End Of Extinction Research Articles

The fear that remains: Associations between trauma, related psychopathology, and fear-potentiated startle in youth resettled as refugees.

Fear-potentiated startle (FPS) can be used to measure fear and safety learning-behaviors affected by trauma that may map onto posttraumatic stress disorder (PTSD). Therefore, FPS could be a candidate biomarker of trauma-related psychopathology and a potential identifier of trauma-exposed youth in need of focused treatment. We enrolled n=71 (35 females, Mage =12.7 years) Syrian youth exposed to civilian war trauma. Eyeblink electromyogram (EMG) data from a differential conditioning FPS paradigm were obtained 2.5 years after resettlement. Youth provided self-report of trauma exposure (Harvard Trauma Questionnaire) and PTSD symptoms (UCLA PTSD Reaction Index). While FPS during conditioning was not associated with symptoms, associations with psychopathology emerged in fear extinction. Probable PTSD was associated with FPS in the last block of extinction, such that FPS to threat cue was significantly greater in the PTSD+ group compared to the PTSD- group at the end of extinction (F=6.25, p=.015). As with adults, we observed a deficit in extinction learning but not fear conditioning in youth with PTSD. These results support the use of trauma-informed cognitive behavioral therapy based on the learning principles of extinction in youth with PTSD.

Measuring fear: Association among different measures of fear learning.

Background and objectivesFear conditioning paradigms use various measures to assess learned fear, including autonomic arousal responses like skin conductance, and self-reports of both associative (US-expectancies) and evaluative (affective ratings) learning. The present study uses a dimensional approach to examine associations among fear indices directly. MethodsSeventy-three participants completed a differential fear conditioning experiment, during which a neutral stimulus (CS+) was paired with an electric shock (US), while another stimulus (CS-) was never paired with the shock (partially instructed fear acquisition). Ten minutes later, both stimuli were presented without any shocks (fear extinction). Skin conductance responses and US-expectancy ratings were recorded during each phase, while self-reported negative affect was assessed for each CS at the end of extinction. ResultsResults showed a positive association among US-expectancy ratings and skin conductance responses during acquisition and early extinction. US-expectancy ratings during overall extinction were positively associated with post-extinction negative affect. LimitationsThe lack of affective ratings post-acquisition may have obscured associations between associative and evaluative learning indices. ConclusionsResults provide evidence for the expected correspondence among different indices of associative fear learning. Findings emphasize the need for incorporating both associative and evaluative learning measures in fear conditioning paradigms.

An experimental investigation into the mediating role of pain-related fear in boosting nocebo hyperalgesia.

Nocebo hyperalgesia refers to increases in perceived pain that putatively result from negative expectations regarding a nocebo stimulus (eg, an inert treatment, compared with no treatment). The precise cognitive-emotional factors contributing to the origins of nocebo effects are poorly understood. We aimed to test the effects of experimentally induced pain-related fear on the acquisition and extinction of nocebo hyperalgesia in healthy participants (N = 72). Acquisition and extinction of nocebo hyperalgesia were compared between a group receiving standard nocebo conditioning (Control group) and 2 groups receiving distinct fear inductions: high intensity of pain stimulations (High-pain group) or a threat manipulation (High-threat group). During nocebo acquisition, the Control and High-threat groups were administered thermal pain stimulations of moderate intensity paired with sham electrical stimulation (nocebo trials), whereas high pain intensity was administered to the High-pain group. During extinction, equivalent pain intensities were administered across all trials. Pain-related fear was measured by eyeblink startle electromyography and self-report. Nocebo hyperalgesia occurred in all groups. Nocebo effects were significantly larger in the High-pain group than those in the Control group. This effect was mediated by self-reported fear, but not by fear-potentiated startle. Groups did not differ in the extinction rate. However, only the High-pain group maintained significant nocebo responses at the end of extinction. Anticipatory pain-related fear induced through a threat manipulation did not amplify nocebo hyperalgesia. These findings suggest that fear of high pain may be a key contributor to the amplification of nocebo hyperalgesia, only when high pain is experienced and not when it is merely anticipated.

