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PubMed2004

Dissociation between taste and tactile extinction on the tongue after right brain damage.

In patients with right brain damage (RBD) or left brain damage (LBD) and healthy subjects, tactile and three basic gustatory stimuli (sour, salty, bitter) were applied to the left or right hemitongues or to both hemitongues simultaneously. Tactile stimuli were detected and localized by verbal report, whereas gustatory stimuli were identified by pointing to the corresponding name on cards bearing the names of the three tastes. In the tactile test, 9 of 18 RBD patients showed extinction of left hemitongue stimuli, whereas the remaining RBD patients, 9 LBD patients and 14 healthy subjects detected virtually all stimuli in all conditions. In the gustatory test, healthy subjects outperformed the two brain damaged groups which nevertheless responded well above chance and did not differ from one another. Unexpectedly, the nine RBD patients with left hemitongue tactile extinction showed no gustatory extinction, since performance did not differ significantly between the two hemitongues on both unilateral and bilateral stimulations. To account for these findings, some evidence suggests that the tongue representation is bilateral in both modalities, but predominantly ipsilateral in the gustatory modality and predominantly contralateral in the tactile modality. The RBD patients with left hemitongue tactile extinction were those with more marked symptoms of left-sided extinction in the visual and auditory modalities, making it likely that their brain damage was also responsible for left lingual tactile extinction. The absence of left gustatory extinction in those patients can be attributed to the predominant channelling of left hemitongue taste inputs into the intact left hemisphere.

Aged↗
PubMed2005

Chronic stress impairs recall of extinction of conditioned fear.

Chronic restraint stress produces retraction of apical dendrites of pyramidal neurons in medial prefrontal cortex. To begin to examine the functional significance of this dendritic reorganization, we assessed the effects of chronic restraint stress on a prefrontally mediated behavior, extinction of conditioned fear. After bar press training to obtain a baseline of activity against which to measure freezing, rats were either unstressed or stressed via placement in a plastic restrainer (3 h/day for 1 week). After an additional day of bar press training, rats underwent fear conditioning and extinction. Rats received five habituation trials to a 30-s tone (4.5 kHz, 80 db) followed by seven pairings of tone and footshock (500 ms, 0.5 mA). One hour later, rats received tone-alone extinction trials to criterion. The next day, rats received 15 additional extinction trials. Percent freezing was assessed during all phases of training. Stress did not significantly affect unconditioned responding to tone, acquisition of conditioned fear, or initial extinction, but significantly increased freezing on extinction day 2. Thus, consistent with the regressive dendritic changes seen in medial prefrontal cortex, one week of restraint stress specifically impaired recall of extinction, a pattern of deficits typical of animals with impaired medial prefrontal function.

Animals↗
PubMed2000

Protection from extinction in human fear conditioning.

Two experiments examined the ability of an added stimulus to interfere with extinction of a target excitatory fear stimulus (a predictor of shock) in human autonomic conditioning. Both experiments demonstrated disruption of extinction when the added stimulus was inhibitory (a predictor of no shock, or safety signal). Subjects showed a return of fear when the target stimulus was tested alone, on both self-reported shock expectancy and skin conductance measures. The second experiment also demonstrated disruption of extinction when the added stimulus was excitatory. This results suggests that protection from extinction may occur even when the added stimulus is not inhibitory. Additional factors that may contribute to protection from extinction include context-specificity, occasion-setting and external inhibition. The results highlight the role that concurrent stimuli play in extinction, and emphasise the need to keep concurrent stimuli as similar as possible to the desired transfer context in practical applications of extinction such as exposure therapy for anxiety.

Adolescent↗
PubMed1984

The effects of quipazine and fluoxetine on extinction of a previously-reinforced operant response in rats.

