Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “extinction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources

Key pecking during extinction after intermittent or continuous reinforcement as a function of the number of reinforcers delivered during training.

Key pecking by 7 pigeons was established and maintained on a multiple variable-ratio variable-ratio (VR) schedule of food presentation. The schedule in one of the components was then changed to fixed-ratio (FR) 1 for a predetermined number of reinforcers. Both components were then changed to extinction (i.e., multiple extinction, extinction). This sequence was repeated a different number of times for each pigeon to determine the relation between the number of reinforcers delivered during each component of the multiple VR FR 1 schedule and the number of responses during extinction. For most pigeons, there were fewer responses during extinction in the presence of a stimulus recently correlated with FR 1, regardless of the number of reinforcers received. The ratio of the total responses in extinction in the former VR component to the total responses in the former FR 1 component increased as the number of reinforcers delivered during each component of the multiple schedule increased. Within-subject replications of the partial-reinforcement extinction effect generally occurred, and there were no overall reductions in the number of responses in extinction with repeated exposures to extinction.

Animals↗

Extinction of responding maintained by timeout from avoidance.

The resistance to extinction of lever pressing maintained by timeout from avoidance was examined. Rats were trained under a concurrent schedule in which responses on one lever postponed shock on a free-operant avoidance (Sidman) schedule (response-shock interval = 30 s) and responses on another lever produced 2 min of signaled timeout from avoidance on a variable-ratio 15 schedule. Following extended training (106 to 363 2-hr sessions), two experiments were conducted. In Experiment 1 two different methods of extinction were compared. In one session, all shocks were omitted, and there was some weakening of avoidance but little change in timeout responding. In another session, responding on the timeout lever was ineffective, and under these conditions timeout responding showed rapid extinction. The within-session patterns produced by extinction manipulations were different than the effects of drugs such as morphine, which also reduces timeout responding. In Experiment 2 shock was omitted for many consecutive sessions. Response rates on the avoidance lever declined relatively rapidly, with noticeable reductions within 5 to 10 sessions. Extinction of the timeout lever response was much slower than extinction of avoidance in all 4 rats, and 2 rats continued responding at baseline levels for more than 20 extinction sessions. These results show that lever pressing maintained by negative reinforcement can be highly resistant to extinction. The persistence of responding on the timeout lever after avoidance extinction is not readily explained by current theories.

Animals↗

Prefrontal cortex long-term potentiation, but not long-term depression, is associated with the maintenance of extinction of learned fear in mice.

Considerable efforts have been made to identify changes of brain synaptic plasticity associated with fear conditioning. However, for both clinical applications and our fundamental understanding of memory processes, it appears also necessary to investigate synaptic plasticity related to extinction. We previously showed that extinction of freezing to a tone conditioned stimulus (CS; previously paired with footshock) in mice results in a sequence of depression and potentiation of synaptic efficacy in the medial prefrontal cortex (mPFC). These data as well as those from lesion studies suggest that the direction of changes in prefrontal synaptic plasticity may modulate extinction of learned fear. To test this, we analyzed the effects of low-frequency stimulation (LFS) and high-frequency stimulation (HFS) of the mediodorsal thalamic nucleus, known to induce prefrontal long-term depression (LTD) and potentiation (LTP), respectively, on extinction. We found that maintenance of the depression phase, using thalamic LFS, was associated with resistance to extinction. Thalamic HFS applied before extinction testing had no effect on the rate of extinction. However, 1 week follow-up tests revealed that the memory of extinction was intact in these mice (with prefrontal LTP) and in control mice displaying prefrontal LTP-like changes, whereas control mice that did not exhibit such changes displayed a return of freezing to the CS. The results suggest that after extinction the lack of depression-LTP-like conversion sequence in the mPFC synaptic efficacy may profoundly alter the process of consolidation.

Acoustic Stimulation↗

Extinction requires new RNA and protein synthesis and the soma of the cell right pedal dorsal 1 in Lymnaea stagnalis.