Exposure to violence and neglect images differentially influences fear learning and extinction

The mechanisms by which exposure to adversity contributes to psychopathology development are poorly understood. Recent models link experiences of threat of harm and deprivation to psychopathology via disruptions in learning mechanisms underlying fear acquisition and extinction. We empirically tested dimensional elements of this model, by examining whether exposure to images of community violence or neglect differentially influenced fear learning and extinction relative to exposure to neutral images. Participants were randomly allocated to one of three exposure conditions: viewing images depicting neglect (n = 25), violence (n = 25) or control images (n = 24). All participants then completed a fear conditioning and extinction task in which the CS+ was paired with an aversive tone, and the CS- was presented alone during conditioning. Both CSs were presented alone during extinction and extinction retest. Skin conductance responses (SCR) and subjective ratings were assessed. Relative to control images, viewing scenes of neglect attenuated SCRs to the CSs during conditioning, extinction and extinction retest. Exposure to images of community violence accentuated SCRs during US anticipation on CS+ trials and impaired the retention of safety learning (larger SCRs to the CS+ compared to the CS- at retest and the CS+ at the end of extinction). No significant group differences emerged in subjective ratings. Findings lend preliminary support for suggestions that adverse experiences may be linked to impairments in fear and safety learning and provide key evidence suggesting that the expression of these impairments may differ as a function of the type of adversity.

L-DOPA improves extinction memory retrieval after successful fear extinction

RationaleA promising strategy to prevent a return of fear after exposure-based therapy in anxiety disorders is to pharmacologically enhance the extinction memory consolidation presumed to occur after exposure. Accumulating evidence suggests that the effect of a number of pharmacological consolidation enhancers depends on a successful fear reduction during exposure. Here, we employed the dopamine precursor L-DOPA to clarify whether its documented potential to enhance extinction memory consolidation is dependent on successful fear extinction.MethodsIn two double-blind, randomized and placebo-controlled experiments (experiment 1: N = 79, experiment 2: N = 32) comprising fear conditioning (day 1), extinction followed by administration of 150 mg L-DOPA or placebo (day 2) and a memory test (day 3) in healthy male adults, conditioned responses were assessed as differential skin conductance responses. We tested whether the effect of L-DOPA on conditioned responses at test depended on conditioned responses at the end of extinction in an experiment with a short (10 trials, experiment 1) and long (25 trials, experiment 2) extinction session.ResultsIn both experiments, the effect of L-DOPA was dependent on conditioned responses at the end of extinction. That is, post-extinction L-DOPA compared to placebo administration reduced conditioned responses at test only in participants showing a complete reduction of conditioned fear at the end of extinction.ConclusionThe results support the potential use of L-DOPA as a pharmacological adjunct to exposure treatment, but point towards a common boundary condition for pharmacological consolidation enhancers: a successful reduction of fear in the exposure session.

Generalization and Extinction of Concept-BasedPain-Related Fear

In chronic pain, pain-related fear seems to overgeneralize to safe stimuli, thus contributing to excessive fear and avoidance behavior. Evidence shows that pain-related fear can be acquired and generalized based on conceptual knowledge. Using a fear conditioning paradigm, we investigated whether this concept-based pain-related fear could also be extinguished. During acquisition, exemplars of 1 action category (conditioned stimuli [CSs]; eg, opening boxes) were followed by pain (CS+), whereas exemplars of another action category were not (CS–; eg, closing boxes). Participants reported more pain-related fear and expectancy toward exemplars of the CS+ category compared with those of the CS– category. During generalization, fear and expectancy spread to novel exemplars (generalization stimuli [GSs]) of the CS+ category (GS+), but not to those of the CS– category (GS–). During extinction, exemplars of both categories were presented in the absence of pain. At the end of extinction, participants no longer reported elevated fear or expectancy toward CS+ exemplars compared to CS– exemplars. These findings were not replicated in either the eye-blink startle or skin conductance measures. This is the first study to demonstrate extinction of concept-based pain-related fear, thus providing evidence for the potential of extinction-based techniques in the treatment of conceptual pain-related fear. PerspectiveThis study demonstrates the acquisition, generalization, and extinction of concept-based pain-related fear in healthy participants. These are the first results to show that concept-based pain-related fear can be extinguished, suggesting that conceptual relationships between fear-inducing stimuli may also be important to consider in clinical practice.

