is a fundamental principle of brain functioning. It allows for efficient representation over a large range of inputs and thereby alleviates the limited coding range of neurons. In the present study, we investigated for the first time potential alterations in context-dependent reward adaptation and its association with symptom dimensions in the schizophrenia spectrum. We studied 27 patients with first-episode psychosis, 26 individuals with schizotypal personality traits and 25 healthy controls. We used functional MRI in combination with a variant of the monetary incentive delay task and assessed adaptive reward coding in two reward conditions with different reward ranges. Compared to healthy controls, patients with first-episode psychosis and healthy individuals with schizotypal personality traits showed a deficit in increasing the blood oxygen level-dependent response slope in the right caudate for the low reward range compared to the high reward range. In other words, the two groups showed inefficient neural adaptation to the current reward context. In addition, we found impaired adaptive coding of reward in the caudate nucleus and putamen to be associated with total symptom severity across the schizophrenia spectrum. Symptom severity was more strongly associated with neural deficits in adaptive coding than with the neural coding of absolute reward outcomes. Deficits in adaptive coding were prominent across the schizophrenia spectrum and even detectable in unmedicated (healthy) individuals with schizotypal personality traits. Furthermore, the association between total symptom severity and impaired adaptive coding in the right caudate and putamen suggests a dimensional mechanism underlying imprecise neural adaptation. Our findings support the idea that impaired adaptive coding may be a general information-processing deficit explaining disturbances within the schizophrenia spectrum over and above a simple model of blunted absolute reward signals.
Assuntos
Adaptação Psicológica/fisiologia , Transtornos Psicóticos/fisiopatologia , Esquizofrenia/fisiopatologia , Adulto , Núcleo Caudado/fisiopatologia , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/fisiopatologia , Dopamina/metabolismo , Dopamina/fisiologia , Processamento Eletrônico de Dados/métodos , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Motivação , Neuropsiquiatria/métodos , Testes Neuropsicológicos , Transtornos Psicóticos/metabolismo , Recompensa , Transtorno da Personalidade Esquizotípica/metabolismo , Transtorno da Personalidade Esquizotípica/fisiopatologiaRESUMO
Deficits in empathy enhance conflicts and human suffering. Thus, it is crucial to understand how empathy can be learned and how learning experiences shape empathy-related processes in the human brain. As a model of empathy deficits, we used the well-established suppression of empathy-related brain responses for the suffering of out-groups and tested whether and how out-group empathy is boosted by a learning intervention. During this intervention, participants received costly help equally often from an out-group member (experimental group) or an in-group member (control group). We show that receiving help from an out-group member elicits a classical learning signal (prediction error) in the anterior insular cortex. This signal in turn predicts a subsequent increase of empathy for a different out-group member (generalization). The enhancement of empathy-related insula responses by the neural prediction error signal was mediated by an establishment of positive emotions toward the out-group member. Finally, we show that surprisingly few positive learning experiences are sufficient to increase empathy. Our results specify the neural and psychological mechanisms through which learning interacts with empathy, and thus provide a neurobiological account for the plasticity of empathic reactions.
Assuntos
Córtex Cerebral/fisiologia , Empatia/fisiologia , Aprendizagem/fisiologia , Processos Grupais , Humanos , Imageamento por Ressonância Magnética , Masculino , Neuroimagem , Plasticidade Neuronal/fisiologia , Distribuição Aleatória , Adulto JovemRESUMO
Neuromodulators such as dopamine can alter the intrinsic firing properties of neurons and may thereby change the configuration of larger functional circuits. The primate orbitofrontal cortex (OFC) receives dopaminergic input from midbrain nuclei, but the role of dopamine in the OFC is still unclear. Here we tested the idea that dopaminergic activity changes the pattern of connectivity between the OFC and the rest of the brain and thereby reconfigures functional networks in the OFC. To this end, we combined double-blind, placebo-controlled pharmacology [D2 receptor (D2R) antagonist amisulpride] in humans with resting-state functional magnetic resonance imaging and clustering methods. In the placebo group, we replicated previously observed parcellations of the OFC into two and six subregions based on connectivity patterns with the rest of the brain. Most importantly, while the twofold clustering did not differ significantly between groups, blocking D2Rs significantly changed the composition of the sixfold parcellation, suggesting a dopamine-dependent reconfiguration of functional OFC subregions. Moreover, multivariate decoding analyses revealed that amisulpride changed the whole-brain connectivity patterns of individual OFC subregions. In particular, D2R blockade shifted the balance of OFC connectivity from associative areas in the temporal and parietal lobe toward functional connectivity with the frontal cortex. In summary, our results suggest that dopamine alters the composition of functional OFC circuits, possibly indicating a broader role for neuromodulators in the dynamic reconfiguration of functional brain networks.SIGNIFICANCE STATEMENT A key role of any neuromodulator may be the reconfiguration of functional brain circuits. Here we test this idea with regard to dopamine and the organization of functional networks in the orbitofrontal cortex (OFC). We show that blockade of dopamine D2 receptors has profound effects on the functional connectivity patterns of the OFC, yielding altered connectivity-based subdivisions of this region. Our results suggest that dopamine changes the connectional configuration of the OFC, possibly leading to transitions between different operating modes that favor either sensory input or recurrent processing in the prefrontal cortex. More generally, our findings support a broader role for neuromodulators in the dynamic reconfiguration of functional brain networks and may have clinical implications for understanding the actions of antipsychotic agents.