How Fast is Fear?

The minimum latency of potentiated startle after delay and trace fear conditioning was investigated. Delay conditioning is hypothesized to be mediated by automatic processes, whereas trace conditioning is hypothesized to involve controlled cognitive processes. In a group receiving delay conditioning, a tone conditioned stimulus (CS) signaled an electric shock unconditioned stimulus (US) presented 1,000 ms after CS onset. In a group receiving trace conditioning, a 200 ms tone CS was followed by an 800 ms gap prior to US presentation. Two control groups received unpaired CS/US presentations. It was hypothesized that fear-potentiated startle should be observed at shorter time intervals after CS onset in the group receiving delay conditioning compared to the group receiving trace conditioning. The results showed increased startle at 100 and 150 ms after CS onset in the group receiving delay conditioning compared to the unpaired group. In the group receiving trace conditioning, increased startle was observed at 1,500 ms after CS onset compared to the unpaired group. This supports the idea that conditioned fear after delay conditioning may be due to automatic processes, whereas trace conditioning is dependent on controlled processes.

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Adaptively Timed Learning

Conscious Mind, Resonant Brain ◽

10.1093/oso/9780190070557.003.0015 ◽

2021 ◽

pp. 539-571

Author(s):

Stephen Grossberg

Keyword(s):

Memory Consolidation ◽

Social Cognitive ◽

Fragile X ◽

Trace Conditioning ◽

Incentive Motivation ◽

Time Intervals ◽

Delay Conditioning ◽

Adaptive Timing ◽

Causal Event ◽

Dopamine Modulation

This chapter explains how humans and other animals learn to adaptively time their behaviors to match external environmental constraints. It hereby explains how nerve cells learn to bridge big time intervals of hundreds of milliseconds or even several seconds, and thereby associate events that are separated in time. This is accomplished by a spectrum of cells that each respond in overlapping time intervals and whose population response can bridge intervals much larger than any individual cell can. Such spectral timing occurs in circuits that include the lateral entorhinal cortex and hippocampal cortex. Trace conditioning, in which CS and US are separated in time, requires the hippocampus, whereas delay conditioning, in which they overlap, does not. The Weber law observed in trace conditioning naturally emerges from spectral timing dynamics, as later confirmed by data about hippocampal time cells. Hippocampal adaptive timing enables a cognitive-emotional resonance to be sustained long enough to become conscious of its feeling and its causal event, and to support BDNF-modulated memory consolidation. Spectral timing supports balanced exploratory and consummatory behaviors whereby restless exploration for immediate gratification is replaced by adaptively timed consummation. During expected disconfirmations of reward, orienting responses are inhibited until an adaptively timed response is released. Hippocampally-mediated incentive motivation supports timed responding via the cerebellum. mGluR regulates adaptive timing in hippocampus, cerebellum, and basal ganglia. Breakdowns of mGluR and dopamine modulation cause symptoms of autism and Fragile X syndrome. Inter-personal circular reactions enable social cognitive capabilities, including joint attention and imitation learning, to develop.

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Muscimol-induced inactivation of the anterior cingulate cortex does not impair trace fear conditioning in the rat

Journal of Psychopharmacology ◽

10.1177/0269881120965914 ◽

2020 ◽

Vol 34 (12) ◽

pp. 1457-1460

Author(s):

Marie A Pezze ◽

Hayley J Marshall ◽

Helen J Cassaday

Keyword(s):

Anterior Cingulate Cortex ◽

Fear Conditioning ◽

Trace Conditioning ◽

Cingulate Cortex ◽

Anterior Cingulate ◽

Trace Interval ◽

Noise Stimulus ◽

Trace Fear Conditioning ◽

Trace Fear

Previous studies suggest that trace conditioning depends on the anterior cingulate cortex (ACC). To examine the role of ACC in trace fear conditioning further, 48 rats were surgically prepared for infusion with saline or 62.5 or 125 µg/side muscimol to inactivate ACC reversibly prior to conditioning. A noise stimulus was followed by a 1 mA footshock, with or without a 10-second trace interval between these events in a conditioned suppression procedure. The trace-conditioned groups (10 seconds) showed less test suppression than the control-conditioned groups (0 seconds). Counter to prediction, there was no effect of muscimol infusion on suppression to the noise stimulus in the 10-second trace groups.

