Mechanisms responsible for reduced contextual conditioning with massed unsignaled unconditional stimuli.

Fanselow, Michael S.; DeCola, Joseph P.; Young, Stacey L.

doi:10.1037/0097-7403.19.2.121

Cited by 93 publications

(89 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Third, perhaps freezing that occurs while an animal is in the black box during a context preference test results in the animal spending a relatively long time in the former shock context. If this happens, then the inference that the former shock context's excitatory strength is low would be incorrect (see also Fanselow, DeCola, & Young, 1993). With regard to Odling-Smee's finding that signaled-shock rats spent more time in the black box than unsignaled-shock rats, the latter two arguments actually imply that the signaled-shock rats were more fearful than the unsignaled-shock rats.…”

mentioning

confidence: 82%

The Effect of a Discrete Signal on Context Conditioning: Assessment by Preference and Freezing Tests

Maes

LoLordo

1996

Learning and Motivation

View full text Add to dashboard Cite

Four experiments with rats assessed conditioning to contextual cues after the delivery of footshocks that were either signaled by a discrete stimulus or unsignaled. Two different tests were used. The first was a context preference test in which subjects were allowed to move freely in a brightly lit, unconditionally aversive context and the former shock context. The second test consisted of scoring freezing behavior while the animals were confined to the former conditioning context. During context preference tests, signaled-shock animals spent more time in the conditioning context and/or entered that context more frequently than did unsignaled-shock subjects. However, freezing tests largely failed to detect a difference between groups. These results were discussed in terms of possible interactions between the formation of contextshock, signal-shock, and context-signal associations and their effect on performance in each of the two types of tests. ᭧

show abstract

mentioning

confidence: 82%

The Effect of a Discrete Signal on Context Conditioning: Assessment by Preference and Freezing Tests

Maes

LoLordo

1996

Learning and Motivation

View full text Add to dashboard Cite

show abstract

“…Glutamatergic modifications in excitatory neurotransmission-in particular, NMDAR and AMPAR-within the amygdala participate in different components of fear learning, including acquisition, expression, and extinction (Miserendino et al, 1990;Fanselow and Kim, 1994;Walker and Davis, 2002). Increased excitatory neurotransmission in the BLA could also enhance fear conditioning (Fanselow et al, 1993).…”

Section: Stress-enhanced Fear Expressionmentioning

confidence: 99%

“…By contrast, there were no differences in GluA2 or GluN1 levels in stressed or metyrapone-treated groups. Because facilitating glutamatergic activity at AMPAR enhances the rate of fear conditioning (Kim et al, 1993) and SEFL occurs predominantly by increasing the rate of fear conditioning (Fanselow et al, 1993), the long-term increase in GluA1 subunits is a highly plausible mechanism for the expression of SEFL.…”

Section: Metyrapone Prevents a Post-stressor Glua1 Increasementioning

confidence: 99%

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Perusini

Meyer

Long

et al. 2015

Neuropsychopharmacol

100

View full text Add to dashboard Cite

Fear promotes adaptive responses to threats. However, when the level of fear is not proportional to the level of threat, maladaptive fear-related behaviors characteristic of anxiety disorders result. Post-traumatic stress disorder develops in response to a traumatic event, and patients often show sensitized reactions to mild stressors associated with the trauma. Stress-enhanced fear learning (SEFL) is a rodent model of this sensitized responding, in which exposure to a 15-shock stressor nonassociatively enhances subsequent fear conditioning training with only a single trial. We examined the role of corticosterone (CORT) in SEFL. Administration of the CORT synthesis blocker metyrapone prior to the stressor, but not at time points after, attenuated SEFL. Moreover, CORT co-administered with metyrapone rescued SEFL. However, CORT alone without the stressor was not sufficient to produce SEFL. In these same animals, we then looked for correlates of SEFL in terms of changes in excitatory receptor expression. Western blot analysis of the basolateral amygdala (BLA) revealed an increase in the GluA1 AMPA receptor subunit that correlated with SEFL. Thus, CORT is permissive to trauma-induced changes in BLA function.

