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Results for “EXTINCTION LEARNING”

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At least 19 recordsLinked to original sources
PubMed2001

Consolidation of extinction learning involves transfer from NMDA-independent to NMDA-dependent memory.

Extinction of conditioned fear to a tone paired with foot shock is thought to involve the formation of new memory. In support of this, previous studies have shown that extinction of conditioned fear depends on NMDA receptor-mediated plasticity. To further investigate the role of NMDA receptors in extinction, we examined the effects of the NMDA antagonist d(-)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP) on the extinction of conditioned freezing and suppression of bar pressing (conditioned emotional response). Rats extinguished normally during a 90 min session in the presence of systemic CPP (10 mg/kg), but were unable to recall extinction learning 24 hr later. This suggests that an NMDA-independent form of plasticity supports short-term extinction memory, but NMDA receptors are required for consolidation processes leading to long-term extinction memory. Surprisingly, extinction learned in the presence of CPP was recalled normally when tested 48 hr after training, suggesting a delayed consolidation process that was able to improve memory in the absence of further training. Delayed consolidation involves NMDA receptors because CPP injected on the rest day between training and test prevented 48 hr recall of extinction learned under CPP. Control experiments showed that the effect of CPP on memory consolidation was not caused by state-dependent learning or reduced expression of freezing under CPP. These findings demonstrate that NMDA receptor activation is critical for consolidation of extinction learning and that this process can be initiated after training has taken place. We suggest that consolidation of extinction involves off-line relearning that reinforces extinction memory through NMDA-mediated plasticity, perhaps in prefrontal-amygdala circuits.

Amygdala↗
PubMed1998

Reward-produced memories regulate memory-discrimination learning, extinction, and other forms of discrimination learning.

In memory-discrimination learning, reward-produced memories are differentially rewarded such that they are the only stimuli available to support discriminative responding. Memory-discrimination learning was used in this study as follows: Reward-produced memories that were assumed to regulate instrumental performance in previously reported extinction and discrimination learning investigations were isolated and explicitly differentially reinforced (prior to a shift to extinction) in each of 4 runway investigations with rats. Results obtained here in the explicit discrimination learning stage and in the subsequent extinction stage were consistent with the prediction of the memory view and with prior discrimination learning and extinction findings. The memory interpretation was applied to memory-discrimination learning, to extinction, and to 2 other types of discrimination learning. It appears that a theory must use reward-produced memories to explain all 4 types of discrimination learning.

Animals↗
PubMedDate not supplied

Extinction learning before trauma and subsequent posttraumatic stress.

OBJECTIVE: Fear conditioning theories propose that persistent stress reactions may occur as a result of impaired extinction learning, and a poor capacity for extinction learning may predispose some individuals to posttraumatic stress disorder development. This study indexed the extent to which deficits in extinction learning before trauma exposure are a risk factor for persistent posttraumatic stress after trauma exposure. METHODS: Eighty-four firefighters were assessed during cadet training (before trauma) and 70 were reassessed within 24 months of commencing active firefighting duties (after trauma). Measures of posttraumatic stress were used before and after trauma exposure. In addition, skin conductance and corrugator electromyogram (EMG) responses were obtained during fear conditioning and extinction paradigms before trauma exposure. RESULTS: Reduced extinction of an aversively conditioned corrugator EMG response pretrauma predicted 31% of the variance in posttraumatic stress severity. CONCLUSIONS: This result provides preliminary support for reduced extinction of a conditioned emotional response as a vulnerability factor for posttraumatic stress.

Adult↗
PubMed2004

Human orbitofrontal cortex mediates extinction learning while accessing conditioned representations of value.

