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The Neuroscience of Emotion: From Reaction to Regulation
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Scientists who emphasize that humans are animals focus on one set of facts when defining and studying emotion. Scientists who emphasize human uniqueness focus on a different set. What the field needs is a model that can account for all the facts, where species-general and species-specific aspects of emotion are incorporated within one unifying framework. I will suggest one possible framework, and illustrate how it is consistent with a broad array of observations about the human brain.
Visual cues depicting unpleasant and pleasant objects and events elicit measurable neural and peripheral activity in human observers. Using dense sensor EEG arrays, the timing and topography of neural processes associated with perceptual, attentional, and attentional engagement can be investigated. Studies are described that explore perceptual (e.g., complexity, repetition) and attentional manipulations (e.g., startle probe, task-relevance) on event-related potentials during affective picture perception. The resulting data suggest a cascade of neural processes from sensory detection to stimulus identification to motivational activation, with different processes modulated by perceptual, attentional, and affective variables. The data are consistent with the view that cues that activate fundamental defensive and appetitive neural systems naturally engage attention in the service of determining appropriate action and that this activation serves as the basis of affective experience.
Anxiety disorders are the most common type of psychiatric illness, afflicting an estimated 19 million children and adults in the US alone. Although medications have been extremely helpful in treating many of these individuals, they can have unpleasant side effects, can be addictive, and do not work for all patients. Cognitive behavioral therapy has also proven to be very helpful in treating many of these disorders and is based on the well-researched phenomenon known as fear extinction, in which a fearful situation is confronted repeatedly in the absence of any aversive event. Extensive empirical work by psychologists has revealed the basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Much of this work has been done using a paradigm known as fear conditioning, in which an initially neutral stimulus, such as a tone, is paired with an aversive event, such as footshock (in rats) or an air blast to the throat (in people). Following this conditioning procedure, the tone produces a variety of behavioral effects (freezing, increased startle, increased blood pressure, sweating) that serve as an objective measure of conditioned fear. If the tone is then presented repeatedly in the absence of the aversive shock or air blast (extinction training), it is much less likely to elicit these conditioned fear responses. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved in extinction, including the brain regions where extinction-related plasticity occurs and the cellular and molecular processes that are engaged. I will review key experiments demonstrating the behavioral characteristics of extinction, and briefly review what is currently known about the neurotransmitters involved. Finally, I will describe the role of NMDA receptors in extinction has that has led to new ways to combine drugs, such as D-cycloserine, with cognitive behavioral therapy to produce clinical benefits.
Memory biases for negative information have been theorized to play an etiological role in major depression. Event-related brain potentials provide a unique window into the processes underlying this phenomenon.
In this talk I will provide neurophysiological evidence for memory biases in both healthy and major depressive research participants, delineating the specific affected processes and the contexts in which they occur.
Functional neuroimaging is revealing how brain mechanisms mediate diversity and individuality in emotion processing. I will review evidence that variation in personality, gender, and age relates to variation in emotion processing in the human brain.
Neuroimaging, especially BOLD fMRI, has begun to identify how variability in brain function contributes to individual differences in complex behavioral traits. In parallel, pharmacological fMRI and multimodal PET/fMRI is identifying how variability in molecular signaling pathways influences individual differences in brain function. Against this background, functional genetic polymorphisms are being utilized to understand the origins of variability in signaling pathways as well as to efficiently model how such emergent variability impacts behaviorally relevant brain function. My talk will provide an overview of a research strategy seeking to integrate these complimentary technologies and utilize existing empirical data to illustrate its effectiveness in illuminating the neurobiology of individual differences in complex behavioral traits. I will also discusses how such efforts can contribute to the identification of predictive disease risk markers as well as the development of more effective and individually tailored treatment regimes.
Serotonin and GABA, more than any other neurotransmitters, and their receptors have been the focus of molecular pharmacology and genetics studies of anxiety and aggression. They are evolutionary old molecules, the former characterized by discrete low concentration. The most successful translation of preclinical data with models in rodents and primates to the clinic pertain to the positive allosteric modulation of GABAA receptors. For example, molecular and behavioral biology studies have begun to differentiate the anxiety-relieving, sedative, anticonvulsant, amnesic and aggression-modulating effects of benzodiazepines and alcohol and link them to very specific subunits of the GABAA receptors in discrete mesocorticolimbic pathways. Similarly, at least half a dozen serotonin receptor subtypes and transporter molecules at somatodendritic, pre- and post-synaptic sites in the mesocorticolimbic pathways have emerged as critical for the modulation of escalated aggression. These anatomical and receptor-selective mechanisms begin to match the clinical complexity of different anxiety disorders and different types of escalated aggressive behavior.