Lymnaea stagnalis were operantly conditioned to not perform aerial respiratory behavior. This learned response was subsequently extinguished. Here, we show that spaced extinction training is more effective than massed extinction training, in addition to the occurrence of spontaneous recovery. We also find evidence of a critical period within the first hour after extinction training in which new RNA and protein synthesis must occur for a memory of extinction training to be established. The memory for extinction training can also be extended using cooling and by preventing aerial respiration from occurring after extinction training. In addition, we demonstrate that memory formation of extinction training requires the soma of the cell right pedal dorsal 1, a cell that we have previously shown to be necessary for long-term memory consolidation and reconsolidation. This finding implies that the events that lead to the formation of extinction memory occur in the same cell that is responsible for long-term memory of operant conditioning. All of these data are consistent with the hypothesis that, during extinction, a new associative memory is being formed and that this new memory covers up, but does not abolish, the "old" memory.

Animals↗

Crystal thickness and extinction distance determination using energy filtered CBED pattern intensity measurement and dynamical diffraction theory fitting.

A new method for measuring thickness and extinction distance of single crystals based on computed adjustment of measured and calculated CBED pattern intensity profiles is presented and discussed. The experimental beam intensity distribution is measured from an energy filtered CBED pattern recorded on a CCD camera. The calculated profile is based on dynamical diffraction theory, and with the two-beam approximation the analytical expression contains only two free parameters: specimen thickness t and extinction distance xig. Parameter refinement through minimization of the difference between experimental and calculated intensity profiles is carried out using Origin 5.0 software from Microcal. The iterative procedure always converges to a unique solution in a few seconds, yielding an accurate value for both thickness and extinction distance. The method is extensively tested on silicon using the (0 0 4) Bragg reflection. On specimens in the usual TEM thickness range, the method gives result similar to the conventional (P.M. Kelly et al., Phys. Stat. Sol. A31 (1975) 771; S.M. Allen, Philos. Mag. A 43 (1981) 325) graphical methods, both based on the measurement of fringe spacing. Moreover, it is shown that the calculation matches perfectly both the positions of the minimums and maximums as well as the amplitude of maximums. For any single intensity profile, specimen thickness and extinction distance can be determined with a precision of about 0.2%. A statistical comparison of our method with the Kelly and Allen techniques, based on more than 50 experiments, shows an improvement in measured extinction distance dispersion. Using 197 keV electrons, and liquid-nitrogen cryo-holder, the new technique yields an experimental value of 161+/-3 nm for the extinction distance for silicon with the (0 0 4) Bragg reflection. The equivalent tabulated value at 0 K is about 156 nm. Using the Kelly and Allen methods, the extinction distance is found to be 162+/-6 nm. The improvement in precision is a direct consequence of matching the intensity profile envelope, which contains information on the extinction distance. Also the accuracy of thickness determination is improved and is around 0.5 to 1% for common specimen thickness. The minimum measurable sample thickness is shown to be two to three times thinner than with the Kelly and Allen methods (0.3 xig, as opposed to 0.8 xig). With no independent calculation of the extinction distance needed, the method is also applicable on unknown crystals. The method is fast, simple and can be easily automated.

Journal Article↗

Extinction and synesthesia in patients with spinal cord injuries.

