scholarly journals Dynamic neural activity during stress signals resilient coping

2016 ◽  
Vol 113 (31) ◽  
pp. 8837-8842 ◽  
Author(s):  
Rajita Sinha ◽  
Cheryl M. Lacadie ◽  
R. Todd Constable ◽  
Dongju Seo
Keyword(s):  
Prefrontal Cortex ◽  
Stress Response ◽  
Emotional Eating ◽  
Behavioral Control ◽  
Real Life ◽  
Active Coping ◽  
Anterior Cingulate ◽  
Neural Activation ◽  
Dorsal Anterior Cingulate Cortex ◽  
Dynamic Activity

Active coping underlies a healthy stress response, but neural processes supporting such resilient coping are not well-known. Using a brief, sustained exposure paradigm contrasting highly stressful, threatening, and violent stimuli versus nonaversive neutral visual stimuli in a functional magnetic resonance imaging (fMRI) study, we show significant subjective, physiologic, and endocrine increases and temporally related dynamically distinct patterns of neural activation in brain circuits underlying the stress response. First, stress-specific sustained increases in the amygdala, striatum, hypothalamus, midbrain, right insula, and right dorsolateral prefrontal cortex (DLPFC) regions supported the stress processing and reactivity circuit. Second, dynamic neural activation during stress versus neutral runs, showing early increases followed by later reduced activation in the ventrolateral prefrontal cortex (VLPFC), dorsal anterior cingulate cortex (dACC), left DLPFC, hippocampus, and left insula, suggested a stress adaptation response network. Finally, dynamic stress-specific mobilization of the ventromedial prefrontal cortex (VmPFC), marked by initial hypoactivity followed by increased VmPFC activation, pointed to the VmPFC as a key locus of the emotional and behavioral control network. Consistent with this finding, greater neural flexibility signals in the VmPFC during stress correlated with active coping ratings whereas lower dynamic activity in the VmPFC also predicted a higher level of maladaptive coping behaviors in real life, including binge alcohol intake, emotional eating, and frequency of arguments and fights. These findings demonstrate acute functional neuroplasticity during stress, with distinct and separable brain networks that underlie critical components of the stress response, and a specific role for VmPFC neuroflexibility in stress-resilient coping.

scholarly journals Dissociable roles of cortical excitation-inhibition balance during patch-leaving versus value-guided decisions

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Luca F. Kaiser ◽  
Theo O. J. Gruendler ◽  
Oliver Speck ◽  
Lennart Luettgau ◽  
Gerhard Jocham
Keyword(s):  
Decision Making ◽  
Prefrontal Cortex ◽  
Neuronal Activity ◽  
Ventromedial Prefrontal Cortex ◽  
Anterior Cingulate ◽  
Mutual Inhibition ◽  
Dorsal Anterior Cingulate Cortex ◽  
Cortical Excitation ◽  
The Cost

AbstractIn a dynamic world, it is essential to decide when to leave an exploited resource. Such patch-leaving decisions involve balancing the cost of moving against the gain expected from the alternative patch. This contrasts with value-guided decisions that typically involve maximizing reward by selecting the current best option. Patterns of neuronal activity pertaining to patch-leaving decisions have been reported in dorsal anterior cingulate cortex (dACC), whereas competition via mutual inhibition in ventromedial prefrontal cortex (vmPFC) is thought to underlie value-guided choice. Here, we show that the balance between cortical excitation and inhibition (E/I balance), measured by the ratio of GABA and glutamate concentrations, plays a dissociable role for the two kinds of decisions. Patch-leaving decision behaviour relates to E/I balance in dACC. In contrast, value-guided decision-making relates to E/I balance in vmPFC. These results support mechanistic accounts of value-guided choice and provide evidence for a role of dACC E/I balance in patch-leaving decisions.

scholarly journals Neural Correlates of True and False Recognition Memory for Socially Relevant Information in Schizophrenia

