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PubMed2002

Role of NMDA receptors and MAP kinase in the amygdala in extinction of fear: clinical implications for exposure therapy.

Infusions into the amygdala (a brain area essential for excitatory fear conditioning) of either NMDA receptor antagonists or inhibitors of the NMDA receptor-linked mitogen activated protein kinase cascade block extinction learning. Conversely, the NMDA receptor agonist D-cycloserine facilitates extinction after either systemic administration or intra-amygdala infusion. Because therapeutic interventions based on extinction procedures are commonly used to treat fear disorders, and because D-cycloserine is a widely available and safe compound, D-cycloserine or similar agents might be usefully combined with traditional extinction-based approaches in the treatment of clinical fear.

Amygdala↗
PubMed2002

Common processes may contribute to extinction and habituation.

Psychologists routinely attribute the characteristics of conditioned behavior to complicated cognitive processes. For example, many of the characteristics of behavior undergoing extinction have been attributed to retrieval from memory. The authors argue that these characteristics may result from the simpler process of habituation. In particular, conditioned responding may decrease during extinction partially because habituation occurs to the stimuli that control responding when those stimuli are presented repeatedly or for a prolonged time (e.g., the experimental context, the conditioned stimulus in classical conditioning). This idea is parsimonious, has face validity, and evokes only processes that are well established by other evidence. In addition, behavior undergoing extinction shows 12 of the fundamental properties of behavior undergoing habituation. However, this model probably cannot provide a complete theory of extinction. It provides no obvious explanation for some of the other characteristics of extinguished behavior.

Animals↗
PubMed2001

Tests for inhibition after extinction of a conditioned stimulus in the flavour aversion procedure.

In four experiments, rats received flavour aversion conditioning followed by extinction. The flavour was then subjected to retardation and summation tests. Experiment 1 showed that reacquisition of an extinguished flavour aversion was retarded with respect to the performance shown by rats for whom the flavour was novel. No retardation was found, however, with respect to a control group that had been given non-reinforced pre-exposure to the flavour. Experiment 2 demonstrated that extinction showed the same sensitivity to the effects of a retention interval as did latent inhibition, consistent with the view that the retardation effect was a consequence of the occurrence of latent inhibition during extinction. An extinguished stimulus was also found to alleviate the response governed by a separately trained excitor in a summation test (Experiments 3 and 4), but the size of this effect did not exceed that produced by a control stimulus when the procedure used ensured an equivalent aversion to the test excitor in the two cases. These results challenge the proposal that extinction can turn a stimulus into a net inhibitor.

Animals↗
PubMed2006

Metapopulation extinction thresholds in rain forest remnants.

Although habitat fragmentation is a major threat to global biodiversity, the demographic mechanisms underlying species loss from tropical forest remnants remain largely unexplored. In particular, no studies at the landscape scale have quantified fragmentation's impacts on colonization, extinction, and local population growth simultaneously. In central Amazonia, we conducted a multiyear demographic census of 292 populations of two leaf-inhabiting (i.e., epiphyllous) bryophyte species transplanted from continuous forest into a network of 10 study sites ranging from 1, 10, and 100 to > 10,000 ha in size. All populations experienced significantly positive local growth (lambda > 1) and a nearly constant per-generational extinction probability (15%). However, experimental leaf patches in reserves of > or = 100 ha experienced nearly double (48%) the colonization probability observed in small reserves (27%), suggesting that the proximate cause of epiphyll species loss in small fragments (< or = 10 ha) is reduced colonization. Nonetheless, populations of small fragments exhibit rates of colonization above patch extinction, positive local growth, and low temporal variation, which are features that should theoretically reduce the probability of extinction. This result suggests that for habitat-tracking metapopulations subject to frequent and stochastic turnover events, including epiphylls, colonization/extinction ratios must be maintained well above unity to ensure metapopulation persistence.

Bryophyta↗
PubMed2000

Vision and touch through the looking glass in a case of crossmodal extinction.