Extinction and synesthesia were studied in 50 patients with spinal cord injury with various levels and extents. Extinction was found in 20 (40 per cent) and synesthesia in 6 (12 per cent) of the 40 males and 10 females. No correlations were found between either of the two phenomena and parameters of patient's age, lesion's age, lesion's level and extent, or accompanying head injury. The latter occurred in 22/50 patients (44 per cent), diagnosed by a history of amnesia. Extinction was tested by synchronous double stimulation unilaterally and bilaterally, symmetrically and asymmetrically. It was more frequent unilaterally than bilaterally. The modalities of superficial sensibility were prone to be extinct but those of deep sensibility (pallesthesia from bone conduction and kinesthesia) were not. Extinction of tactile responses did not imply that all other skin modalities (pain, temperature, pressure, skin pallesthesia) will also be extinct in an all or nothing fashion. Modalities could become extinct either singly or in combination. Extinction in spinal man was presumed to be caused by a reduction of perception in hypesthetic areas and was of diagnostic value insofar as its segmental distribution suggested the longitudinal extent of a cord lesion. This concept is in accord with the results of monkey experiments by Eidelberg and Schwartz (1971). Synesthia in spinal man is not identical with synchiria of the monkey. It is not in a reciprocal relationship with extinction and both phonemena co-existed in four of the six patients. Synesthesia is elicited by a stimulus delivered to the normesthetic skin above the level of the lesion with two responses: one well localised at the site of stimulation and the other unilaterally or bilaterally in anaesthetic parts of the body. Five of the six patients reported volitional phantom movements of somatic (toes) and/or visceral (micturition-defaecation) structures. Such sensations are elicited by remembering the engrams of pre-traumatic experiences in areas of the body image connected with motor function. Synesthesia could be understood as a sensory counterpart in areas of the body image when ascending impules of actual perception are mixed with impulses modulated at the artifical synapse of the rostral cord stump creating a phantom sensation.

Adolescent↗

Lessons from the past: biotic recoveries from mass extinctions.

Although mass extinctions probably account for the disappearance of less than 5% of all extinct species, the evolutionary opportunities they have created have had a disproportionate effect on the history of life. Theoretical considerations and simulations have suggested that the empty niches created by a mass extinction should refill rapidly after extinction ameliorates. Under logistic models, this biotic rebound should be exponential, slowing as the environmental carrying capacity is approached. Empirical studies reveal a more complex dynamic, including positive feedback and an exponential growth phase during recoveries. Far from a model of refilling ecospace, mass extinctions appear to cause a collapse of ecospace, which must be rebuilt during recovery. Other generalities include the absence of a clear correlation between the magnitude of extinction and the pace of recovery or the resulting ecological and evolutionary disruption the presence of a survival interval, with few originations, immediately after an extinction and preceding the recovery phase, and the presence of many lineages that persist through an extinction event only to disappear during the subsequent recovery. Several recoveries include numerous missing lineages, groups that are found before the extinction, then latter in the recovery, but are missing during the initial survival-recovery phase. The limited biogeographic studies of recoveries suggest considerable variability between regions.

Animals↗

A complete classification of Darwinian extinction in ecological interactions.

The evolution of a population by individual-level natural selection can result in the population's extinction. Selection causes the spread of phenotypes with higher relative fitness, but at the same time, selection can also indirectly produce changes in the physical, biotic, or genotypical environment through population interactions (e.g., environment modification, interspecific interactions, and genomic conflict). Because fitness is environment dependent, this can cause mean fitness to decrease, resulting in extinction. I call this process "Darwinian extinction." Examples of Darwinian extinction include a variety of dynamics and modes of extinction, but the variation is constrained. I determine the complete classification of possible dynamics and modes of Darwinian extinction due to ecological interactions, using bifurcation theory and models with ecological and evolutionary changes occurring on different timescales. This classification is also extended to extinctions due to interactions within the population. The mode of extinction may be either sudden or gradual (requiring additional stochastic processes), and each mode has specific types of dynamics associated with it. Darwinian extinction is a robust and normal phenomenon, and this reasonably complete classification can help us understand more thoroughly its role in nature.

Animals↗

Determinants of loss of mammal species during the Late Quaternary 'megafauna' extinctions: life history and ecology, but not body size.