The effect of positive mood induction on reducing reinstatement fear: Relevance for long term outcomes of exposure therapy

While exposure therapy is effective in treating anxiety, fear can return after exposure. Return of fear can be understood through mechanisms of extinction learning. One form of return of fear is reinstatement, or, the fear that results from an unsignaled unconditional stimulus (US) presentation after extinction. Though the conditional response (CR; e.g., fear) typically reduces during extinction, the excitatory conditional stimulus (CS+) valence remains negative. The more negative the CS+ valence after the end of extinction, the greater the fear at reinstatement. The current study evaluated the degree to which positive mood induction (positive imagery training; PIT) compared to control (positive verbal training; PVT) before extinction a) decreased CS+ negative valence during extinction and b) reduced reinstatement fear. Compared to PVT, PIT a) increased positive affect, b) decreased post-extinction CS+ negative valence, and c) reduced reinstatement responding as measured by eye blink startle reflex (when shock was used at reinstatement) and self-report fear (regardless of reinstatement US type). Results suggest that increasing positive affect prior to exposure therapy could reduce relapse through reinstatement.

Morphine administration during low ovarian hormone stage results in transient over expression of fear memories in females.

Acute exposure to morphine after a traumatic event reduces trauma related symptoms in humans and conditioned fear expression in male rats. We aimed to determine whether acute administration of morphine alters consolidation of fear learning and extinction. Male and female rats in proestrus and metaestrus (high and low ovarian hormones respectively) underwent fear conditioning and received saline or morphine (2.5 mg/kg s.c.). The next day they underwent extinction. Results showed increased freezing during extinction only in the morphine metaestrus group while morphine did not affect males or proestrus females. Recall of extinction was similar on all groups. On a second experiment, a subset of rats conditioned during metaestrus was administered morphine prior to extinction producing no effects. We then measured mu opioid receptor (MOR) expression in the amygdala and periaqueductal gray (PAG) at the end of extinction (day 2). In males and proestrus females, morphine caused an increase in MOR in the amygdala but no in the PAG. In metaestrus females, morphine did not change MOR expression in either structure. These data suggests that ovarian hormones may interact with MORs in the amygdala to transiently alter memory consolidation. Morphine given after trauma to females with low ovarian hormones might increase the recall of fear responses, making recovery harder.

Hemodynamic responses in amygdala and hippocampus distinguish between aversive and neutral cues during Pavlovian fear conditioning in behaving rats

Lesion and electrophysiological studies in rodents have identified the amygdala and hippocampus (HPC) as key structures for Pavlovian fear conditioning, but human functional neuroimaging studies have not consistently found activation of these structures. This could be because hemodynamic responses cannot detect the sparse neuronal activity proposed to underlie conditioned fear. Alternatively, differences in experimental design or fear levels could account for the discrepant findings between rodents and humans. To help distinguish between these alternatives, we used tissue oxygen amperometry to record hemodynamic responses from the basolateral amygdala (BLA), dorsal HPC (dHPC) and ventral HPC (vHPC) in freely-moving rats during the acquisition and extinction of conditioned fear. To enable specific comparison with human studies we used a discriminative paradigm, with one auditory cue [conditioned stimulus (CS)+] that was always followed by footshock, and another auditory cue (CS−) that was never followed by footshock. BLA tissue oxygen signals were significantly higher during CS+ than CS− trials during training and early extinction. In contrast, they were lower during CS+ than CS− trials by the end of extinction. dHPC and vHPC tissue oxygen signals were significantly lower during CS+ than CS− trials throughout extinction. Thus, hemodynamic signals in the amygdala and HPC can detect the different patterns of neuronal activity evoked by threatening vs. neutral stimuli during fear conditioning. Discrepant neuroimaging findings may be due to differences in experimental design and/or fear levels evoked in participants. Our methodology offers a way to improve translation between rodent models and human neuroimaging.