When observing ourselves in a mirror, we see our body and adjacent objects (e.g. a comb or razor) projecting the image of distant objects. Are these recoded by the brain as reflecting stimuli in peripersonal space? To address this, we exploited the neuropsychological phenomenon of crossmodal, visual-tactile extinction, as shown by patient BV following right-hemisphere stroke. In such crossmodal extinction, a right visual event impairs the perception of a simultaneous left tactile event. In BV, the right visual stimulus (an LED flash) induced more extinction of touch on the contralesional left hand when presented near the ipsilesional right hand, than when distant from it. This agrees with previous data in patients and monkeys showing that visual-tactile interactions are strongest within peripersonal space. Crucially, we also found that an ipsilesional flash produced more extinction when observed as the distant mirror-reflection of an LED that lay close to the ipsilesional hand, rather than as a distant LED flash projecting an equivalent visual image directly. This suggests that in BV, seeing his own hand via a mirror activates a representation of peripersonal space around that hand, not of the extrapersonal space suggested by the distant visual image in the mirror. We discuss the possible neural basis of interpreting mirror reflections.

Aged↗
PubMed2001

Modulation of visual perception by eye gaze direction in patients with spatial neglect and extinction.

Parietal neurons have retinotopic receptive fields whose response is modulated by eye gaze signals. We examined the role of eye position and eye movement direction on visual extinction in three patients with parietal damage and left neglect, characterized by impaired perception of contralesional field stimuli despite intact visual cortex. Patients tracked a horizontally moving fixation point, while discriminating fine changes at the fixated point and detecting more salient targets flashed on either side of fixation. Eye position modulated extinction, with worse detection of left field targets during eccentric fixation towards the left. Direction of eye movement also modulated extinction, with worse detection of left targets during rightward scanning. These results demonstrate that extinction in contralesional field is influenced by extra-retinal factors related to eye position and eye movements, consistent with a convergence of these signals in parietal cortex.

Aged↗
PubMed2002

Effect of cocaine and sucrose withdrawal period on extinction behavior, cue-induced reinstatement, and protein levels of the dopamine transporter and tyrosine hydroxylase in limbic and cortical areas in rats.

Lever pressing during tests for resistance to extinction and cue-induced reinstatement of cocaine seeking in rats progressively increases over the first 2 months of withdrawal. In the present report, we investigated the generality of these findings in rats trained to self-administer sucrose, a non-drug reinforcer. We also examined whether the time-dependent changes in cocaine seeking correlate with the levels of the dopamine transporter (DAT) and tyrosine hydroxylase (TH) proteins in the amygdala, nucleus accumbens, prefrontal cortex and orbitofrontal cortex. Rats were trained to self-administer cocaine (0.5 mg/kg/i.v. infusion) or 10% sucrose (0.2 ml/infusion into a liquid drop receptacle) for 10 days (6 h/day); each reward delivery was paired with a tone+light cue. Tests for cocaine seeking were conducted following 1 or 15 reward-free days. On the test day, rats were initially tested for resistance to extinction during 6-7 60-min extinction sessions in the absence of the tone-light cue, until they reached the extinction criterion of less than 15 responses/60 min. Subsequently, rats were tested for cue-induced reinstatement during a 60-min session in which each lever press led to a contingent presentation of the tone-light cue. Lever pressing during the tests for reward seeking was significantly greater on day 15 than on day 1 following withdrawal from both cocaine and sucrose self-administration training. The levels of DAT, but not TH, were greater in the prefrontal cortex of cocaine-trained rats than in sucrose-trained rats on both days 1 and 15 of withdrawal. The levels of DAT and TH in other brain areas were not altered following withdrawal from cocaine or sucrose self-administration. These data suggest that the withdrawal can modulate reward seeking of both drug and non-drug reinforcers, and that alterations in DAT and TH levels in the brain regions examined do not mediate this effect.

Animals↗
PubMedDate not supplied

Extinction of conditioned taste aversion depends on functional protein synthesis but not on NMDA receptor activation in the ventromedial prefrontal cortex.

We investigated the role of the ventromedial prefrontal cortex (vmPFC) in extinction of conditioned taste aversion (CTA) by microinfusing a protein synthesis inhibitor or N-methyl-d-asparate (NMDA) receptors antagonist into the vmPFC immediately following a non-reinforced extinction session. We found that the protein synthesis blocker anisomycin, but not the NMDA receptors antagonist D,L-2-amino-5-phosphonovaleric acid, impaired CTA extinction in the vmPFC. Anisomycin microinfusion into vmPFC had no effect on CTA acquisition and by itself did not induce CTA. These findings show the necessary role functional protein synthesis is playing in the vmPFC during the learning of CTA extinction.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Conditioned fear extinction and reinstatement in a human fear-potentiated startle paradigm.