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Amy M Jimenez ◽  
Junghee Lee ◽  
Eric A Reavis ◽  
Jonathan K Wynn ◽  
Michael F Green
Keyword(s):  
Prefrontal Cortex ◽  
Recognition Memory ◽  
False Recognition ◽  
Cingulate Cortex ◽  
Posterior Cingulate Cortex ◽  
Anterior Cingulate ◽  
False Alarms ◽  
Neural Activation ◽  
Lateral Prefrontal Cortex ◽  
Socially Relevant

Abstract Individuals with schizophrenia (SZ) demonstrate poor recognition memory, even when information is socially relevant. The neural alterations associated with responses to old information that is accurately recognized (true recognition) vs new information inaccurately identified as old (false recognition) are not known. Twenty SZ patients and 16 healthy controls performed a recognition paradigm during functional magnetic resonance imaging (fMRI) using 78 learned target and 78 new distractor words (all socially relevant trait adjectives). Participants were asked to indicate whether they had seen the word before or not. Words were classified according to the subjects’ responses, as hits (true recognition), false alarms (false recognition), correct rejections, or misses and compared for blood-oxygen-level-dependent (BOLD) activation. During hits, patients with SZ and controls showed similar BOLD activation in expected areas of lateral prefrontal cortex, parietal cortex, and anterior cingulate cortex. During false alarms, controls activated many of the same regions as were activated during hits. In contrast, patients had reduced activation in lateral prefrontal cortex (Brodmann Area, BA, 9, 46), anterior cingulate/paracingulate (BA 24/32, 6), and posterior cingulate cortex (BA 23/31). These results indicate that, compared to controls, patients with SZ exhibit a lack of correspondence between behavior (ie, falsely identifying new items as old) and neural activation patterns (ie, overlap in activation of regions associated with true and false recognition). These findings shed light on the neural mechanisms associated with false recognition memory in SZ.

scholarly journals Distinguishing neural correlates of context-dependent advantageous- and disadvantageous-inequity aversion

2018 ◽  
Vol 115 (33) ◽  
pp. E7680-E7689 ◽  
Author(s):  
Xiaoxue Gao ◽  
Hongbo Yu ◽  
Ignacio Sáez ◽  
Philip R. Blue ◽  
Lusha Zhu ◽  
...  
Keyword(s):  
Decision Making ◽  
Prefrontal Cortex ◽  
Computational Models ◽  
Social Contexts ◽  
Inequity Aversion ◽  
Context Dependency ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex ◽  
Decision Making Processes ◽  
Context Dependent

Humans can integrate social contextual information into decision-making processes to adjust their responses toward inequity. This context dependency emerges when individuals receive more (i.e., advantageous inequity) or less (i.e., disadvantageous inequity) than others. However, it is not clear whether context-dependent processing of advantageous and disadvantageous inequity involves differential neurocognitive mechanisms. Here, we used fMRI to address this question by combining an interactive game that modulates social contexts (e.g., interpersonal guilt) with computational models that enable us to characterize individual weights on inequity aversion. In each round, the participant played a dot estimation task with an anonymous coplayer. The coplayer would receive pain stimulation with 50% probability when either of them responded incorrectly. At the end of each round, the participant completed a variant of dictator game, which determined payoffs for him/herself and the coplayer. Computational modeling demonstrated the context dependency of inequity aversion: when causing pain to the coplayer (i.e., guilt context), participants cared more about the advantageous inequity and became more tolerant of the disadvantageous inequity, compared with other conditions. Consistently, neuroimaging results suggested the two types of inequity were associated with differential neurocognitive substrates. While the context-dependent processing of advantageous inequity was associated with social- and mentalizing-related processes, involving left anterior insula, right dorsolateral prefrontal cortex, and dorsomedial prefrontal cortex, the context-dependent processing of disadvantageous inequity was primarily associated with emotion- and conflict-related processes, involving left posterior insula, right amygdala, and dorsal anterior cingulate cortex. These results extend our understanding of decision-making processes related to inequity aversion.