Previous studies have shown that treatments that reduce serotonergic neurotransmission lead to enhanced responding during extinction. To evaluate the generality of this effect, the present study examined the effects of the serotonin agonists, quipazine and fluoxetine on responding in extinction. In Experiment 1, 72 rats were trained to lever press on a continuous reinforcement schedule for 5 30-min sessions. Four sessions of extinction followed; 30-min prior to each, 3 groups (n = 16) received quipazine (0, 1.0, 5.0 mg/kg) and 3 groups (n = 8) received fluoxetine (0, 1.0, 5.0 mg/kg). The 5.0 mg/kg dose of quipazine resulted in a significant reduction in responding on day 1; the lower dose of quipazine and both doses of fluoxetine were without significant effect. In Experiment 2, 3 similarly trained groups (n = 8) received either saline or quipazine (5.0 mg/kg) prior to each extinction session; additionally, one quipazine group was injected twice with the 5.0 mg/kg dose in its home cage several days before the beginning of extinction. The results of the drug-naive quipazine group replicated those of that group from Experiment 1 whereas the drug-experienced group showed no significant effect of quipazine in extinction. The results suggested that prior drug experience could modify the effects of quipazine on behaviour. Apart from this drug novelty effect the lack of significant effect of either quipazine or fluoxetine suggested that the effects of manipulations believed to increase and decrease serotonin functioning on responding in extinction may not be symmetrical. These results may be understood with reference to the hypothesis that serotonin plays a role in tuning out or reducing responsiveness to nonreinforced or irrelevant stimuli.

Animals↗
PubMed1999

Presentation of an ethanol-paired stimulus complex alters response patterns during extinction.

It has been hypothesized that environmental stimuli previously paired with ethanol consumption play a role in excessive ethanol intake. This study examined the ability of orally self-administered ethanol to establish a tone-light stimulus complex as a conditioned reinforcer (CSR). Male Long-Evans rats were trained to orally self-administer 10% ethanol (10E) using the sucrose-substitution procedure. During training, a tone-light stimulus complex was paired with ethanol presentation in a stimulus complex paired (SC-paired) group but not in a control group. Responding during extinction in the presence and absence of the stimulus complex was then examined. Following the initiation of ethanol self-administration, 10E maintained greater responding in the SC-paired group compared to the control group. When the stimulus complex was presented contingent on responding during extinction, the rate of extinction was slightly attenuated in the SC-paired group but not in the control group. The altered rate of extinction in the SC-paired group was characterized by: 1) a slight decrease in total session responding over successive days of extinction and 2) a transient attenuation of extinction burst response rate during the first extinction session. These data suggest the stimulus complex could function as a weak CS(R), but overall its ability to maintain lever pressing was minimal.

Animals↗
PubMed2004

Response disinhibition may be explained as an extinction deficit in an animal model of attention-deficit/hyperactivity disorder (ADHD).

Attention-deficit/hyperactivity disorder (ADHD) is a disorder affecting between 2 and 12% of grade-school children disturbing social, academic, and occupational functioning. Problems related to social adjustment and functioning and/or psychiatric problems will exist in 50-70% of adolescents and young adults diagnosed with ADHD as children. It has been suggested that altered reinforcement and extinction processes may cause the symptoms of ADHD. The present study investigated extinction processes in spontaneously hypertensive rats (SHR), possibly the best-validated animal model of ADHD. Extinction was tested after either a variable interval (VI) or a fixed interval (FI) schedule of reinforcement with and without the presence of a conditioned reinforcer (light in the water cubicle). The results indicate a slower extinction process in the SHR compared to the normal controls, especially during the initial transition from scheduled reinforcement to extinction. Also, more responses were retained in the SHR during the later part of extinction. The extinction deficit in the SHR may be linked to reinforcer unpredictability and the presence of conditioned reinforcers, and may explain response disinhibition seen in children with ADHD.

Analysis of Variance↗
PubMed2002

Vasopressin content in select brain regions during extinction of a conditioned taste aversion.