Humans in different cultures develop a similar capacity to recognize the emotional signals of diverse facial expressions. This capacity is mediated by a brain network that involves emotion-related brain circuits and higher-level visual-representation areas. Recent studies suggest that the key components of this network begin to emerge early in life. The studies also suggest that initial biases in emotion-related brain circuits and the early coupling of these circuits and cortical perceptual areas provide a foundation for a rapid acquisition of representations of those facial features that denote specific emotions.
The ability to effectively manage our emotions is essential to the maintenance of both mental and physical well-being. One of the most flexible and powerful regulatory strategies is reappraisal, which involves cognitively changing our interpretation of the meaning of an event in order to change our emotional response to it. In this talk I will present a series of studies designed to unpack the basic psychological and neural mechanisms underlying reappraisal, and how they function differently in clinical groups. The first part of the talk seeks to establish a model of basic reappraisal mechanisms by comparing and contrasting different forms reappraisal to each other and to related regulatory strategies. The second part translates this model to help clarify how emotion dysregulation plays a role in both substance abuse and borderline personality disorder.
I will explore how animal models of fear learning extend to
humans in a social context. Specifically, I will demonstrate how the
neural circuitry of fear conditioning forms the basis to fears
learned through social communication and changing fears in humans
through social and non-social means relies on overlapping neural
My long-term research goal is to identify specific abnormalities in neural systems underlying different subprocesses supporting emotion processing and emotion regulation in individuals with major psychiatric disorders, including bipolar disorder and unipolar depression. Identifying neural system abnormalities that may represent objective biomarkers of psychiatric disorders is a crucially important step toward the long-term goal of improving diagnostic accuracy of these disorders, and informing management in individuals presenting in the early stages of psychiatric illness. My research has also focused on examination of the extent to which neuroimaging can help identify as early as possible neural system abnormalities in those individuals at genetic risk of psychiatric disorder that in turn can be used as predictors of subsequent development of the disorder.
I will present findings from several neuroimaging studies from my group in which we have employed different neuroimaging techniques, including functional Magnetic Resonance Imaging (fMRI), diffusion tensor imaging (DTI), functional connectivity and dynamic causal modeling (DCM), to examine structural and functional connectivity in neural systems underlying emotion regulation in healthy, bipolar and unipolar depressed adults. I will also present findings from studies in which we have begun to examine the extent to which these neuroimaging techniques are beginning to identify abnormalities in neural systems supporting emotion processing and emotion regulation in individuals at high genetic risk of subsequently developing bipolar disorder and unipolar depression, that in turn will facilitate identification of potential risk markers of disorder development.
Anhedonia, the lack of reactivity to pleasurable stimuli, plays an important role in a variety of psychiatric disorders, and is a cardinal symptom of depression. Although anhedonia confers increased vulnerability to psychopathology, few studies have employed laboratory-based measures to objectively characterize this important phenotype. In addition, the neurobiological underpinnings of anhedonia remain largely unknown. To address these issues we have developed a probabilistic reward task based on a differential reinforcement schedule that allows us to objectively assess participants' propensity to modulate behavior as a function of reward history. Our findings indicate that depression is characterized by an impaired tendency to modulate behavior in response to prior reinforcements, and provide initial clues about which aspects of hedonic processing might be dysfunctional in depression. In addition, recent functional magnetic resonance imaging (fMRI) findings suggest that blunted hedonic responses are associated with dysfunction within basal ganglia regions previously implicated in reward processing. We are currently investigating the effects of genetic vulnerability and stress on hedonic deficits and associated neurobiological dysfunctions.