Extinctions of megafauna species during the Late Quaternary dramatically reduced the global diversity of mammals. There is intense debate over the causes of these extinctions, especially regarding the extent to which humans were involved. Most previous analyses of this question have focused on chronologies of extinction and on the archaeological evidence for human-megafauna interaction. Here, I take an alternative approach: comparison of the biological traits of extinct species with those of survivors. I use this to demonstrate two general features of the selectivity of Late Quaternary mammal extinctions in Australia, Eurasia, the Americas and Madagascar. First, large size was not directly related to risk of extinction; rather, species with slow reproductive rates were at high risk regardless of their body size. This finding rejects the 'blitzkrieg' model of overkill, in which extinctions were completed during brief intervals of selective hunting of large-bodied prey. Second, species that survived despite having low reproductive rates typically occurred in closed habitats and many were arboreal or nocturnal. Such traits would have reduced their exposure to direct interaction with people. Therefore, although this analysis rejects blitzkrieg as a general scenario for the mammal megafauna extinctions, it is consistent with extinctions being due to interaction with human populations.

Animals↗

Tactile extinction to simple (elementary) and complex stimuli.

Thirty patients with cerebrovascular disease and 85 control subjects were examined using both the classical tactile extinction test and a modified Quality Extinction Test (modified QET) in order to investigate the so-called tactile extinction phenomenon to complex stimuli from the qualitative standpoint. As a result, 1) the patients with tactile extinction to simple (elementary) stimuli also manifested extinction to complex tactile stimuli in the modified QET; 2) there were patients who exhibited extinction only to complex tactile stimuli. Our results provide support for the concept that the so-called tactile extinction phenomenon could result from competition between tactile stimuli presented to both hands at at least 2 different levels of tactile processing, i.e. the process of perception and the process of recognition. When discussing the phenomenon of extinction to complex tactile stimuli, therefore, one should consider these 2 forms of extinction separately.

Adult↗

Biological extinction in earth history.

Virtually all plant and animal species that have ever lived on the earth are extinct. For this reason alone, extinction must play an important role in the evolution of life. The five largest mass extinctions of the past 600 million years are of greatest interest, but there is also a spectrum of smaller events, many of which indicate biological systems in profound stress. Extinction may be episodic at all scales, with relatively long periods of stability alternating with short-lived extinction events. Most extinction episodes are biologically selective, and further analysis of the victims and survivors offers the greatest chance of deducing the proximal causes of extinction. A drop in sea level and climatic change are most frequently invoked to explain mass extinctions, but new theories of collisions with extraterrestrial bodies are gaining favor. Extinction may be constructive in a Darwinian sense or it may only perturb the system by eliminating those organisms that happen to be susceptible to geologically rare stresses.

Animals↗

Opioid receptors in the midbrain periaqueductal gray regulate extinction of pavlovian fear conditioning.

Four experiments studied the role of opioid receptors in the midbrain periaqueductal gray matter (PAG), an important structure eliciting conditioned fear responses, in the extinction of Pavlovian fear. Rats received pairings of an auditory conditioned stimulus (CS) with a foot shock unconditioned stimulus (US). The freezing conditioned response (CR) elicited by the CS was then extinguished via nonreinforced presentations of the CS. Microinjection of the opioid receptor antagonist naloxone into the ventrolateral PAG (vlPAG) before nonrein-forced CS presentations impaired development of extinction, but such microinjections at the end of extinction did not reinstate an already extinguished freezing CR. This role for opioid receptors in fear extinction was specific to the vlPAG because infusions of naloxone into the dorsal PAG did not impair fear extinction. Finally, the impairment of fear extinction produced by vlPAG infusions of naloxone was dose-dependent. These results show for the first time that the midbrain PAG contributes to fear extinction and specifically identify a role for vlPAG opioid receptors in the acquisition but not the expression of such extinction. Taken together with our previous findings, we suggest that, during fear conditioning, activation of vlPAG opioid receptors contributes to detection of the discrepancy between the actual and expected outcome of the conditioning trial. vlPAG opioid receptors regulate the learning that accrues to the CS and other stimuli present on a trial because they instantiate an associative error correction process influencing US information reaching the site of CS-US convergence in the amygdala. During nonreinforcement, this vlPAG opioid receptor contribution signals extinction.