Extinction under a behavioral microscope: Isolating the sources of decline in operant response rate

Extinction performance is often used to assess underlying psychological processes without the interference of reinforcement. For example, in the extinction/reinstatement paradigm, motivation to seek drug is assessed by measuring responding elicited by drug-associated cues without drug reinforcement. However, extinction performance is governed by several psychological processes that involve motivation, memory, learning, and motoric functions. These processes are confounded when overall response rate is used to measure performance. Based on evidence that operant responding occurs in bouts, this paper proposes an analytic procedure that separates extinction performance into several behavioral components: (1-3) the baseline bout initiation rate, within-bout response rate, and bout length at the onset of extinction; (4-6) their rates of decay during extinction; (7) the time between extinction onset and the decline of responding; (8) the asymptotic response rate at the end of extinction; (9) the refractory period after each response. Data that illustrate the goodness of fit of this analytic model are presented. This paper also describes procedures to isolate behavioral components contributing to extinction performance and make inferences about experimental effects on these components. This microscopic behavioral analysis allows the mapping of different psychological processes to distinct behavioral components implicated in extinction performance, which may further our understanding of the psychological effects of neurobiological treatments.

Explicit disassociation of a conditioned stimulus and unconditioned stimulus during extinction training reduces both time to asymptotic extinction and spontaneous recovery of a conditioned taste aversion

Conditioned taste aversions (CTAs) may be acquired when an animal consumes a novel taste (CS) and then experiences the symptoms of poisoning (US). This aversion may be extinguished by repeated exposure to the CS alone. However, following a latency period in which the CS is not presented, the CTA will spontaneously recover (SR). In the current study we employed an explicitly unpaired extinction procedure (EU-EXT) to determine if it could thwart SR of a CTA. Sprague–Dawley rats acquired a strong CTA after three pairings of saccharin (SAC the CS) and Lithium Chloride (LiCl the US). CTA acquisition was followed by extinction (EXT) training consisting of either (a) CS-only exposure (CSO) or (b) exposure to saccharin and Lithium Chloride on alternate days (i.e., explicitly unpaired: EU). Both extinction procedures resulted in ⩾90% reacceptance of SAC, although the EU extinction procedure (EU-EXT) significantly decreased the time necessary for rats to reach this criterion (compared to CSO controls). Rats were subsequently tested for SR of the CTA upon re-exposure to SAC following a 30-day latency period of water drinking. Rats that acquired a CTA and then underwent the CSO extinction procedure exhibited a significant suppression of SAC drinking during the SR test (as compared to their SAC drinking at the end of extinction). However, animals in the EU-EXT group did not show such suppression in drinking compared to CSO controls. These data suggest that the EU-EXT procedure may be useful in reducing both time to extinction and the spontaneous recovery of fears.

Prevalence, magnitude, and correlates of an extinction burst in drug-seeking behavior in rats trained to self-administer nicotine during unlimited access (23 h/day) sessions

Animals trained to self-administer a variety of addictive drugs exhibit a temporary increase in response rate when saline is substituted for the drug (i.e., an "extinction burst"). However, the presence of an extinction burst in animal models of nicotine self-administration (NSA) has not been studied extensively. The objective of the study was to examine the prevalence, magnitude, and correlates of an extinction burst in nicotine-seeking behavior using data from a previously published study and recently trained animals. Rats were trained to self-administer nicotine (0.03 mg/kg per infusion) during daily 23-h sessions. Saline extinction was subsequently arranged, followed by reacquisition of NSA for some animals. There was no increase in the daily infusion rate on the first day of extinction. However, a significant increase (35%) in mean peak 2-h infusion rates was observed within the first extinction session, indicative of an extinction burst. Greater extinction burst magnitude was correlated with higher infusion rates during the first 2 h of baseline sessions and smaller decreases in infusion rate at the end of extinction. In addition, animals with the slowest initial rates of extinction exhibited the fastest rates of reacquisition when unlimited access to nicotine was restored. A modest increase in drug-seeking behavior occurred early within the first extinction session in rats trained to self-administer nicotine in unlimited access sessions. The presence of an extinction burst in nicotine-seeking behavior suggests similar mechanisms underlying extinction of NSA and self-administration of other drugs of abuse in animals and also parallels a similar phenomenon sometimes observed in smokers.