In extinction, an animal learns that a previously conditioned stimulus (CS+) no longer predicts delivery of a salient reinforcer (unconditioned stimulus, UCS). Rodent studies indicate that extinction relies on amygdala-prefrontal interactions and involves formation of memories that inhibit, without actually erasing, the original conditioning trace. Whether extinction learning in humans follows similar neurobiological principles is unknown. We used functional magnetic resonance imaging to measure human brain activity evoked during olfactory aversive conditioning and extinction learning. Neural responses in orbitofrontal cortex and amygdala were preferentially enhanced during extinction, suggesting potential cross-species preservation of learning mechanisms that oppose conditioning. Moreover, by manipulating UCS aversiveness via reinforcer inflation, we showed that a CS+ retains access to representations of UCS value in distinct regions of ventral prefrontal cortex, even as extinction proceeds.

Adolescent↗
PubMed2006

Extinction learning, reconsolidation and the internal reinforcement hypothesis.

Retrieving a consolidated memory--by exposing an animal to the learned stimulus but not to the associated reinforcement--leads to two opposing processes: one that weakens the old memory as a result of extinction learning, and another that strengthens the old, already-consolidated memory as a result of some less well-understood form of learning. This latter process of memory strengthening is often referred to as "reconsolidation", since protein synthesis can inhibit this form of memory formation. Although the behavioral phenomena of the two antagonizing forms of learning are well documented, the mechanisms behind the corresponding processes of memory formation are still quite controversial. Referring to results of extinction/reconsolidation experiments in honeybees, we argue that two opposing learning processes--with their respective consolidation phases and memories--are initiated by retrieval trials: extinction learning and reminder learning, the latter leading to the phenomenon of spontaneous recovery from extinction, a process that can be blocked with protein synthesis inhibition.

Animals↗
PubMed2007

Facilitation of extinction learning for contextual fear memory by PEPA: a potentiator of AMPA receptors.

Contextual fear memory is attenuated by the re-exposure of mice to the context without aversive stimulus. This phenomenon is called extinction. Here, we report that a potentiator of AMPA receptors, 4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluorophenoxyacetamide (PEPA), potently facilitates extinction learning in mice. C57BL/6J mice were exposed to novel context and stimulated by electrical footshock. After 24 h (extinction training) and 72 h (extinction test), the mice were repeatedly exposed to the context without footshock and the duration of their freezing response was measured. The duration of freezing response in the extinction test was consistently shorter than the value in extinction training. Intraperitoneal injection of PEPA 15 min before extinction training remarkably reduced the duration of freezing responses during the extinction training and test, compared with the vehicle-injected control mice. This action of PEPA on extinction was dose-dependent and inhibited by NBQX (1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide), an AMPA receptor antagonist. PEPA had no effect on acquisition and consolidation of fear memory itself. Electrophysiological studies suggested that PEPA activates the neural network much more potently in the medial prefrontal cortex (mPFC) than in the basolateral amygdala and hippocampal CA1 field. Quantitative PCR studies suggested the pronounced expression of PEPA-preferring AMPA receptor subunits (GluR3 and GluR4) and a splice variant (flop) in the mPFC. An intra-mPFC injection of PEPA facilitated the extinction much more potently than an intra-amygdala injection of PEPA did. These results suggest that PEPA facilitates extinction learning through AMPA receptor activation mainly in the mPFC.

Adaptation, Physiological↗
PubMed2005

A requirement for memory retrieval during and after long-term extinction learning.

Current learning theories are based on the idea that learning is driven by the difference between expectations and experience (the delta rule). In extinction, one learns that certain expectations no longer apply. Here, we test the potential validity of the delta rule by manipulating memory retrieval (and thus expectations) during extinction learning. Adrenergic signaling is critical for the time-limited retrieval (but not acquisition or consolidation) of contextual fear. Using genetic and pharmacologic approaches to manipulate adrenergic signaling, we find that long-term extinction requires memory retrieval but not conditioned responding. Identical manipulations of the adrenergic system that do not affect memory retrieval do not alter extinction. The results provide substantial support for the delta rule of learning theory. In addition, the timing over which extinction is sensitive to adrenergic manipulation suggests a model whereby memory retrieval occurs during, and several hours after, extinction learning to consolidate long-term extinction memory.

