Spaced sessions of avoidance extinction reduce spontaneous recovery and promote infralimbic cortex activation

Tapias-Espinosa, Carles; Kádár, Elisabet; Segura-Torres, Pilar

doi:10.1016/j.bbr.2017.08.025

Cited by 5 publications

(9 citation statements)

References 35 publications

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“…A longer span of extinction has been shown to suppress spontaneous recovery (Tapias-Espinosa, Kádár, & Segura-Torres, 2018). However, as in most studies of recovery, recovery was probed at only one postextinction delay.…”

Section: The Time Scale Of Recoverymentioning

confidence: 99%

“…extinction sessions should also be varied (Rescorla, 2004). The span of extinction should also be varied (Tapias-Espinosa et al, 2018). Fortunately, this can be done in such a way as to also vary the intervals between the end of extinction and the probe for recovery: As we have just noted, probes for recovery are further extinction sessions.…”

Section: The Time Scale Of Recoverymentioning

confidence: 99%

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Number and time in acquisition, extinction and recovery

Gallistel

Papachristos

2019

J Exper Analysis Behavior

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We measured rate of acquisition, trials to extinction, cumulative responses in extinction, and the spontaneous recovery of anticipatory hopper poking in a Pavlovian protocol with mouse subjects. We varied by factors of 4 number of sessions, trials per session, intersession interval, and span of training (number of days over which training extended). We find that different variables affect each measure: Rate of acquisition [1/(trials to acquisition)] is faster when there are fewer trials per session. Terminal rate of responding is faster when there are more total training trials. Trials to extinction and amount of responding during extinction are unaffected by these variables. The number of training trials has no effect on recovery in a 4-trial probe session 21 days after extinction. However, recovery is greater when the span of training is greater, regardless of how many sessions there are within that span. Our results and those of others suggest that the numbers and durations and spacings of longer-duration "episodes" in a conditioning protocol (sessions and the spans in days of training and extinction) are important variables and that different variables affect different aspects of subjects' behavior. We discuss the theoretical and clinical implications of these and related findings and conclusions-for theories of conditioning and for neuroscience.The work reported here comprised a portion of a dissertation submitted to Rutgers University in partial fulfillment of the requirements for the doctoral degree. EBP designed and did the experiments, did the initial data analyses, and wrote a draft, with some advice from CRG. CRG did several further analyses and wrote the final draft.

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Section: The Time Scale Of Recoverymentioning

confidence: 99%

Section: The Time Scale Of Recoverymentioning

confidence: 99%

Number and time in acquisition, extinction and recovery

Gallistel

Papachristos

2019

J Exper Analysis Behavior

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“…Behavioral tests were performed at both prepubertal and adult stages. In animals with whole period exposure to AGIQ, spontaneous recovery was also examined after the facilitation of fear extinction learning because preventing fear recovery is important for therapy related to anxiety disorders such as PTSD 18 . In animals subjected to spontaneous recovery, the number of immunoreactive cells for synaptic plasticity-related IEGs and their regulator, as well as constitutive changes in gene expression, in the brain regions of interest were compared among the different exposure periods.…”

Section: Introductionmentioning

confidence: 99%

Continuous exposure to α-glycosyl isoquercitrin from developmental stages to adulthood is necessary for facilitating fear extinction learning in rats

et al. 2020

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We previously reported that exposure to α-glycosyl isoquercitrin (AGIQ) from the fetal stage to adulthood facilitated fear extinction learning in rats. The present study investigated the specific AGIQ exposure period sufficient for inducing this behavioral effect. Rats were dietarily exposed to 0.5% AGIQ from the postweaning stage to adulthood (PW-AGIQ), the fetal stage to postweaning stage (DEV-AGIQ), or the fetal stage to adulthood (WP-AGIQ). Fear memory, anxiety-like behavior, and object recognition memory were assessed during adulthood. Fear extinction learning was exclusively facilitated in the WP-AGIQ rats. Synaptic plasticity-related genes showed a similar pattern of constitutive expression changes in the hippocampal dentate gyrus and prelimbic medial prefrontal cortex (mPFC) between the DEV-AGIQ and WP-AGIQ rats. However, WP-AGIQ rats revealed more genes constitutively upregulated in the infralimbic mPFC and amygdala than DEV-AGIQ rats, as well as FOS-immunoreactive (+) neurons constitutively increased in the infralimbic cortex. Ninety minutes after the last fear extinction trial, many synaptic plasticity-related genes (encoding Ephs/Ephrins, glutamate receptors/transporters, and immediate-early gene proteins and their regulator, extracellular signal-regulated kinase 2 [ERK2]) were upregulated in the dentate gyrus and amygdala in WP-AGIQ rats. Additionally, WP-AGIQ rats exhibited increased phosphorylated ERK1/2 + neurons in both the prelimbic and infralimbic cortices. These results suggest that AGIQ exposure from the fetal stage to adulthood is necessary for facilitating fear extinction learning. Furthermore, constitutive and learning-dependent upregulation of synaptic plasticity-related genes/molecules may be differentially involved in brain regions that regulate fear memory. Thus, new learning-related neural circuits for facilitating fear extinction can be established in the mPFC.

