Mechanism for Temporal Encoding in Fear Conditioning

Faulkner, Billie; Tieu, Kinh; Brown, Thomas H.

doi:10.1007/978-1-4757-9800-5_99

Cited by 9 publications

(13 citation statements)

References 12 publications

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“…This hypothesis was partly based on a simple model (Faulkner et al, 1997;Faulkner and Brown, 1999;Tieu et al, 1999) of fear conditioning in which timing emerges through chains of socalled "late-spiking" PR neurons McGann et al, 2001;Moyer et al, 2002;Moyer and Brown, 2007). These chains formed a suite of what might be termed "analog tap delay lines."…”

Section: Isi Encoding As Revealed In Behavior and Neurophysiologymentioning

confidence: 99%

Single-Unit Firing in Rat Perirhinal Cortex Caused by Fear Conditioning to Arbitrary and Ecological Stimuli

Furtak¹,

Allen²,

Brown³

2007

J. Neurosci.

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Pretraining lesions of rat perirhinal cortex (PR) severely impair pavlovian fear conditioning to a 22 kHz ultrasonic vocalization (USV) cue. However, PR lesions are without significant effect when the cue is a continuous tone at the same or a lower frequency. Here we examined fear-conditioning-produced changes in single-unit firing elicited in rat PR by a 22 kHz tone cue or a 22 kHz USV cue. Chronic recording electrodes were introduced from the lateral surface of the skull. Altogether, 200 well isolated units were studied in 28 rats. Overall, 73% of the recorded single units (145 of 200 units) evidenced statistically significant firing changes in response to the tone or USV conditional stimulus (CS) after it had been paired several times with an aversive unconditional stimulus (US). Interestingly, 33% of units (66 of 200 units) that were initially CS-unresponsive became CS-responsive after conditioning. After conditioning, there were two notable differences between single-unit responses elicited by the USV cue and those elicited by the tone cue. First, 11% of the units (14 of 123 units) recorded from the USV-conditioned group displayed a precisely timed increase in firing rate during the 260 ms interval in which the US had previously occurred. This US-timed response was unique to the USV-conditioned group. Second, the mean latency of cue-elicited firing was ϳ30 ms longer in the USV-conditioned group than in the tone-conditioned group. These cue-specific differences in acquired firing latencies and acquired firing patterns suggest that spectrotemporal properties of a CS can control the essential circuitry or neurophysiological mechanisms underlying fear conditioning.

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Section: Isi Encoding As Revealed In Behavior and Neurophysiologymentioning

confidence: 99%

Single-Unit Firing in Rat Perirhinal Cortex Caused by Fear Conditioning to Arbitrary and Ecological Stimuli

Furtak¹,

Allen²,

Brown³

2007

J. Neurosci.

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“…For paradigms in which the critical associative structures lack delay neurons, or in which the ISI span minutes to hours, it is thought that small populations of neurons may maintain a representation of a stimulus for extended periods of time. Network models based on this type of connectivity have been described for both the amygdala (Faulkner et al, 1997;Tieu et al, 1999) and the hippocampus (Kesner and Rolls, 2001).…”

Section: Criticisms Of Ltp As a Mechanism For Conditioningmentioning

confidence: 99%

Long‐term potentiation as a substrate for memory: Evidence from studies of amygdaloid plasticity and Pavlovian fear conditioning

Goosens¹,

Maren

2002

Hippocampus

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ABSTRACT:Recent reports have raised concerns about the ability of long-term potentiation (LTP) to account for associative learning and memory. In this paper, we review the many mechanistic similarities between one form of associative learning, Pavlovian fear conditioning, and amygdaloid LTP. We then address many of the criticisms levied against LTP within the framework of fear conditioning. We believe that many of the apparent discrepancies between LTP and behavior can be generally accounted for by a failure to appreciate that learned behavior is supported by multiple synapses in an extensive network of brain structures. We conclude that LTP remains a viable substrate for memory. Hippocampus 2002;12:592-599.

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“…In addition to receiving both CS-and US-related information, the amygdala sends projections, via its central nucleus (ACe), to motor regions that are directly responsible for organizing the production of many defensive CRs (Kapp et al, 1979;LeDoux et al, 1988;Canli and Brown, 1996;LeDoux, 2000). In one neurophysiological model (Faulkner et al, 1997;Tieu et al, 1999;Mc-Gann and Brown, 2000) that captures several aspects of current thinking (Fanselow and LeDoux, 1999;Blair et al, 2001), CS-US pairings create CS-CR pathways by inducing associative long-term potentiation (Levy and Steward, 1979; Barrionuevo and Brown, 1983; in the amygdala (for review, see Brown and Lindquist, 2003).…”

Section: Introductionmentioning

confidence: 99%

Central Amygdala Lesions Block Ultrasonic Vocalization and Freezing as Conditional But Not Unconditional Responses

Choi

Brown

2003

J. Neurosci.

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Bilateral amygdala (AM) lesions prevent the acquisition of fear-related conditional responses (CRs) in rats, a result that is most commonly concluded to reflect a learning or memory deficit. An alternative hypothesis is that AM-lesioned animals fail to acquire certain fear CRs simply because they cannot perform these behaviors. This performance-deficit hypothesis is usually invoked in regard to studies in which the CR is freezing, the most commonly measured behavior. Here we explore this interpretation by measuring two different behaviors [freezing and 22 kHz ultrasonic vocalization (USV)] elicited under three conditions (during context conditioning, during subsequent retention testing, and after ejaculation) in experimental rats [that received electrolytic lesions of the central nucleus of the amygdala (ACe)] and control animals (that received a sham operation). If ACe damage produces a discrete motor deficit that specifically renders the animal unable to remain immobile, then freezing should be blocked or impaired when elicited under all three conditions, whereas USV should be spared. Alternatively, if ACe damage selectively interferes with CR formation, maintenance, or expression, then both freezing and USV should be blocked or impaired when elicited as CRs during acquisition and retention testing but spared when evoked as unconditional responses (URs) to ejaculation. ACe damage blocked or severely impaired both freezing and USV elicited as CRs but had no effect on either behavior elicited as URs. We reject the motor-deficit hypothesis and discuss some viable alternatives.

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Mechanism for Temporal Encoding in Fear Conditioning

Cited by 9 publications

References 12 publications

Single-Unit Firing in Rat Perirhinal Cortex Caused by Fear Conditioning to Arbitrary and Ecological Stimuli

Single-Unit Firing in Rat Perirhinal Cortex Caused by Fear Conditioning to Arbitrary and Ecological Stimuli

Long‐term potentiation as a substrate for memory: Evidence from studies of amygdaloid plasticity and Pavlovian fear conditioning

Central Amygdala Lesions Block Ultrasonic Vocalization and Freezing as Conditional But Not Unconditional Responses

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