Alpha-2 Adrenoreceptor Antagonist Yohimbine Potentiates Consolidation of Conditioned Fear

Sperl, Matthias F.J.; Panitz, Christian; Skoluda, Nadine; Nater, Urs M.; Pizzagalli, Diego A.; Hermann, Christiane; Mueller, Erik M.

doi:10.1093/ijnp/pyac038

Cited by 10 publications

(3 citation statements)

References 137 publications

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“…For statistical analysis, we calculated the mean IBI signal between 2000 and 5000 ms relative to stimulus onset. This time range was chosen based on previous studies demonstrating fear bradycardia (slowing of the heartbeat) during the presentation of threat‐predictive cues (Panitz et al, 2015; Sperl et al, 2022). Mean IBI values were imported to R for statistical analysis.…”

Section: Methodsmentioning

confidence: 99%

Oscillatory and non‐oscillatory brain activity reflects fear expression in an immediate and delayed fear extinction task

2023

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Fear extinction is pivotal for inhibiting fear responding to former threat‐predictive stimuli. In rodents, short intervals between fear acquisition and extinction impair extinction recall compared to long intervals. This is called Immediate Extinction Deficit (IED). Importantly, human studies of the IED are sparse and its neurophysiological correlates have not been examined in humans. We, therefore, investigated the IED by recording electroencephalography (EEG), skin conductance responses (SCRs), an electrocardiogram (ECG), and subjective ratings of valence and arousal. Forty male participants were randomly assigned to extinction learning either 10 min after fear acquisition (immediate extinction) or 24 h afterward (delayed extinction). Fear and extinction recall were assessed 24 h after extinction learning. We observed evidence for an IED in SCR responses, but not in the ECG, subjective ratings, or in any assessed neurophysiological marker of fear expression. Irrespective of extinction timing (immediate vs. delayed), fear conditioning caused a tilt of the non‐oscillatory background spectrum with decreased low‐frequency power (<30 Hz) for threat‐predictive stimuli. When controlling for this tilt, we observed a suppression of theta and alpha oscillations to threat‐predictive stimuli, especially pronounced during fear acquisition. In sum, our data show that delayed extinction might be partially advantageous over immediate extinction in reducing sympathetic arousal (as assessed via SCR) to former threat‐predictive stimuli. However, this effect was limited to SCR responses since all other fear measures were not affected by extinction timing. Additionally, we demonstrate that oscillatory and non‐oscillatory activity is sensitive to fear conditioning, which has important implications for fear conditioning studies examining neural oscillations.

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Section: Methodsmentioning

confidence: 99%

Oscillatory and non‐oscillatory brain activity reflects fear expression in an immediate and delayed fear extinction task

2023

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“…Similar contradictions are observed in humans, such that administration of a D 2 ‐like receptor antagonist prior to or after fear acquisition decreased fMRI BOLD activity in the mPFC towards the CS+ during extinction training, displaying an opposite neuroimaging phenotype to those administered the extinction facilitator L‐DOPA. However, electroencephalography, galvanic skin conductance responses and explicit ratings were unaltered (Klass et al, 2021; Lissek et al, 2015; Sperl et al, 2022). Furthermore, those administered a D 2 ‐like receptor agonist after acquisition exhibited exaggerated renewal as explicit ratings towards the CS+ increased (Lissek et al, 2018).…”

Section: Resultsmentioning

confidence: 99%

65 years of research on dopamine's role in classical fear conditioning and extinction: A systematic review

Hamati,

Ahrens,

Shvetz

et al. 2023

Eur J of Neuroscience

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Dopamine, a catecholamine neurotransmitter, has historically been associated with the encoding of reward, whereas its role in aversion has received less attention. Here, we systematically gathered the vast evidence of the role of dopamine in the simplest forms of aversive learning: classical fear conditioning and extinction. In the past, crude methods were used to augment or inhibit dopamine to study its relationship with fear conditioning and extinction. More advanced techniques such as conditional genetic, chemogenic and optogenetic approaches now provide causal evidence for dopamine's role in these learning processes. Dopamine neurons encode conditioned stimuli during fear conditioning and extinction and convey the signal via activation of D1–4 receptor sites particularly in the amygdala, prefrontal cortex and striatum. The coordinated activation of dopamine receptors allows for the continuous formation, consolidation, retrieval and updating of fear and extinction memory in a dynamic and reciprocal manner. Based on the reviewed literature, we conclude that dopamine is crucial for the encoding of classical fear conditioning and extinction and contributes in a way that is comparable to its role in encoding reward.

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“…Humans administered a D 2 -like receptor antagonist tiapride or sulpiride prior to or after acquisition exhibited decreased fMRI BOLD activity in the PFC towards the CS+ during extinction, but EEG, galvanic skin conductance responses, and explicit ratings were unaltered (Klass et al, 2021;Lissek et al, 2015;Sperl et al, 2022). In humans administered a D 2 -like receptor agonist after acquisition, fMRI BOLD activity in the hippocampus increased during extinction and renewal, and explicit ratings towards the CS+ increased during renewal (Lissek et al, 2018).…”

Section: Evidence From Non-selective D 2 -Like Receptor Drug Interven...mentioning

confidence: 98%

50 Years of Research on Dopamine’s Role in Passive Aversive Conditioning and Extinction: A Systematic Review

Hamati

Ahrens

Holahan

et al. 2023

Preprint

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Dopamine, a catecholamine neurotransmitter, has historically been associated with the encoding of reward, whereas its role in aversion has received less attention. Here, we systematically gather the vast evidence for a role of dopamine in the simplest form of aversive learning: passive aversive conditioning and extinction. In the past, crude methods were used to augment or inhibit dopamine in order to study its relationship with fear conditioning and extinction. More advanced techniques such as conditional genetic, chemogenic, and optogenetic approaches now provide causal evidence for dopamine’s role in these learning processes. Dopamine neurons encode fear and extinction-related information and convey the signal via activation of D1, D2, D3, and D4 receptor sites particularly in the amygdala, prefrontal cortex, and striatum in order to continuously form, consolidate, retrieve, and update fear and extinction memory in a dynamic and reciprocal manner. Based on the reviewed literature, we conclude that dopamine is crucial for the encoding of passive aversive conditioning and contributes in a way that is comparable to its role in encoding reward.

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Alpha-2 Adrenoreceptor Antagonist Yohimbine Potentiates Consolidation of Conditioned Fear

Cited by 10 publications

References 137 publications

Oscillatory and non‐oscillatory brain activity reflects fear expression in an immediate and delayed fear extinction task

Oscillatory and non‐oscillatory brain activity reflects fear expression in an immediate and delayed fear extinction task

65 years of research on dopamine's role in classical fear conditioning and extinction: A systematic review

50 Years of Research on Dopamine’s Role in Passive Aversive Conditioning and Extinction: A Systematic Review

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