Animals↗
PubMed2007

The disruptive effects of the CB1 receptor antagonist rimonabant on extinction learning in mice are task-specific.

RATIONALE: Disruption of CB(1) receptor signaling through the use of CB(1) (-/-) mice or the CB(1) receptor antagonist rimonabant (SR141716) has been demonstrated to impair extinction of learned responses in conditioned fear and Morris water maze tasks. In contrast, CB(1) (-/-) mice exhibited normal extinction rates in an appetitively motivated operant conditioning task. OBJECTIVES: The purpose of this study was to test whether rimonabant would differentially disrupt extinction learning between fear-motivated and food-motivated tasks. MATERIALS AND METHODS: Separate groups of C57BL/6J mice were trained in two aversively motivated tasks, conditioned freezing and passive avoidance, and an appetitively motivated operant conditioning task at a fixed ratio (FR-5) schedule of food reinforcement. After acquisition, the respective reinforcers in each task were withheld, and an intraperitoneal injection of vehicle or rimonabant was given 30 min before each extinction session. RESULTS: Rimonabant (3 mg/kg) treatment significantly disrupted extinction in both the conditioned freezing and passive avoidance tasks but failed to affect extinction rates in the operant conditioning task, whether using daily or weekly extinction sessions. Interestingly, rimonabant (3 mg/kg) prevented the significant increases in lever pressing (i.e., extinction burst) that occurred during the first extinction session of the operant conditioning task. CONCLUSIONS: These results support the hypothesis that the CB(1) receptor plays a vital role in the extinction of aversive memories but is not essential for extinction of learned responses in appetitively motivated tasks.

Animals↗
PubMed2004

Extinction learning in humans: role of the amygdala and vmPFC.

Understanding how fears are acquired is an important step in translating basic research to the treatment of fear-related disorders. However, understanding how learned fears are diminished may be even more valuable. We explored the neural mechanisms of fear extinction in humans. Studies of extinction in nonhuman animals have focused on two interconnected brain regions: the amygdala and the ventral medial prefrontal cortex (vmPFC). Consistent with animal models suggesting that the amygdala is important for both the acquisition and extinction of conditioned fear, amygdala activation was correlated across subjects with the conditioned response in both acquisition and early extinction. Activation in the vmPFC (subgenual anterior cingulate) was primarily linked to the expression of fear learning during a delayed test of extinction, as might have been expected from studies demonstrating this region is critical for the retention of extinction. These results provide evidence that the mechanisms of extinction learning may be preserved across species.

Adolescent↗
PubMed2001

Memory extinction, learning anew, and learning the new: dissociations in the molecular machinery of learning in cortex.

The rat insular cortex (IC) subserves the memory of conditioned taste aversion (CTA), in which a taste is associated with malaise. When the conditioned taste is unfamiliar, formation of long-term CTA memory depends on muscarinic and beta-adrenergic receptors, mitogen-activated protein kinase (MAPK), and protein synthesis. We show that extinction of CTA memory is also dependent on protein synthesis and beta-adrenergic receptors in the IC, but independent of muscarinic receptors and MAPK. This resembles the molecular signature of the formation of long-term memory of CTA to a familiar taste. Thus, memory extinction shares molecular mechanisms with learning, but the mechanisms of learning anew differ from those of learning the new.

Adrenergic beta-Antagonists↗
PubMed2006

Relationship of delay aversion and response inhibition to extinction learning, aggression, and sexual behaviour.