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Measuring human trace fear conditioning

10.31234/osf.io/x8bzu ◽

2021 ◽

Author(s):

Jelena Wehrli ◽

Yanfang Xia ◽

Samuel Gerster ◽

Dominik R Bach

Keyword(s):

Fear Conditioning ◽

Skin Conductance ◽

Pupil Size ◽

Recall Test ◽

Trace Fear Conditioning ◽

Skin Conductance Responses ◽

Clinical Scenarios ◽

Fear Potentiated Startle ◽

Conditioned Responses ◽

Trace Fear

Trace fear conditioning is an important research paradigm to model aversive learning in biological or clinical scenarios, where predictors (conditioned stimuli, CS) and aversive outcomes (unconditioned stimuli, US) are separated in time. The optimal measurement of human trace fear conditioning, and in particular of memory recall after consolidation, is currently unclear. We conducted two identical experiments with a 15-s trace interval and a recall test 1 week after acquisition, while recording several psychophysiological observables. We explored learning and memory measures in the first experiment and confirmed the most sensitive measures in the second experiment. Retrodictive validity was used as a metric to estimate measurement error. We found that in the recall test without reinforcement, only fear-potentiated startle but not skin conductance, pupil size, heart period, or respiration amplitude, differentiated CS+ and CS-. During acquisition without startle probes, only skin conductance responses and pupil size responses but none of the other measures differentiated CS+ and CS-. We establish the optimal way of quantifying these conditioned responses. As a side finding, there was no evidence for extinction of fear-potentiated startle over 30 trials without reinforcement. These results may be useful to inform future substantive research using human trace fear conditioning protocols.

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Faculty Opinions recommendation of A role for prefrontal cortex in memory storage for trace fear conditioning.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1017350.202586 ◽

2004 ◽

Author(s):

Karl-Peter Giese

Keyword(s):

Prefrontal Cortex ◽

Fear Conditioning ◽

Memory Storage ◽

Trace Fear Conditioning ◽

Trace Fear

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Trace Fear Conditioning Detects Hypoxic-Ischemic Brain Injury in Neonatal Mice

Developmental Neuroscience ◽

10.1159/000329710 ◽

2011 ◽

Vol 33 (3-4) ◽

pp. 222-230 ◽

Cited By ~ 6

Author(s):

Katarina Järlestedt ◽

Alison L. Atkins ◽

Henrik Hagberg ◽

Marcela Pekna ◽

Carina Mallard

Keyword(s):

Brain Injury ◽

Fear Conditioning ◽

Ischemic Brain Injury ◽

Ischemic Brain ◽

Neonatal Mice ◽

Trace Fear Conditioning ◽

Hypoxic Ischemic Brain Injury ◽

Trace Fear

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Facilitation of Conditioned Fear Extinction by Systemic Administration or Intra-Amygdala Infusions of d-Cycloserine as Assessed with Fear-Potentiated Startle in Rats

Journal of Neuroscience ◽

10.1523/jneurosci.22-06-02343.2002 ◽

2002 ◽

Vol 22 (6) ◽

pp. 2343-2351 ◽

Cited By ~ 542

Author(s):

David L. Walker ◽

Kerry J. Ressler ◽

Kwok-Tung Lu ◽

Michael Davis

Keyword(s):

Conditioned Fear ◽

Fear Extinction ◽

Systemic Administration ◽

Fear Potentiated Startle

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Fear potentiated startle at short intervals following conditioned stimulus onset during delay but not trace conditioning

Psychophysiology ◽

10.1111/j.1469-8986.2009.00809.x ◽

2009 ◽

Vol 46 (4) ◽

pp. 880-888 ◽

Cited By ~ 9

Author(s):

Ole Åsli ◽

Silje Kulvedrøsten ◽

Line E. Solbakken ◽

Magne Arve Flaten

Keyword(s):

Conditioned Stimulus ◽

Trace Conditioning ◽

Stimulus Onset ◽

Short Intervals ◽

Fear Potentiated Startle

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The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the mouse lateral amygdala via cholecystokinin

eLife ◽

10.7554/elife.69333 ◽

2021 ◽

Vol 10 ◽

Author(s):

Hemin Feng ◽

Junfeng Su ◽

Wei Fang ◽

Xi Chen ◽

Jufang He

Keyword(s):

Entorhinal Cortex ◽

Neural Plasticity ◽

Long Term Potentiation ◽

Fear Memory ◽

Memory Formation ◽

Loss Of Function ◽

Trace Fear Conditioning ◽

Term Potentiation ◽

Auditory Response ◽

Trace Fear

Although fear memory formation is essential for survival and fear-related mental disorders, the neural circuitry and mechanism are incompletely understood. Here, we utilized trace fear conditioning to study the formation of trace fear memory in mice. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. We adopted both loss-of-function and gain-of-function experiments to demonstrate that release of the cholecystokinin (CCK) from the EC is required for trace fear memory formation. We discovered that CCK-positive neurons project from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of the auditory response in the LA and formation of trace fear memory. In summary, high-frequency activation of EC neurons triggers the release of CCK in their projection terminals in the LA, potentiating auditory response in LA neurons. The neural plasticity in the LA leads to trace fear memory formation.

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