Acute Effects of Heroin on Negative Emotional Processing: Relation of Amygdala Activity and Stress-Related Responses

ABSTRACTIntroduction:With ∼4 million births each year in the United States, an estimated 760,000 women annually suffer from a clinically significant postpartum depressive illness. Yet even though the relationship between psychiatric disorders and the postpartum period has been documented since the time of Hippocrates, fewer than half of all these cases are recognized.Objective:Because postpartum depression (PPD), the most common complication of childbearing, remains poorly characterized, and its etiology remains unclear, we attempted to address a critical gap in the mechanistic understanding of PPD by probing its systems-level neuropathophysiology, in the context of a specific neurobiological model of fronto-limbic-striatal function.Methods:Using emotionally valenced word probes, with linguistic semantic specificity within an integrated functional magnetic resonance imaging (fMRI) protocol, we investigated emotional processing, behavioral regulation, and their interaction (functions of clinical relevance to PPD), in the context of fronto-limbic-striatal function.Results:We observed attenuated activity in posterior orbitofrontal cortex for negative versus neutral stimuli with greater PPD symptomatology, increased amygdala activity in response to negative words in those without PPD symptomotology, and attenuated striatum activation to positive word conditions with greater PPD symptomotology.Conclusion:Identifying the functional neuroanatomical profile of brain systems involved in the regulation of emotion and behavior in the postpartum period will not only assist in determining whether the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition psychiatric diagnostic specifier of PPD has an associated, unique, functional neuroanatomical profile, but a neurobiological characterization in relation to asymptomatic (postpartum nondepressed) control subjects, will also increase our understanding of the affective disorder spectrum, shed additional light on the possible mechanism(s) responsible for PPD and provide a necessary foundation for the development of more targeted, biologically based diagnostic and therapeutic strategies for PPD.

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The Face of Negative Affect: Trial-by-Trial Corrugator Responses to Negative Pictures Are Positively Associated with Amygdala and Negatively Associated with Ventromedial Prefrontal Cortex Activity

Journal of Cognitive Neuroscience ◽

10.1162/jocn_a_00622 ◽

2014 ◽

Vol 26 (9) ◽

pp. 2102-2110 ◽

Cited By ~ 33

Author(s):

Aaron S. Heller ◽

Regina C. Lapate ◽

Kaitlyn E. Mayer ◽

Richard J. Davidson

Keyword(s):

Emotional Processing ◽

Emotional Valence ◽

Neural Circuitry ◽

Emg Activity ◽

Reciprocal Relation ◽

Physiological Measures ◽

Facial Muscle ◽

The Face ◽

Amygdala Activity ◽

Human Participants

The ability to simultaneously acquire objective physiological measures of emotion concurrent with fMRI holds the promise to enhance our understanding of the biological bases of affect and thus improve our knowledge of the neural circuitry underlying psychiatric disorders. However, the vast majority of neuroimaging studies to date examining emotion have not anchored the examination of emotion-responding circuitry to objective measures of emotional processing. To that end, we acquired EMG activity of a valence-sensitive facial muscle involved in the frowning response (corrugator muscle) concurrent with fMRI while twenty-six human participants viewed negative and neutral images. Trial-by-trial increases in corrugator EMG activity to negative pictures were associated with greater amygdala activity and a concurrent decrease in ventromedial PFC activity. Thus, this study highlights the reciprocal relation between amygdalar and ventromedial PFC in the encoding of emotional valence as reflected by facial expression.