Impulsivity is an important symptom of many psychiatric disorders, and can be divided into two subtypes: response inhibition deficits and delay aversion. In the present study, we investigated the relationship between delay aversion and response inhibition, both to each other and to locomotion, extinction of conditioned responses, sexual behaviour, and aggressive behaviour. To that end, we quantified the behaviour of 24 rats in several tests. To measure response inhibition, rats were trained in a stop-signal task. In this operant task, rats were rewarded food if they inhibited execution of a response after presentation of an audible stop-signal. Delay aversion was measured in an operant task in which rats made a choice between a small, immediately available reward and a large reward available after a delay. The results showed that delay aversion and response inhibition were independent. Responses during extinction and various measures of aggressive behaviour were positively correlated to delay aversion. The speed of go-trials in the stop-task was correlated to non-aggressive behaviour. We conclude that the role of response inhibition in various behaviours is small, but delay aversion in particular contributes to several other behaviours, such as aggressive behaviour and extinction.

Aggression↗
PubMed2005

D-cycloserine facilitates extinction of learned fear: effects on reacquisition and generalized extinction.

BACKGROUND: d-cycloserine (DCS) facilitates extinction of learned fear. The aim of this study was to examine whether DCS 1) affects reacquisition of fear (Experiment 1) and 2) produces generalized extinction of fear (Experiment 2). METHODS: Following fear conditioning, where a light or a tone conditioned stimulus (CS) was paired with a white-noise burst unconditioned stimulus (US), rats received nonreinforced exposure to one CS (i.e., extinction training). Fear was assessed by measuring CS-elicited freezing, a species-specific defense response. RESULTS: Rats given DCS exhibited facilitated extinction of fear but were able to reacquire fear of that CS in a similar manner as saline-treated control animals (Experiment 1). Furthermore, DCS-treated rats exhibited generalized extinction (i.e., they were less fearful of a non-extinguished CS) in comparison to controls (Experiment 2). CONCLUSIONS: DCS facilitates extinction of learned fear to the extinguished CS, but also appears to reduce fear of a nonextinguished CS. These findings suggest that this drug may have substantial clinical value in the treatment of anxiety disorders.

Animals↗
PubMed1997

[Effects of item-arrangement on serial pattern learning and extinction in rats].

Two experiments using rats as subjects examined effects of item-arrangement on acquisition and extinction in serial learning. In Experiment 1, Group A received series of 16-0-16 and 1-0-1 food pellets in a runway, while Group D received 1-0-16 and 16-0-1 series. Both groups manifested a remote anticipation of the third item on Run 2, and current anticipation of the third item on Run 3. In extinction phase, resistance was greater in Group D than Group A. These results indicate that the first item signaled not only the second item, but also the third item. In Experiment 2, two of the four groups were trained with either of the following monotonic series: 0-16-0-8-0-4- 0-2-0-1 (Group M16) or 0-1-0-2-0-4-0-8-0-16 (Group M1), while the other two groups were given one of the following nonmonotonic series: 0-16-0-2-0-4-0-8-0-1 (Group NM16) or 0-1-0-8-0-4-0-2-0-16 (Group NM1). In extinction phase, Group M16 showed the least resistance. These results are discussed mainly on the basis of remote association view and structural complexity theory of serial learning.

Animals↗
PubMed2006

The role of the amygdala in the extinction of conditioned fear.

The amygdala has long been known to play a central role in the acquisition and expression of fear. More recently, convergent evidence has implicated the amygdala in the extinction of fear as well. In rodents, some of this evidence comes from the infusion of drugs directly into the amygdala and, in particular, into the basolateral complex of the amygdala, during or after extinction learning. In vivo electrophysiology has identified cellular correlates of extinction learning and memory in the lateral nucleus of that structure. Human imaging experiments also indicate that amygdaloid activity correlates with extinction training. In addition, some studies have directly identified changes in molecular constituents of the basolateral amygdala. Together these experiments strongly indicate that the basolateral amygdala plays a crucial role in extinction learning. Interpreted in the light of these findings, several recent in vitro electrophysiology studies in amygdala-containing brain slices are suggestive of potential synaptic and circuit bases of extinction learning.

Amygdala↗