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“…For example, increased neuronal activity in the amygdala is associated with both renewal and spontaneous recovery of extinguished fear (Hobin et al 2003 ; Herry et al 2008 ; Lin et al 2011 ; Huang et al 2013 ; Orsini et al 2013 ; Tapias-Espinosa et al 2018 ), as well as reinstatement of drug-seeking (Weiss et al 2000 ; Ciccocioppo et al 2001 ; Thiel et al 2010 ; Polston et al 2012 ; Hitora-Imamura et al 2015 ). Similarly, gamma oscillations in the amygdala during extinction have been shown to correlate with levels of spontaneous recovery during retrieval (Courtin et al 2014 ) and electrical stimulation of the amygdala can induce fear relapse (Kellett and Kokkinidis 2004 ).…”

Section: Introductionmentioning

confidence: 99%

“…Consistent with these reports, pharmacological inactivation of the IL results in a loss of extinguished fear and results in relapse (Laurent and Westbrook 2009 ; Hitora-Imamura et al 2015 ; Marek et al 2018a ), while pharmacological activation of the IL impairs relapse and promotes extinction retrieval (Marek et al 2018a )—provided that the spontaneous recovery of fear does not mask these effects (Do-Monte et al 2015 ; Marek et al 2018a ). That said, reduced spontaneous recovery (in a two-way active avoidance paradigm) is associated with greater IL activity (Tapias-Espinosa et al 2018 ). In drug-seeking paradigms, several studies demonstrate that lesion or inactivation of the IL results in the emergence (or even, enhancement) of drug reinstatement (for both cue- and drug prime-induced reinstatement), stress-induced drug relapse, and drug renewal across numerous drug types (Capriles et al 2003 ; McLaughlin and See 2003 ; McFarland et al 2004 ; Peters et al 2008b ).…”

Section: Introductionmentioning

confidence: 99%

Common neurocircuitry mediating drug and fear relapse in preclinical models

Goode

2018

Psychopharmacology

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Background Comorbidity of anxiety disorders, stressor- and trauma-related disorders, and substance use disorders is extremely common. Moreover, therapies that reduce pathological fear and anxiety on the one hand, and drug-seeking on the other, often prove short-lived and are susceptible to relapse. Considerable advances have been made in the study of the neurobiology of both aversive and appetitive extinction, and this work reveals shared neural circuits that contribute to both the suppression and relapse of conditioned responses associated with trauma or drug use. Objectives The goal of this review is to identify common neural circuits and mechanisms underlying relapse across domains of addiction biology and aversive learning in preclinical animal models. We focus primarily on neural circuits engaged during the expression of relapse. Key findings After extinction, brain circuits involving the medial prefrontal cortex and hippocampus come to regulate the expression of conditioned responses by the amygdala, bed nucleus of the stria terminalis, and nucleus accumbens. During relapse, hippocampal projections to the prefrontal cortex inhibit the retrieval of extinction memories resulting in a loss of inhibitory control over fear- and drug-associated conditional responding. Conclusions The overlapping brain systems for both fear and drug memories may explain the co-occurrence of fear and drug-seeking behaviors.

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Spaced sessions of avoidance extinction reduce spontaneous recovery and promote infralimbic cortex activation

Cited by 5 publications

References 35 publications

Number and time in acquisition, extinction and recovery

Number and time in acquisition, extinction and recovery

Continuous exposure to α-glycosyl isoquercitrin from developmental stages to adulthood is necessary for facilitating fear extinction learning in rats

Common neurocircuitry mediating drug and fear relapse in preclinical models

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