scholarly journals Neural mechanisms of economic commitment in the human medial prefrontal cortex

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Konstantinos Tsetsos ◽  
Valentin Wyart ◽  
S Paul Shorkey ◽  
Christopher Summerfield
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Neural Mechanisms ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex ◽  
Financial Return ◽  
Economic Decisions ◽  
Decision Biases ◽  
Stimulus Value ◽  
Over Time

Neurobiologists have studied decisions by offering successive, independent choices between goods or gambles. However, choices often have lasting consequences, as when investing in a house or choosing a partner. Here, humans decided whether to commit (by acceptance or rejection) to prospects that provided sustained financial return. BOLD signals in the rostral medial prefrontal cortex (rmPFC) encoded stimulus value only when acceptance or rejection was deferred into the future, suggesting a role in integrating value signals over time. By contrast, the dorsal anterior cingulate cortex (dACC) encoded stimulus value only when participants rejected (or deferred accepting) a prospect. dACC BOLD signals reflected two decision biases–to defer commitments to later, and to weight potential losses more heavily than gains–that (paradoxically) maximised reward in this task. These findings offer fresh insights into the pressures that shape economic decisions, and the computation of value in the medial prefrontal cortex.

Neurocircuitry Underlying OCD

2017 ◽  
Author(s):  
Suzanne N. Haber
Keyword(s):  
Prefrontal Cortex ◽  
Orbitofrontal Cortex ◽  
Treatment Strategies ◽  
Reward Processing ◽  
Ventromedial Prefrontal Cortex ◽  
Anterior Cingulate ◽  
Reward Learning ◽  
Imaging Studies ◽  
Dorsal Anterior Cingulate Cortex ◽  
Individual Level

Structural and functional imaging studies have identified abnormalities in the brains of individuals with OCD. The most consistent findings point to pathology in the circuitry connecting the prefrontal cortex with the basal ganglia, and especially to abnormalities in the orbitofrontal cortex (OFC), ventromedial prefrontal cortex (vmPFC), dorsal anterior cingulate cortex (dACC), and striatum. This chapter describes the detailed anatomy and interconnectivity of these structures, together with its functional correlates, to provide context for the more detailed treatment of abnormalities seen in OCD provided in the chapters that follow. These corticostriatal circuits are critical for reward processing, reward learning, and action selection, and so disruption in these circuitries in OCD may underlie abnormalities in these domains. Precisely defining the anatomy of these circuits and how it is disrupted in OCD, at both the group and individual level, is increasingly important, as it may help us to optimize anatomically targeted treatment strategies.

scholarly journals Motor system dysfunction in the schizophrenia diathesis: Neural systems to neurotransmitters

2017 ◽  
Vol 44 ◽  
pp. 125-133 ◽  
Author(s):  
R. Abboud ◽  
C. Noronha ◽  
V.A. Diwadkar
Keyword(s):  
Motor Control ◽  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Motor System ◽  
Primary Motor Cortex ◽  
Multiple Scales ◽  
Motor Dysfunction ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex

AbstractMotor control is a ubiquitous aspect of human function, and from its earliest origins, abnormal motor control has been proposed as being central to schizophrenia. The neurobiological architecture of the motor system is well understood in primates and involves cortical and sub-cortical components including the primary motor cortex, supplementary motor area, dorsal anterior cingulate cortex, the prefrontal cortex, the basal ganglia, and cerebellum. Notably all of these regions are associated in some manner to the pathophysiology of schizophrenia. At the molecular scale, both dopamine and γ-Aminobutyric Acid (GABA) abnormalities have been associated with working memory dysfunction, but particularly relating to the basal ganglia and the prefrontal cortex respectively. As evidence from multiple scales (behavioral, regional and molecular) converges, here we provide a synthesis of the bio-behavioral relevance of motor dysfunction in schizophrenia, and its consistency across scales. We believe that the selective compendium we provide can supplement calls arguing for renewed interest in studying the motor system in schizophrenia. We believe that in addition to being a highly relevant target for the study of schizophrenia related pathways in the brain, such focus provides tractable behavioral probes for in vivo imaging studies in the illness. Our assessment is that the motor system is a highly valuable research domain for the study of schizophrenia.