Decades of psychological research have taught us that extinction of classical conditioning reduces the expression of the conditioned response, but does not eliminate the conditioning memory, suggesting that extinction is inhibitory learning. Recent advances in rodent research have delineated the neural circuits involved in the acquisition and expression of extinction. While the basolateral amygdala (BLA) is a site of inhibitory learning in extinction, the medial prefrontal cortex modulates the expression of extinction memory, via projections to the amygdala. Converging lines of evidence indicate that the infralimbic (IL) prefrontal cortex inhibits the expression of conditioned fear by inhibiting amygdala output. Extinction induced plasticity in IL occurs via both synaptic and intrinsic mechanisms. Furthermore electrical stimulation of IL reduces fear and strengthens extinction. Manipulations of the prelimbic (PL) prefrontal cortex have the opposite effect, suggesting that this area works with the amygdala to activate fear. Thus, PL and IL serve as �on� and �off� switches for fear expression. Extinction failure is associated with over and under activity in PL and IL respectively, suggesting that the ability to retrieve extinction is governed by prefrontal cortex, in conjunction with hippocampal and amygdala inputs. Human homologues of rodent IL and PL show predicted changes in activity levels in people undergoing extinction, as well as extinction failure in PTSD patients. Strategies to ameliorate prefrontal deficits could facilitate extinction-based therapies for anxiety disorders.
Recent neuroimaging studies have reported functional abnormalities in several limbic and paralimbic brain regions in PTSD. Specifically, the amygdala and dorsal anterior cingulate cortex (dACC) appear to be hyperresponsive in PTSD, whereas the rostral anterior cingulate cortex (rACC) and adjacent medial prefrontal cortex (mPFC) appear to be hyporesponsive in this disorder. These findings are consistent with fear conditioning models of PTSD as well as the role of these brain regions in the assessment of emotional stimuli and emotion regulation. New research will be presented to help determine whether these functional abnormalities can predict response to treatment. In addition, the results of a new study of monozygotic twins discordant for trauma exposure will be presented to help determine whether the functional abnormalities in PTSD are acquired signs of the disorder or familial vulnerability factors that increase the risk of PTSD after exposure to psychological trauma.
Early adversity, for example poor caregiving, can have profound effects on emotional development. Orphanage rearing, even in the best circumstances, lies outside of the bounds of a species-typical caregiving environment and is often followed by difficulty in the socio-emotional domain. This talk will describe the developmental trajectory of socio-emotional behaviors (self regulation in the context of highly arousing social information) and associated neuro-development in a population of previously institutionalized children using behavioral data as well as structural and functional neuroimaging. The individual differences in neural phenotypes we observed co-occur with behavioral atypicalities, including peer relationship difficulties. These findings are consistent with previous reports describing negative socio-affective effects of prolonged orphanage care and with animal models that show long term changes in the amygdala and emotional behavior following early postnatal stress. Thus, stress-related changes in limbic circuitry may be the mediating factor between early adversity and residual emotional and social problems experienced by children who have been internationally adopted.
Functional neuroimaging studies indicate that regions of prefrontal cortex (PFC) and the amygdala are implicated in using cognitive reappraisal to regulate negative affect. Interestingly, older people exhibit decrements in performance on cognitive tasks associated with regions of PFC that are implicated in reappraisal processes, including poorer visual working memory performance, and decreased ability to ignore task-irrelevant information. Yet, at the same time, there is substantial evidence to suggest that older people actually experience higher levels of affective functioning than younger adults on a daily basis. This raises important questions as to the emotion regulatory processes that underlie such salutary functioning. This talk will review evidence to suggest that functioning in PFC and amygdala regions during reappraisal is related to affective functioning in older adults, and that older adults choose emotion regulatory strategies that provide the best fit with the cognitive, social, and neural systems at their disposal.
My research seeks to demonstrate that the amygdala, part of a circuitry originally designed for fear and fear-related learning (in an evolutionary sense), now supports subtle fluctuations in state more appropriately referred to as vigilance. These fluctuations, observed in response to stimuli that predict biologically relevant outcomes, then give rise to a host of central and peripheral responses that facilitate the processing of biologically relevant information. We have answered questions about the fundamental role of the amygdala in humans using expressions on the faces of others, which produce robust activation of the amygdala. We suggest that this activation is related to the fact that facial expressions are, in essence, conditioned stimuli; that is, they have predicted biologically relevant outcomes for you in the past, thus, upon their presentation in an experimental study, they will command the respect of this system (at least initially). While these signals will often be comparable across a group of subjects, we can also find evidence of individual differences between subjects.
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