Animals↗

Mass extinction: a commentary.

Four neocatastrophist claims about mass extinction are currently being debated; they are that: 1, the late Cretaceous mass extinction was caused by large body impact; 2, as many as five other major extinctions were caused by impact; 3, the timing of extinction events since the Permian is uniformly periodic; and 4, the ages of impact craters on Earth are also periodic and in phase with the extinctions. Although strongly interconnected the four claims are independent in the sense that none depends on the others. Evidence for a link between impact and extinction is strong but still needs more confirmation through bed-by-bed and laboratory studies. An important area for future research is the question of whether extinction is a continuous process, with the rate increasing at times of mass extinctions, or whether it is episodic at all scales. If the latter is shown to be generally true, then species are at risk of extinction only rarely during their existence and catastrophism, in the sense of isolated events of extreme stress, is indicated. This is line of reasoning can only be considered an hypothesis for testing. In a larger context, paleontologists may benefit from a research strategy that looks to known Solar System and Galactic phenomena for predictions about environmental effects on earth. The recent success in the recognition of Milankovitch Cycles in the late Pleistocene record is an example of the potential of this research area.

Animals↗

Reversible inactivations of the cerebellum with muscimol prevent the acquisition and extinction of conditioned nictitating membrane responses in the rabbit.

Lesions of the cerebellum severely impair the classically conditioned nictitating membrane response (NMR) in rabbits. Thus, the cerebellum is essential for the production of conditioned responses (CRs), either because it is actively involved in NMR conditioning or because damage to it causes motor or other general deficits. To distinguish between these alternatives, the cerebellum may be inactivated during training. Inactivation of the cerebellum during acquisition training might result in the absence of CRs on initial trials of subsequent training without the neuronal blockade. The blockade may have prevented learning but it may have produced other deficits that require time or further training to overcome. This problem can be addressed by inactivating the cerebellum during extinction training. If inactivation during extinction training results in the immediate production of CRs when training is resumed without the blockade, then it may be concluded that extinction learning was prevented by the blockade-the presence of CRs argues against any deficits not associated with learning. We used muscimol to inactivate the cerebellum and test its involvement in acquisition and extinction of NMR conditioning in the same subjects. We injected muscimol close to the interpositus nucleus of the cerebellum 1 h before each of four daily training sessions of delay conditioning. Almost no CRs were produced in these training sessions-there was little or no acquisition of NMR conditioning during cerebellar inactivation. The subjects were then trained for four daily sessions without injections of muscimol. There were no CRs on initial trials of the first session of retraining, but all subjects produced CRs by the end of this session. The subjects then received four daily sessions of extinction training with muscimol inactivation of the nuclei-no CRs were produced. Extinction training then continued for four daily sessions without muscimol inactivation. On the first of these sessions, all subjects immediately produced high levels of CRs. These responses then extinguished within and between sessions with characteristic beginning-of-session spontaneous recovery. There was little or no extinction of NMR conditioning during cerebellar inactivation. After inactivation, the muscimol- inactivated subjects went on to acquire and extinguish NM responses at rates similar to those of appropriate controls. We conclude that cerebellar circuitry is essential for, and actively engaged in, both acquisition and extinction of this simple form of motor learning.

Animals↗

The abolition of the partial reinforcement extinction effect (PREE) by amphetamine.

The effects of amphetamine administration on the partial reinforcement extinction effect (PREE) at one trial a day, were examined. Two groups of rats were trained to run in a straight alley. The continuously reinforced (CRF) group received food reward on every trial. The partially reinforced (PRF) group was rewarded on a quasirandom 50% schedule. All animals were then tested in extinction. dl-Amphetamine 1.5 mg/kg was administered in a 2 X 2 design, i.e., drug-no drug in acquisition and drug-no drug in extinction. The PREE, i.e., increased resistance to extinction exhibited by PRF animals as compared to CRF animals, was obtained in animals that received saline in acquisition, independently of drug treatment in extinction. In contrast, amphetamine administered in acquisition abolished the PREE irrespective of drug treatment in extinction. In addition, amphetamine administered in extinction alone increased resistance to extinction in PRF animals.