The purpose of this study was to analyze fear extinction and reinstatement in humans using fear-potentiated startle. Participants were fear conditioned using a simple discrimination procedure with colored lights as the conditioned stimuli (CSs) and an airblast to the throat as the unconditioned stimulus (US). Participants were extinguished 24 h after fear conditioning. Upon presentation of unsignaled USs after extinction, participants displayed significant fear reinstatement. In summary, these procedures produced robust fear-potentiated startle, significant CS+/CS- discrimination, within-session extinction, and significant reinstatement. This is the first demonstration of fear extinction and reinstatement in humans using startle measures.

Conditioning, Classical↗
PubMedDate not supplied

CB1 cannabinoid receptors modulate kinase and phosphatase activity during extinction of conditioned fear in mice.

Cannabinoid receptors type 1 (CB1) play a central role in both short-term and long-term extinction of auditory-cued fear memory. The molecular mechanisms underlying this function remain to be clarified. Several studies indicated extracellular signal-regulated kinases (ERKs), the phosphatidylinositol 3-kinase with its downstream effector AKT, and the phosphatase calcineurin as potential molecular substrates of extinction behavior. To test the involvement of these kinase and phosphatase activities in CB1-dependent extinction of conditioned fear behavior, conditioned CB1-deficient mice (CB1(-/-)) and wild-type littermates (CB1(+/+)) were sacrificed 30 min after recall of fear memory, and activation of ERKs, AKT, and calcineurin was examined by Western blot analysis in different brain regions. As compared with CB1(+/+), the nonreinforced tone presentation 24 h after auditory-cued fear conditioning led to lower levels of phosphorylated ERKs and/or calcineurin in the basolateral amygdala complex, ventromedial prefrontal cortex, dorsal hippocampus, and ventral hippocampus of CB1(-/-). In contrast, higher levels of phosphorylated p44 ERK and calcineurin were observed in the central nucleus of the amygdala of CB1(-/-). Phosphorylation of AKT was more pronounced in the basolateral amygdala complex and the dorsal hippocampus of CB1(-/-). We propose that the endogenous cannabinoid system modulates extinction of aversive memories, at least in part via regulation of the activity of kinases and phosphatases in a brain structure-dependent manner.

1-Phosphatidylinositol 4-Kinase↗
PubMedDate not supplied

Like extinction, latent inhibition of conditioned fear in mice is blocked by systemic inhibition of L-type voltage-gated calcium channels.

Having recently shown that extinction of conditioned fear depends on L-type voltage-gated calcium channels (LVGCCs), we have been seeking other protocols that require this unusual induction mechanism. We tested latent inhibition (LI) of fear, because LI resembles extinction except that cue exposures precede, rather than follow, cue-shock pairing. Systemic injections of two LVGCC inhibitors, nifedipine and diltiazem, before pre-exposure blocked LI completely with no evidence of state-dependent learning. The results indicate that extinction and LI share a common molecular requirement and may support the notion that LI, like extinction, is a form of inhibitory learning.

Analysis of Variance↗
PubMedDate not supplied

Factors regulating the effects of hippocampal inactivation on renewal of conditional fear after extinction.

After extinction of fear to a Pavlovian conditional stimulus (CS), contextual stimuli come to regulate the expression of fear to that CS. There is growing evidence that the context dependence of memory retrieval after extinction involves the hippocampus. In the present experiment, we examine whether hippocampal involvement in memory retrieval after extinction is related to the history of CS presentations in the context used for retrieval testing. We used infusions of muscimol to inactivate the dorsal hippocampus (DH) during postextinction retrieval tests that were conducted in contexts that differed in their history of CS presentations in that context. We found that DH inactivation affected the context-dependent retrieval of extinction (i.e., renewal) when testing occurred in a context that had no history of CS exposure, but not in a context that reliably predicted the CS. These results are discussed in terms of theories regarding the role of the hippocampus in contextual memory retrieval.

Animals↗
PubMedDate not supplied

Context and behavioral processes in extinction.

This article provides a selective review and integration of the behavioral literature on Pavlovian extinction. The first part reviews evidence that extinction does not destroy the original learning, but instead generates new learning that is especially context-dependent. The second part examines insights provided by research on several related behavioral phenomena (the interference paradigms, conditioned inhibition, and inhibition despite reinforcement). The final part examines four potential causes of extinction: the discrimination of a new reinforcement rate, generalization decrement, response inhibition, and violation of a reinforcer expectation. The data are consistent with behavioral models that emphasize the role of generalization decrement and expectation violation, but would be more so if those models were expanded to better accommodate the finding that extinction involves a context-modulated form of inhibitory learning.