Previous studies have shown that low levels of vasopressin during extinction of conditioned taste avoidance are associated with a faster extinction, that fluid deprivation differentially alters vasopressin levels in various neural areas, and that extinction of conditioned taste avoidance is accelerated in fluid deprived male rats. The following study was designed to identify areas of the brain in which vasopressin levels are different in fluid deprived and nondeprived males during extinction of conditioned taste avoidance. Arginine vasopressin content was determined by radioimmunoassay in the paraventricular nucleus (PVN), medial amygdala (AMe), bed nucleus of the stria terminalis (BNST), nucleus tractus solitarius (NTS), medial septum (MS), lateral septum (LS), and insular cortex (IC) of unconditioned nondeprived males and conditioned males that were maintained on a 23-h fluid deprivation schedule or that were nondeprived. Vasopressin content in the PVN of deprived and nondeprived males differed during extinction. Based on comparisons with unconditioned nondeprived males, this difference was due to an elevation in the vasopressin content of the nondeprived but not the deprived males. These results raise the possibility that a vasopressinergic system in the PVN plays a critical role in the differential extinction rate of fluid deprived and nondeprived males, which will need to be verified by manipulating vasopressin levels in this brain site during extinction of a conditioned taste avoidance.

Animals↗
PubMed1999

The importance of a compound stimulus in conditioned drug-seeking behavior following one week of extinction from self-administered cocaine in rats.

Previous studies have demonstrated that conditioned stimuli can increase responding on a drug-associated lever after extinction from drug self-administration. The present study investigated singular stimuli (tone or light) or a compound stimulus (tone + light) for their ability to increase extinguished responding following chronic cocaine self-administration. Rats self-administered cocaine for 2 weeks on a fixed ratio (FR1) schedule of reinforcement, in which lever responding resulted in varied presentation of a tone, light, or tone + light combination. The rats were then exposed to 1 week of daily extinction sessions. Presentation of the tone + light on day 8 of extinction in the absence of cocaine reinforcement resulted in a significant increase in responding, while either stimulus component alone was much weaker or failed to produce any changes from extinction rates of responding. In addition, changing the duration of the single elements of the compound did not affect the magnitude of increased responding to the compound. Following three final extinction sessions, robust lever responding for cocaine infusions on day 12 of extinction was seen across all groups. These findings suggest that compound stimuli may be critical to fully activate drug-seeking behavior in conditions of craving and relapse following prolonged extinction.

Acoustic Stimulation↗
PubMed2000

Extinction can be enhanced by a concurrent excitor.

Five experiments used rat subjects to investigate the impact on extinction of the presence of other conditioned stimuli. In Experiments 1 (Pavlovian magazine approach) and 2 (instrumental discriminative training), an excitatory stimulus (X) was extinguished alone, in conjunction with a previously reinforced other stimulus (A), in conjunction with previously nonreinforced other stimulus (B), or it was spared extinction. Responding during extinction was greatest to AX, and subsequent testing of X alone showed AX extinction to have produced the most decrement to X. Experiment 3 found similar results using a within-subject design. Experiment 5 continued separate reinforced presentations of A during extinction. This procedure not only promoted extinction of X but also converted it into a conditioned inhibitor. These experiments bear on the mechanisms of overshadowing and stimulus processing, as well as provide information on the determinants of extinction.

Analysis of Variance↗
PubMed2005

Facilitation of fear extinction by midbrain periaqueductal gray infusions of RB101(S), an inhibitor of enkephalin-degrading enzymes.

Mu-opioid receptors in the ventrolateral quadrant midbrain periaqueductal gray (vIPAG) contribute to extinction of conditioned fear. The present experiment studied whether fear extinction could be facilitated by infusions of a peptidase inhibitor that reduces catabolism of vIPAG enkephalins. Rats were trained to fear an auditory conditioned stimulus. Fear was then extinguished. Extinction training was preceded by infusions of vehicle or RB101(S), an inhibitor of enkephalin catabolising enzymes. RB101(S) dose dependently facilitated extinction as indexed by performance during extinction and on a drug-free test. This facilitation was not observed when RB101(S) was infused outside the vIPAG. These results confirm that vIPAG endogenous opioids contribute to fear extinction and show that extinction can be facilitated by manipulations that increase vIPAG opioid neuromodulation.

Animals↗
PubMed2006

The effects of acquisition training schedule on extinction and reinstatement of cocaine self-administration in male rats.