show abstract

“…A very general excitatory learning rule is that memory is stronger when training trials are "spaced" or distributed in time (Ebbinghaus 1885(Ebbinghaus /1913Carew and Kandel 1973;Fanselow and Tighe 1988;Fanselow et al 1993;Tully et al 1994;Kogan et al 1997;Freudenthal et al 1998;Barela 1999;Josselyn et al 2001). We recently reported that, in contrast to most acquisition learning, more short-and long-term extinction of cue fear followed temporally massed CS presentations than spaced presentations (Cain et al 2003).…”

mentioning

confidence: 99%

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Ponnusamy¹,

Nissim²,

Barad³

2005

Learn. Mem.

123

101

View full text Add to dashboard Cite

Extinction of conditioned fear in animals is the explicit model of behavior therapy for human anxiety disorders, including panic disorder, obsessive-compulsive disorder, and post-traumatic stress disorder. Based on previous data indicating that fear extinction in rats is blocked by quinpirole, an agonist of dopamine D2 receptors, we hypothesized that blockade of D2 receptors might facilitate extinction in mice, while agonists should block extinction, as they do in rats. One day after fear conditioning mice with three pairings of a white noise conditional stimulus (CS) with moderate footshock, we injected the D2 antagonist, sulpiride, the D2 agonist, quinpirole, or vehicle, just before repeated CS presentations to generate extinction. We assayed fear by measuring behavioral freezing during extinction presentations and then drug-free during CS presentations 1 d later. We found that sulpiride injections before extinction training facilitated extinction memory 24 h later, while quinpirole partially blocked extinction memory compared with vehicle-injected controls. Notably, sulpiride treatment yielded significant extinction after spaced CS presentations, which yield no extinction at all in vehicle-treated mice. These findings suggest that dopamine D2-mediated signaling contributes physiological inhibition of extinction, and that D2 antagonists may be useful adjuncts to behavior therapy of human anxiety disorders.Extinction of conditioned fear in mammals is an important preclinical model of behavior therapy, one of the most effective treatments for human anxiety disorders (Wolpe 1969;Craske 1999). Despite the efficacy of behavior therapy for human anxiety disorders, extinction-like treatments require repeated cue exposures and are vulnerable to reversal by a number of environmental factors. Thus, a deeper understanding of the synaptic mechanisms of extinction may permit the development of adjunctive medications to facilitate extinction learning, and perhaps, to make it more permanent.Anxiety disorders affect about 16% of the American population and include panic disorder (PD, 1.7%), obsessivecompulsive disorder (OCD, 2.3%), post-traumatic stress disorder (PTSD, 3.6%), generalized anxiety disorder (GAD, 2.8%), social phobia (2%), and simple phobias (8%) (US-Surgeon-General 1999). The rate of PTSD may well go higher in the context of current wars and terrorist acts. Given the enormous burden of such anxiety disorders, we are fortunate in having a reasonable animal model for the acquisition of some of these fears, that is, classically conditioned fear, and an even better animal model of an effective treatment method for those disorders, extinction of conditioned fear.Pavlovian, or classical, fear conditioning has long been an important model both of associative learning and of the etiology of human anxiety (Watson and Rayner 1920;Eysenck 1979;Wolpe and Rowan 1988). Temporal pairing of a neutral conditional stimulus (CS) with an aversive unconditional stimulus (US) generates robust conditional fear responses upon subseque...

show abstract

Mechanisms responsible for reduced contextual conditioning with massed unsignaled unconditional stimuli.

Cited by 93 publications

References 73 publications

The Effect of a Discrete Signal on Context Conditioning: Assessment by Preference and Freezing Tests

The Effect of a Discrete Signal on Context Conditioning: Assessment by Preference and Freezing Tests

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

Contact Info

Product

Resources

About