Early Triassic recovery of the brachiopod faunas from the end-Permian mass extinction: A global review

Brachiopod faunas in Lower Triassic deposits from Spitzbergen, Primorye of Russia, Japan, Mangyslak of Kazakhstan, Alpine Europe, the Caucasus, the Middle East, the Himalaya, South China, New Zealand, and western USA are taxonomically and stratigraphically reviewed. They comprise survivors of the end-Permian extinction and taxa originating in the Early Triassic. Origination of the Mesozoic-type taxa represents the recovery of Early Triassic brachiopods. The initial recovery of brachiopod faunas began in the late Griesbachian, and the time interval between the end of extinction and the onset of the recovery of brachiopods is much shorter than previously suspected. The Early Triassic recovery of brachiopod faunas is characterized by widespread brachiopod dispersal, multiprovincialism, and the presence of rare Lazarus genera at that time. Taxonomic selectivity of the recovery brachiopod faunas favors the rhynchonellids. The re-population of post-extinction brachiopods varies geographically: there is a preference for regions either previously barren of latest Permian taxa or regions where the pre-extinction Changhsingian and surviving brachiopods are very rare. This unique biogeographic selectivity is probably partly responsible for the impoverished nature of brachiopod faunas in the Triassic (even Mesozoic) oceans. Five intervals of extinction, survival, survival–recovery, recovery–dispersal, and radiation are recognized based on variations in brachiopod faunas from the latest Permian to the Early Triassic. A dramatic reduction in brachiopod diversity at the end-Permian mass extinction is followed by several stepwise declines in diversity in the survival interval, the time during which the surviving brachiopods are dominated by geographically widespread generalist faunas that adapted to a wide variety of environments. The survival interval was followed by a slow re-population of new lineages dominated by progenitor taxa.

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.

Extinction in fear conditioning: Effects on startle modulation and evaluative self‐reports

A basic feature of human evaluative conditioning is that the reported acquired valence of a previously neutral conditioned stimulus (CS) that has been paired with a valenced unconditioned stimulus (US), is resistant to extinction. The present study investigated whether startle modulation, sometimes presented as an index of acquired valence, reflected this basic feature. In a differential fear conditioning paradigm (n = 38) with an electrocutaneous stimulus as the US, a strong extinction manipulation was conducted by removing the US-electrodes and by extended extinction trials. At the end of extinction, the results corroborated previous findings of evaluative conditioning in that the reported valence for CS+ was still more negative than for CS-, despite disappearance of the differential skin conductance responses. However, startle modulation did not show resistance-to-extinction. Results were discussed in terms of recent conceptualizations of extinction.

Intralimbic evoked potentials during the formation of an alimentary conditioned reflex in response to the electrostimulation of the hippocampus of dogs.

Instrumental alimentary conditioned reflexes (CR) in response to the electrostimulation of the hippocampus were developed in experiments on dogs with electrodes implanted in various divisions of the hippocampus, the amygdala, the septum, and the hypothalamus. During their development the evoked potentials (EP) were investigated in the hippocampus itself and in other limbic structures, as well as in the hippocampus during the testing of the latter for the purpose of verifying generalization. The formation and extinction of the CR was accompanied by changes in the amplitude-temporal characteristics primarily of late components of the EP picked up from the lateral hypothalamus and the amygdaloid complex in response to the hippocampal electrostimulation. During the carrying out of this stimulation of signal functions (pedal pressing to obtain food), the average amplitude of the trace positivity and of the late negative wave were found to be lower than by the end of extinction in the presence of ineffectiveness of the signal. The average amplitudes of the late components of the hippocampal EP which arose in response to electrostimulation of the amygdala were lower in those tests in which the instrumental movement appeared when the generalization of the CR was tested.