Partial reinforcement is known to increase resistance to extinction (Rn) relative to training with continuous reinforcement. This phenomenon, referred to as the partial reinforcement extinction effect, is one of the most robust in learning and conditioning studies. Experiment 1 investigated manipulations known to affect the partial reinforcement extinction effect and determined their possible relevance for drug use patterns. Male rats received intravenous cocaine self-administration training under partial reinforcement (FR-10) training or continuous reinforcement (FR-1) conditions with either a low (0.25 mg/kg infusion) or a high cocaine dose (1.00 mg/kg infusion). Animals were placed on an extinction (recurrent nonreward) schedule for 10 days (1-hr sessions) prior to being tested for cue-induced reinstatement (single 2-hr session). Experiment 2 involved acquisition of cocaine self-administration under FR-1 conditions of short training (15 days) or extended training (30 days) with a low dose (0.25 mg/kg infusion) or a medium dose (0.50 mg/kg infusion) of cocaine reward prior to extinction or reinstatement. Experiment 1 showed that rats trained with FR-10-high dose outcomes exhibited greater Rn than the remaining groups. Additionally, FR-10-high dose and FR-10-low dose rats were more likely to return to active drug seeking during the reinstatement test. In Experiment 2, rats trained under FR-1-medium dose conditions were more persistent during extinction following short acquisition training than comparable rats experiencing extended acquisition training. The reinstatement test was conducted following extinction, in which it was observed that overtraining under FR-1-medium dose reward schedules resulted in a decrease in the tendency to return to active drug seeking.

Animals↗
PubMed1975

Interhemispheric transfer of extinction of the active avoidance reaction in rats.

Cortical spreading depression (CSD) was employed in rats to study the lateralization of extinction of a jumping avoidance reaction. Under unilateral CSD, 181 nonreinforced trials were needed to extinguish the avoidance reaction acquired in three 100-trial sessions of intact-brain training. During a second extinction session, either with the same or with the contralateral hemisphere depressed, the mean number of trials to the extinction criterion (9/10) was 39 (n = 12) or 186 (n = 15), respectively. Five extinction trials performed with the brain intact 1 hr before extinction with contralateral CSD decreased the number of trials to extinction of 98 (n = 11). Thus, extinction of active avoidance can be lateralized and interhemispherically transferred in the same way as acquisition of this habit.

Animals↗
PubMed2003

Extinction-induced upregulation in AMPA receptors reduces cocaine-seeking behaviour.

Cocaine addiction is thought to involve persistent neurobiological changes that facilitate relapse to drug use despite efforts to abstain. But the propensity for relapse may be reduced by extinction training--a form of inhibitory learning that progressively reduces cocaine-seeking behaviour in the absence of cocaine reward. Here we show that extinction training during withdrawal from chronic cocaine self-administration induces experience-dependent increases in the GluR1 and GluR2/3 subunits of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward. Increases in the GluR1 subunit are positively associated with the level of extinction achieved during training, suggesting that GluR1 may promote extinction of cocaine seeking. Indeed, viral-mediated overexpression of both GluR1 and GluR2 in nucleus accumbens shell neurons facilitates extinction of cocaine- but not sucrose-seeking responses. A single extinction training session, when conducted during GluR subunit overexpression, attenuates stress-induced relapse to cocaine seeking even after GluR overexpression declines. Our findings indicate that extinction-induced plasticity in AMPA receptors may facilitate control over cocaine seeking by restoring glutamatergic tone in the nucleus accumbens, and may reduce the propensity for relapse under stressful situations in prolonged abstinence.

Animals↗
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↗
PubMed2001

Retrieval of memory for fear-motivated training initiates extinction requiring protein synthesis in the rat hippocampus.