Amphetamine↗

Effects of haloperidol on the multitrial partial reinforcement extinction effect (PREE): evidence for neuroleptic drug action on nonreinforcement but not on reinforcement.

Two experiments investigated the effects of haloperidol (0.1 mg/kg) on the partial reinforcement extinction effect (PREE). In experiment 1 two groups of rats were trained to run in a straight alley using six trials/day with an intertrial interval (ITI) of 5-8 min. The continuously reinforced (CRF) group received food reward on every trial. The partially reinforced (PRF) group was rewarded on a quasi-random 50% schedule. All animals were then tested in extinction. Haloperidol was administered in a 2 x 2 design, i.e., drug-no drug in acquisition and drug-no drug in extinction. In experiment 2 two groups of rats were trained to press a lever in an operant chamber using a discrete trial procedure of ten trials/day with an ITI of 60 s. The CRF group was rewarded on each trial and the PRF group was rewarded on a quasi-random 50% schedule. Haloperidol was administered for 22 days prior to the start of the PREE procedure as well as throughout acquisition and extinction. The PREE, i.e., increased resistance to extinction of PRF as compared to CRF animals, was obtained in both experiments in all drug conditions. In both experiments haloperidol increased the rate of extinction. Experiment 1 revealed that this effect was entirely due to the administration of the drug in extinction, independently of the drug condition in acquisition. In contrast to previous results in a one trial/day procedure, the administration of haloperidol to CRF animals did not increase resistance to extinction, failing to support the notion that neuroleptics attenuate the rewarding properties of reinforcement.

Animals↗

Extinction: [corrected] does it or doesn't it? The requirement of altered gene activity and new protein synthesis.

Many accounts of memory suggest that an initial learning experience initiates a cascade of cellular and molecular events that are required for the consolidation of memory from a labile into a more permanent state. Studies of memory in many species have routinely found that altered gene activity and new protein synthesis are the critical components of this memory consolidation process. During extinction, when organisms learn that previously established relations between stimuli have been severed, new memories are formed and consolidated. However, the nature of the learning that underlies extinction remains unclear and there are many processes that may contribute to the weakening of behavior that occurs during extinction. In this review, we suggest that the molecular mechanisms that underlie extinction may differ depending on the learning process that is engaged by extinction. We review evidence that extinction, like initial learning, requires transcription and translation, as well as evidence that extinction occurs when protein synthesis is inhibited. We suggest that extinction occurs through the interaction of multiple behavioral and molecular mechanisms.

Animals↗

When supine is better than upright: evidence from postural effects in extinction patients.

There is no clear consensus on the specific effects of gravitational inputs on the manifestations of neglect and extinction. While some studies provided evidence that neglect patients improved their performance in supine position, other studies supported instead the notion that the manipulation of body posture has no effect on neglect and extinction. To investigate the effects of the postural manipulation of the entire body in space on visual extinction, a total of 24 right- and left-brain-damaged patients (with or without signs of visual extinction) and 8 healthy control subjects were tested in a visual detection task in two different gravitational conditions: upright and supine. Two dependent variables were considered: accuracy and speed of response. The results were clear-cut. Changing body posture had only a mild effect on the performance of healthy controls and non-extinction patients, but it clearly modulated the performance of extinction patients. In fact, extinction patients markedly improved their performance on contralesional stimuli in supine position in terms of both accuracy and speed of response. This suggests that the reduction of gravitational inputs obtained by placing patients in supine position results in a significant amelioration of visual extinction.

Aged↗