Animals↗
PubMedDate not supplied

Emotional perseveration: an update on prefrontal-amygdala interactions in fear extinction.

Fear extinction refers to the ability to adapt as situations change by learning to suppress a previously learned fear. This process involves a gradual reduction in the capacity of a fear-conditioned stimulus to elicit fear by presenting the conditioned stimulus repeatedly on its own. Fear extinction is context-dependent and is generally considered to involve the establishment of inhibitory control of the prefrontal cortex over amygdala-based fear processes. In this paper, we review research progress on the neural basis of fear extinction with a focus on the role of the amygdala and the prefrontal cortex. We evaluate two competing hypotheses for how the medial prefrontal cortex inhibits amygdala output. In addition, we present new findings showing that lesions of the basal amygdala do not affect fear extinction. Based on this result, we propose an updated model for integrating hippocampal-based contextual information with prefrontal-amygdala circuitry.

Amygdala↗
PubMedDate not supplied

Anisomycin infused into the hippocampus fails to block "reconsolidation" but impairs extinction: the role of re-exposure duration.

Recent studies have reported new evidence consistent with the hypothesis that reactivating a memory by re-exposure to a training context destabilizes the memory and induces "reconsolidation." In the present experiments, rats' memory for inhibitory avoidance (IA) training was tested 6 h (Test 1), 2 d (Test 2), and 6 d (Test 3) after training. On Test 1 the rats were either removed from the shock compartment immediately after entry or retained in the shock context for 200 sec, and intrahippocampal infusions of the protein synthesis inhibitor anisomycin (75 microg/side) were administered immediately after the test. Anisomycin infusions administered after Test 1 impaired IA performance on Test 2 in animals given the brief re-exposure, but impaired extinction in animals exposed to the context for 200 sec. Rats with anisomycin-induced retention impairment on Test 2 demonstrated spontaneous recovery of retention performance on Test 3, whereas rats showing extinction on Test 2 showed further extinction on Test 3. The findings indicate that post-retrieval administration of anisomycin impairs subsequent retention performance only in the absence of extinction and that this impairment is temporary.

Animals↗
PubMed1999

Mass extinction in a dynamical system of evolution with variable dimension.

Introducing the effect of extinction into the so-called replicator equations in mathematical biology, we construct a general model where the diversity of species, i.e., the dimension of the equation, is a time-dependent variable. The system shows very different behavior from the original replicator equation, and leads to mass extinction when the system initially has high diversity. The present theory can serve as a mathematical foundation for the paleontologic theory for mass extinction. This extinction dynamics is a prototype of dynamical systems where the variable dimension is inevitable.

Animals↗
PubMed2004

Resistance to extinction is associated with impaired immediate early gene induction in medial prefrontal cortex and amygdala.

Extinction of classical fear conditioning is thought to involve activity-dependent potentiation of synaptic transmission in the medial prefrontal cortex (mPFC), resulting in the inhibition of amygdala-dependent fear responses. While many studies have addressed the mechanisms underlying extinction learning, it is unclear what determines whether extinction memory is consolidated or whether spontaneous recovery of the fear response occurs. Here we show, using a combined electrophysiological and immunocytochemical approach, that spontaneous recovery of conditioned fear in mice is associated with a prolonged expression of long-term depression of synaptic transmission in the mPFC and the failure of induction of the immediate-early genesc-Fos and zif268 in the mPFC and the basolateral nucleus of the amygdala. This suggests that coordinated activity-dependent changes in gene expression in the mPFC and the amygdala may underlie the formation of long-term fear extinction memory.

Amygdala↗
PubMed1986

Auditory extinction to nonverbal and verbal stimuli.

The so-called auditory extinction phenomenon in a verbal dichotic listening test was investigated in seven brain damaged patients from the qualitative standpoint. As the result, it became evident that the phenomenon could result from competition between verbal materials presented to both ears in at least two different levels of auditory processing i.e., sound perception and linguistic recognition. From the present study, we emphasize the following: If Bender's definition is followed, it is advisable to use the term extinction only for the phenomenon at the acoustic level. If the use of the term extinction for the phenomenon is to be continued at the linguistic level, the presence of auditory extinction and/or obscuration to nonverbal stimuli should be noted.

Acoustic Stimulation↗