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Human Capacities for Emotion Recognition and their Implications for Computer Vision

i-com ◽

10.1515/icom-2015-0032 ◽

2015 ◽

Vol 14 (2) ◽

pp. 126-137 ◽

Cited By ~ 1

Author(s):

Benny Liebold ◽

René Richter ◽

Michael Teichmann ◽

Fred H. Hamker ◽

Peter Ohler

Keyword(s):

Emotion Recognition ◽

Emotional Processing ◽

Affective Computing ◽

Expression Patterns ◽

Connectivity Pattern ◽

Motor Patterns ◽

Emotional Processes ◽

Current State ◽

Amygdala Activity ◽

Cortical Involvement

AbstractCurrent models for automated emotion recognition are developed under the assumption that emotion expressions are distinct expression patterns for basic emotions. Thereby, these approaches fail to account for the emotional processes underlying emotion expressions. We review the literature on human emotion processing and suggest an alternative approach to affective computing. We postulate that the generalizability and robustness of these models can be greatly increased by three major steps: (1) modeling emotional processes as a necessary foundation of emotion recognition; (2) basing models of emotional processes on our knowledge about the human brain; (3) conceptualizing emotions based on appraisal processes and thus regarding emotion expressions as expressive behavior linked to these appraisals rather than fixed neuro-motor patterns. Since modeling emotional processes after neurobiological processes can be considered a long-term effort, we suggest that researchers should focus on early appraisals, which evaluate intrinsic stimulus properties with little higher cortical involvement. With this goal in mind, we focus on the amygdala and its neural connectivity pattern as a promising structure for early emotional processing. We derive a model for the amygdala-visual cortex circuit from the current state of neuroscientific research. This model is capable of conditioning visual stimuli with body reactions to enable rapid emotional processing of stimuli consistent with early stages of psychological appraisal theories. Additionally, amygdala activity can feed back to visual areas to modulate attention allocation according to the emotional relevance of a stimulus. The implications of the model considering other approaches to automated emotion recognition are discussed.

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Reducing Amygdala Activity and Phobic Fear through Cognitive Top–Down Regulation

Journal of Cognitive Neuroscience ◽

10.1162/jocn_a_01537 ◽

2020 ◽

Vol 32 (6) ◽

pp. 1117-1129

Author(s):

Eva Loos ◽

Nathalie Schicktanz ◽

Matthias Fastenrath ◽

David Coynel ◽

Annette Milnik ◽

...

Keyword(s):

Anxiety Disorders ◽

Cognitive Load ◽

Emotional Processing ◽

Psychological Intervention ◽

Causal Modeling ◽

Top Down ◽

Down Regulation ◽

Fmri Study ◽

Amygdala Activity ◽

Healthy Participants

The amygdala is critically involved in emotional processing, including fear responses, and shows hyperactivity in anxiety disorders. Previous research in healthy participants has indicated that amygdala activity is down-regulated by cognitively demanding tasks that engage the PFC. It is unknown, however, if such an acute down-regulation of amygdala activity might correlate with reduced fear in anxious participants. In an fMRI study of 43 participants (11 men) with fear of snakes, we found reduced amygdala activity when visual stimuli were processed under high cognitive load, irrespective of whether the stimuli were of neutral or phobic content. Furthermore, dynamic causal modeling revealed that this general reduction in amygdala activity was partially mediated by a load-dependent increase in dorsolateral PFC activity. Importantly, high cognitive load also resulted in an acute decrease in perceived phobic fear while viewing the fearful stimuli. In conclusion, our data indicate that a cognitively demanding task results in a top–down regulation of amygdala activity and an acute reduction of fear in phobic participants. These findings may inspire the development of novel psychological intervention approaches aimed at reducing fear in anxiety disorders.

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Does alcohol affect emotional face processing via interoceptive pathways?

10.31234/osf.io/43umw ◽

2021 ◽

Author(s):

Mateo Leganes-Fonteneau ◽

Marsha Bates ◽

Anthony Pawlak ◽

Jennifer Buckman

Keyword(s):