Evidence that protein synthesis inhibitors induce amnesia in a variety of species and learning paradigms indicates that the consolidation of newly acquired information into stable memories requires the synthesis of new proteins. Because extinction of a response also requires acquisition of new information, extinction, like original learning, would be expected to require protein synthesis. The present experiments examined the involvement of protein synthesis in the hippocampus in the extinction of a learned fear-based response known to involve the hippocampus. Rats were trained in a one-trial inhibitory avoidance task in which they received footshock after stepping from a small platform to a grid floor. They were then given daily retention tests without footshock. The inhibitory response (e.g., remaining on the platform) gradually extinguished with repeated testing over several days. Footshock administered in a different context, instead of a retention test, prevented the extinction. Infusions of the protein synthesis inhibitor anisomycin (80 microg) into the CA1 region of the hippocampus (bilaterally) 10 min before inhibitory avoidance training impaired retention on all subsequent tests. Anisomycin infused into the hippocampus immediately after the 1st retention test blocked extinction of the response. Infusions administered before the 1st retention test induced a temporary (i.e., 1 day) reduction in retention performance and blocked subsequent extinction. These findings are consistent with other evidence that anisomycin blocks both the consolidation of original learning and extinction.

Animals↗
PubMed2002

Signatures of random and selective mass extinctions in phylogenetic tree balance.

Current models of diversification with evolving speciation rates have trouble mimicking the extreme imbalance seen in estimated phylogenies. However, these models have not incorporated extinction. Here, we report on a simple simulation model that includes heritable and evolving speciation rates coupled with mass extinctions, Random (but not selective) mass extinctions, coupled with evolving among-lineage variation in speciation rates, increase imbalance of postrecovery clades. Thus, random mass extinctions are plausible contributors to the imbalance of modern clades. Paleontological evidence suggests that mass extinctions are often random with respect to ecological and morphological traits, consistent with our simulations. In contrast, evidence that the current anthropogenic mass extinction is phylogenetically selective suggests that the current extinction episode may be qualitatively different from past ones in the way it reshapes future biotas.

Biological Evolution↗
PubMed2006

Does red noise increase or decrease extinction risk? Single extreme events versus series of unfavorable conditions.

Recent theoretical studies have shown contrasting effects of temporal correlation of environmental fluctuations (red noise) on the risk of population extinction. It is still debated whether and under which conditions red noise increases or decreases extinction risk compared with uncorrelated (white) noise. Here, we explain the opposing effects by introducing two features of red noise time series. On the one hand, positive autocorrelation increases the probability of series of poor environmental conditions, implying increasing extinction risk. On the other hand, for a given time period, the probability of at least one extremely bad year ("catastrophe") is reduced compared with white noise, implying decreasing extinction risk. Which of these two features determines extinction risk depends on the strength of environmental fluctuations and the sensitivity of population dynamics to these fluctuations. If extreme (catastrophic) events can occur (strong noise) or sensitivity is high (overcompensatory density dependence), then temporal correlation decreases extinction risk; otherwise, it increases it. Thus, our results provide a simple explanation for the contrasting previous findings and are a crucial step toward a general understanding of the effect of noise color on extinction risk.

Animals↗
PubMedDate not supplied

Adrenergic transmission facilitates extinction of conditional fear in mice.

Extinction of classically conditioned fear, like its acquisition, is active learning, but little is known about its molecular mechanisms. We recently reported that temporal massing of conditional stimulus (CS) presentations improves extinction memory acquisition, and suggested that temporal spacing was less effective because individual CS exposures trigger two opposing processes: (1) fear extinction, which is favored by CS massing, and (2) fear incubation (increase), which is favored by spacing. We here report the effects of manipulating the adrenergic system during massed or spaced CS presentations in fear-conditioned mice. We administered yohimbine (5 mg/kg), an alpha(2)-receptor antagonist, or propranolol (10 mg/kg), a beta-receptor antagonist, systemically prior to CS presentation sessions and recorded both short- and long-term changes in conditional freezing. Yohimbine treatment facilitated extinction of both cue and context fear with massed protocols. When given before spaced CS presentations, propranolol led to a persistent incubation of cue fear, whereas yohimbine led to persistent extinction, compared with vehicle-treated animals, which showed no change in fear. These results suggest that norepinephrine positively modulates the formation of fear extinction memories in mice. They also provide clear evidence that spaced CS presentations trigger both fear-reducing (extinction) and fear-increasing (incubation) mechanisms.

Adrenergic Agonists↗