Researchers have wondered how the brain creates emotions since the early days of psychological science. With a surge of studies in affective neuroscience in recent decades, scientists are poised to answer this question. In this target article, we present a meta-analytic summary of the neuroimaging literature on human emotion. We compare the locationist approach (i.e., the hypothesis that discrete emotion categories consistently and specifically correspond to distinct brain regions) with the psychological constructionist approach (i.e., the hypothesis that discrete emotion categories (...) are constructed of more general brain networks not specific to those categories) to better understand the brain basis of emotion. We review both locationist and psychological constructionist hypotheses of brain–emotion correspondence and report meta-analytic findings bearing on these hypotheses. Overall, we found little evidence that discrete emotion categories can be consistently and specifically localized to distinct brain regions. Instead, we found evidence that is consistent with a psychological constructionist approach to the mind: A set of interacting brain regions commonly involved in basic psychological operations of both an emotional and non-emotional nature are active during emotion experience and perception across a range of discrete emotion categories. (shrink)
In our response, we clarify important theoretical differences between basic emotion and psychological construction approaches. We evaluate the empirical status of the basic emotion approach, addressing whether it requires brain localization, whether localization can be observed with better analytic tools, and whether evidence for basic emotions exists in other types of measures. We then revisit the issue of whether the key hypotheses of psychological construction are supported by our meta-analytic findings. We close by elaborating on commentator suggestions for future research.
Lindquist et al. convincingly argue that the brain implements psychological operations that are constitutive of emotion rather than modules subserving discrete emotions. However, the nature of such psychological operations is open to debate. I argue that considering appraisal theories may provide alternative interpretations of the neuroimaging data with respect to the psychological operations involved.
We agree that conceptualisation is key in understanding the brain basis of emotion. We argue that by conflating facial emotion recognition with subjective emotion experience, Lindquist et al. understate the importance of biological predisposition in emotion. We use examples from the anxiety disorders to illustrate the distinction between these two phenomena, emphasising the importance of both emotional hardware and contextual learning.
Compared to our understanding of positive prediction error signals occurring due to unexpected reward outcomes, less is known about the neural circuitry in humans that drives negative prediction errors during omission of expected rewards. While classical learning theories such as Rescorla–Wagner or temporal difference learning suggest that both types of prediction errors result from a simple subtraction, there has been recent evidence suggesting that different brain regions provide input to dopamine neurons which contributes to specific components of this prediction error (...) computation. Here, we focus on the brain regions responding to negative prediction error signals, which has been well-established in animal studies to involve a distinct pathway through the lateral habenula. We examine the activity of this pathway in humans, using a conditioned inhibition paradigm with high-resolution functional MRI. First, participants learned to associate a sensory stimulus with reward delivery. Then, reward delivery was omitted whenever this stimulus was presented simultaneously with a different sensory stimulus, the conditioned inhibitor. Both reward presentation and the reward-predictive cue activated midbrain dopamine regions, insula and orbitofrontal cortex. While we found significant activity at an uncorrected threshold for the CI in the habenula, consistent with our predictions, it did not survive correction for multiple comparisons and awaits further replication. Additionally, the pallidum and putamen regions of the basal ganglia showed modulations of activity for the inhibitor that did not survive the corrected threshold. (shrink)