Face Processing ◽

Emotional Processing ◽

The Body ◽

Cardiovascular Physiology ◽

Acute Effects ◽

Alcohol Administration ◽

Emotional Face Processing ◽

Before And After ◽

Emotional Face ◽

Physiological Substrates

Background: Our brain uses interoceptive signals from the body to shape how we perceive emotions in others; however, whether interoceptive signals can be manipulated to alter emotional perceptions is unknown. Alcohol has acute effects both on emotional processing and on the physiological substrates supporting interoception. In this registered report, we examine whether alcohol administration triggers physiological changes that alter interoceptive signals and manipulate emotional face processing. Such knowledge will broaden understanding of the mechanisms by which alcohol affects emotional face processing.Methods: Participants (n=36) will be administered an alcohol or placebo beverage. Cardiovascular physiology will be recorded before and after administration. Participants will complete two behavioral tasks in which they view emotional faces presented in synchrony with different phases of the cardiac cycle (i.e., systole, diastole). This manipulation creates an index of how interoceptive signals amplify emotional face processing. Hypotheses: We hypothesize that, compared to placebo, alcohol administration will disrupt the cardiac amplification of emotional face processing. We further explore whether this disruption depends on the nature and magnitude of changes in cardiovascular physiology after alcohol administration.

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Amygdala Plasticity and Pain

Pain Research and Management ◽

10.1155/2017/8296501 ◽

2017 ◽

Vol 2017 ◽

pp. 1-12 ◽

Cited By ~ 43

Author(s):

Jeremy M. Thompson ◽

Volker Neugebauer

Keyword(s):

Cognitive Deficits ◽

Emotional Processing ◽

Basolateral Amygdala ◽

Cell Mass ◽

Central Nucleus ◽

Control Mechanisms ◽

Cortical Control ◽

Amygdala Activity ◽

Preclinical And Clinical Studies ◽

New Strategies

The amygdala is a limbic brain region that plays a key role in emotional processing, neuropsychiatric disorders, and the emotional-affective dimension of pain. Preclinical and clinical studies have identified amygdala hyperactivity as well as impairment of cortical control mechanisms in pain states. Hyperactivity of basolateral amygdala (BLA) neurons generates enhanced feedforward inhibition and deactivation of the medial prefrontal cortex (mPFC), resulting in pain-related cognitive deficits. The mPFC sends excitatory projections to GABAergic neurons in the intercalated cell mass (ITC) in the amygdala, which project to the laterocapsular division of the central nucleus of the amygdala (CeLC; output nucleus) and serve gating functions for amygdala output. Impairment of these cortical control mechanisms allows the development of amygdala pain plasticity. Mechanisms of abnormal amygdala activity in pain with particular focus on loss of cortical control mechanisms as well as new strategies to correct pain-related amygdala dysfunction will be discussed in the present review.

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Serotonergic neurotransmission in emotional processing: New evidence from long-term recreational poly-drug ecstasy use

Journal of Psychopharmacology ◽

10.1177/0269881116662633 ◽

2016 ◽

Vol 30 (12) ◽

pp. 1296-1304 ◽

Cited By ~ 1

Author(s):

Helle Ruff Laursen ◽

Susanne Henningsson ◽

Julian Macoveanu ◽

Terry L Jernigan ◽

Hartwig R Siebner ◽

...

Keyword(s):

Face Processing ◽

Emotional Processing ◽

Neural Basis ◽

Serotonin Depletion ◽

Serotonergic Neurotransmission ◽

Emotional Face Processing ◽

Amygdala Activity ◽

Angry Face ◽

Emotional Face

The brain’s serotonergic system plays a crucial role in the processing of emotional stimuli, and several studies have shown that a reduced serotonergic neurotransmission is associated with an increase in amygdala activity during emotional face processing. Prolonged recreational use of ecstasy (3,4-methylene-dioxymethamphetamine [MDMA]) induces alterations in serotonergic neurotransmission that are comparable to those observed in a depleted state. In this functional magnetic resonance imaging (fMRI) study, we investigated the responsiveness of the amygdala to emotional face stimuli in recreational ecstasy users as a model of long-term serotonin depletion. Fourteen ecstasy users and 12 non-using controls underwent fMRI to measure the regional neural activity elicited in the amygdala by male or female faces expressing anger, disgust, fear, sadness, or no emotion. During fMRI, participants made a sex judgement on each face stimulus. Positron emission tomography with 11C-DASB was additionally performed to assess serotonin transporter (SERT) binding in the brain. In the ecstasy users, SERT binding correlated negatively with amygdala activity, and accumulated lifetime intake of ecstasy tablets was associated with an increase in amygdala activity during angry face processing. Conversely, time since the last ecstasy intake was associated with a trend toward a decrease in amygdala activity during angry and sad face processing. These results indicate that the effects of long-term serotonin depletion resulting from ecstasy use are dose-dependent, affecting the functional neural basis of emotional face processing.