Effects of self-generated rules on the development of schedule-controlled behavior.

College students responded under a multiple differential-reinforcement-of-low-rate 5-s fixed-ratio 8 schedule, with components alternating every 2 min. After 40 programmed minutes of acquisition and 12 min of maintenance, without notice, both schedules changed to extinction for 28 min. During acquisition, between alternations of the multiple schedule, some subjects were asked to develop rules describing the schedule contingencies. Other subjects were given these same rules between alternations, and a third group neither received nor were asked to develop rules. By the end of the acquisition phase, self-generated-rule subjects were more likely to show schedule-typical behavior than were subjects not asked to generate rules. The behavior of those given rules was similar to those asked to generate rules at the end of acquisition, but yoked-rule subjects acquired schedule-typical behavior at a quicker rate. By the end of extinction, during the period corresponding to the previous fixed-ratio interval, all no-rule subjects who had earned points during acquisition and maintenance were responding at a rate of less than 30 responses per minute. Only 3 of the 9 self-generated-rule subjects and 2 of the 5 yoked-rule subjects were similarly responding at this low rate. Results suggest that asking subjects to develop self-rules facilitates acquisition, but can retard extinction. Results also suggest that self-generated rules function similarly to external rules.

Peripheral noradrenaline depletion does not impair extinction of food-rewarded running in the rat

To test whether the sympathetic nervous system influences the inhibition of non-rewarded running in the runway, we examined the effects of peripheral noradrenaline depletion, induced by 6-hydroxydopamine (6-OHDA HBr, 30 mg/kg, i.p.), on extinction of food-rewarded running in rats. This was done in two separate experiments. In the first, in which the inter-trial interval (ITI) was one day and rats were injected before acquisition, running times at the end of extinction did not differ. The 6-OHDA appeared to slow down running times at the end of acquisition and the start of extinction. In the second experiment (15 s ITI) therefore, rats were injected after stable running had been acquired; there was no effect on running in subsequent rewarded trials. In extinction, although the groups ran similarly at first, the 6-OHDA treated animals subsequently ran more slowly than the controls; that is they showed greater extinction. Taken together with other published evidence, the sympathetic nervous system does not appear to contribute to the extinction of continuously reinforced responses.

Acquisition, extinction, and reacquisition of a conditional discrimination to avoid shock by goldfish

Goldfish, trained in the shuttlebox to avoid shock, were tested for the acquisition and extinction of a color-matching or a color-oddity conditional discrimination choice response, and then tested for reacquisition. Extinction affected the accuracy of the choice response but not the number of trials with response (response strength). Half of all groups were extinguished with changed signal colors, and half had the same signal colors experienced in acquisition. All groups had the same signal colors in reacquisition that they had experienced in acquisition. Changed-signal oddity groups decremented slightly faster than same-signal oddity groups, providing some support for a generalization decrement interpretation, but same- and changed-signal matching groups did not differ. All groups extinguished on the choice response by the end of extinction. All matching groups, and all oddity groups, regardless of their respective signal colors in extinction, reacquired at the same rate, and faster than in acquisition. These results imply conceptual generalization of extinction effects. Matching-trained groups were found to be slightly superior to oddity-trained groups in both acquisition and reacquisition. Comparisons of these results to positive reinforcement conditional discrimination extinction work, including some procedural suggestions, are made.

Negative S- contrast with minimally contingent large reward as a function of trial initiation procedure

Three groups of 12 rats received acquisition trials in an alley to a one-pellet reward (G-) followed by extinction trials. Acquisition trials were interspersed with other, “G+,” reward trials in which Ss were placed on a feeding surface holding 12 pellets (Groups S12 and C12) or one pellet (Group S1). On G+ trials, Group C12 Ss were taken directly to the feeding surface from their home cages, whereas Group S12 and S1 Ss were placed into the alley startbox and then removed to the feeding surface. Group S12, but not C12, displayed a strong depression of response speed in S-during acquisition. All three groups differed in start speeds by the end of extinction with C12 the fastest and S12 the slowest.