scholarly journals The Fragile Brain: Stress Vulnerability, Negative Affect and GABAergic Neurocircuits in Psychosis

2019 ◽  
Vol 45 (6) ◽  
pp. 1170-1183 ◽  
Author(s):  
Stephan F Taylor ◽  
Tyler B Grove ◽  
Vicki L Ellingrod ◽  
Ivy F Tso
Keyword(s):  
Prefrontal Cortex ◽  
Negative Affect ◽  
Anterior Cingulate ◽  
Gamma Aminobutyric Acid ◽  
Dorsal Anterior Cingulate Cortex ◽  
Stress Vulnerability ◽  
Neuroimaging Data ◽  
Cortical Regions ◽  
Persons With Schizophrenia ◽  
Gaba Function

Abstract Persons with schizophrenia exhibit sensitivity to stress and negative affect (NA), both strongly correlated with poor functional outcome. This theoretical review suggests that NA reflects a “fragile brain,” ie, vulnerable to stress, including events not experienced as stressful by healthy individuals. Based on postmortem evidence of altered gamma-aminobutyric acid (GABA) function in parvalbumin positive interneurons (PVI), animal models of PVI abnormalities and neuroimaging data with GABAergic challenge, it is suggested that GABAergic disruptions weaken cortical regions, which leads to stress vulnerability and excessive NA. Neurocircuits that respond to stressful and salient environmental stimuli, such as the hypothalamic-pituitary-adrenal axis and the amygdala, are highly dysregulated in schizophrenia, exhibiting hypo- and hyper-activity. PVI abnormalities in lateral prefrontal cortex and hippocampus have been hypothesized to affect cognitive function and positive symptoms, respectively; in the medial frontal cortex (dorsal anterior cingulate cortex and dorsal medial prefrontal cortex), these abnormalities may lead to vulnerability to stress, NA and dysregulation of stress responsive systems. Given that postmortem PVI disruptions have been identified in other conditions, such as bipolar disorder and autism, stress vulnerability may reflect a transdiagnostic dimension of psychopathology.

scholarly journals Single-cell foundations of live social gaze interaction in the prefrontal cortex and amygdala

2021 ◽  
Author(s):  
Olga Dal Monte ◽  
Siqi Fan ◽  
Nicholas Fagan ◽  
Cheng-Chi Chu ◽  
Michael Zhou ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Single Cell ◽  
Interpersonal Communication ◽  
Significant Proportion ◽  
Real Life ◽  
Eye Contact ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Gaze Interaction ◽  
Social Gaze

Social gaze interaction powerfully shapes interpersonal communication in humans and other primates. However, little is known about the neural underpinnings of these social behavioral exchanges. Here, we studied neural responses associated with naturalistic, face-to-face, social gaze interactions between pairs of macaques. We examined spiking activity in a large number of neurons spanning four different brain regions involved in social behaviors - the amygdala, orbitofrontal cortex, anterior cingulate cortex, and dorsomedial prefrontal cortex. We observed widespread single-cell representations of social gaze interaction functionalities in these brain regions - social discriminability, social gaze monitoring, and mutual eye contact selectivity. Many of these neurons discriminated looking at social versus non-social stimuli with rich temporal heterogeneity, or parametrically tracked the gaze positions of oneself or the conspecific. Furthermore, many neurons displayed selectivity for mutual eye contact as a function of the initiator or follower of mutual gaze events. Crucially, a significant proportion of neurons coded for more than one of these three signatures of social gaze interaction, supporting the recruitment of partially overlapping neuronal ensembles. Our findings emphasize integrated contributions of the amygdala and prefrontal circuits within the social interaction networks in processing real-life social interactions.

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