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A systematic review of the effects of psychiatric medications on social cognition

BMC Psychiatry ◽

10.1186/s12888-021-03545-z ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Zoë Haime ◽

Andrew J. Watson ◽

Nadia Crellin ◽

Louise Marston ◽

Eileen Joyce ◽

...

Keyword(s):

Systematic Review ◽

Social Cognition ◽

Emotional Processing ◽

Drug Effects ◽

Small Sample ◽

Narrative Synthesis ◽

Amygdala Activity ◽

Drug Treatments ◽

Small Sample Sizes ◽

The Impact

Abstract Introduction Social cognition is an important area of mental functioning relevant to psychiatric disorders and social functioning, that may be affected by psychiatric drug treatments. The aim of this review was to investigate the effects of medications with sedative properties, on social cognition. Method This systematic review included experimental and neuroimaging studies investigating drug effects on social cognition. Data quality was assessed using a modified Downs and Black checklist (Trac et al. CMAJ 188: E120-E129, 2016). The review used narrative synthesis to analyse the data. Results 40 papers were identified for inclusion, 11 papers investigating benzodiazepine effects, and 29 investigating antipsychotic effects, on social cognition. Narrative synthesis showed that diazepam impairs healthy volunteer’s emotion recognition, with supporting neuroimaging studies showing benzodiazepines attenuate amygdala activity. Studies of antipsychotic effects on social cognition gave variable results. However, many of these studies were in patients already taking medication, and potential practice effects were identified due to short-term follow-ups. Conclusion Healthy volunteer studies suggest that diazepam reduces emotional processing ability. The effects of benzodiazepines on other aspects of social cognition, as well as the effects of antipsychotics, remain unclear. Interpretations of the papers in this review were limited by variability in measures, small sample sizes, and lack of randomisation. More robust studies are necessary to evaluate the impact of these medications on social cognition.

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Serotonin neurons in the dorsal raphe mediate the anticataplectic action of orexin neurons by reducing amygdala activity

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1614552114 ◽

2017 ◽

Vol 114 (17) ◽

pp. E3526-E3535 ◽

Cited By ~ 38

Author(s):

Emi Hasegawa ◽

Takashi Maejima ◽

Takayuki Yoshida ◽

Olivia A. Masseck ◽

Stefan Herlitze ◽

...

Keyword(s):

Emotional Processing ◽

Muscle Tone ◽

Dorsal Raphe ◽

Designer Drugs ◽

Nerve Terminals ◽

Downstream Target ◽

Serotonin Neurons ◽

Amygdala Activity ◽

Neuron Terminals ◽

Dorsal Raphé

Narcolepsy is a sleep disorder caused by the loss of orexin (hypocretin)-producing neurons and marked by excessive daytime sleepiness and a sudden weakening of muscle tone, or cataplexy, often triggered by strong emotions. In a mouse model for narcolepsy, we previously demonstrated that serotonin neurons of the dorsal raphe nucleus (DRN) mediate the suppression of cataplexy-like episodes (CLEs) by orexin neurons. Using an optogenetic tool, in this paper we show that the acute activation of DRN serotonin neuron terminals in the amygdala, but not in nuclei involved in regulating rapid eye-movement sleep and atonia, suppressed CLEs. Not only did stimulating serotonin nerve terminals reduce amygdala activity, but the chemogenetic inhibition of the amygdala using designer receptors exclusively activated by designer drugs also drastically decreased CLEs, whereas chemogenetic activation increased them. Moreover, the optogenetic inhibition of serotonin nerve terminals in the amygdala blocked the anticataplectic effects of orexin signaling in DRN serotonin neurons. Taken together, the results suggest that DRN serotonin neurons, as a downstream target of orexin neurons, inhibit cataplexy by reducing the activity of amygdala as a center for emotional processing.

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