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Mammalian extinctions in the late Pleistocene of northern Eurasia and North America.

The 'mass extinctions' at the end of the Pleistocene were unique, both in the Pleistocene and earlier in the geological record, in that the species lost were nearly all large terrestrial mammals. Although a global phenomenon, late Pleistocene extinctions were most severe in North America, South America and Australia, and moderate in northern Eurasia (Europe plus Soviet Asia). In Africa, where nearly all of the late Pleistocene 'megafauna' survives to the present day, losses were slight. Ruling out epidemic disease or cosmic catastrophe, the contending hypotheses to explain late Pleistocene extinctions are: (a) failure to adapt to climatic/environmental change; and (b) extermination by human hunters ('prehistoric overkill'). This review focuses on extinctions in northern Eurasia (mainly Europe) in comparison with North America. In addition to reviewing the faunal evidence, the highly relevant environmental and archaeological backgrounds are summarized. The latest survival dates of extinct species are estimated from stratigraphic occurrences of fossil remains, radiocarbon dates, or association with archaeological industries. The Middle and Upper Pleistocene (ca. 700,000-10,000 BP) in northern Eurasia and North America was a time of constantly changing climate, ranging from phases of extensive glaciation in cold stages, to temperate periods (interglacials). In the Lateglacial (ca. 15,000-10,000 BP), during which most extinctions occurred, there was a major reorganization of vegetation, mainly involving the replacement of open vegetation by forests. These changes were more profound than earlier in the Last Cold Stage, but similar in nature to vegetational changes that took place at previous cold stage/interglacial transitions. The archaeological record shows that humans have been present in Europe since the early Middle Pleistocene. The arrival in Europe ca. 35,000 BP of 'anatomically modern humans', with their technologically more advanced upper palaeolithic industries, was a 'quantum leap' in human history. Extinctions occurred throughout the European Pleistocene, but until the late Pleistocene most losses were replaced by the evolution or immigration of new species, and most of those lost without replacement were small mammals. In marked contrast, extinctions without replacement in the late Pleistocene were almost entirely confined to the largest mammals (greater than 1000 kg) and some medium-large species (100-1000 kg).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Mutagenesis versus inhibition in the efficiency of extinction of foot-and-mouth disease virus.

RNA viruses replicate near the error threshold for maintenance of genetic information, and an increase in mutation frequency during replication may drive RNA viruses to extinction in a process termed lethal mutagenesis. This report addresses the efficiency of extinction (versus escape from extinction) of foot-and-mouth disease virus (FMDV) by combinations of the mutagenic base analog 5-fluorouracil (FU) and the antiviral inhibitors guanidine hydrochloride (G) and heparin (H). Selection of G- or H-resistant, extinction-escape mutants occurred with low-fitness virus only in the absence of FU and with high-fitness virus with some mutagen-inhibitor combinations tested. The combination of FU, G, and H prevented selection of extinction-escape mutants in all cases examined, and extinction of high-fitness FMDV could not be achieved by equivalent inhibitory activity exerted by the nonmutagenic agents. The G-resistant phenotype was mapped in nonstructural protein 2C by introducing the relevant mutations in infectious cDNA clones. Decreases in FMDV infectivity were accompanied by modest decreases in the intracellular and extracellular levels of FMDV RNA, maximal intracellular concentrations of FU triphosphate, and a decrease in the intracellular concentrations of UTP. In addition to indicating a key participation of mutagenesis in virus extinction, the results suggest that picornaviruses provide versatile experimental systems to approach the problem of extinction failure associated with inhibitor-escape mutants during treatments based on enhanced mutagenesis.

Animals↗

Density-dependent demographic variation determines extinction rate of experimental populations.

Understanding population extinctions is a chief goal of ecological theory. While stochastic theories of population growth are commonly used to forecast extinction, models used for prediction have not been adequately tested with experimental data. In a previously published experiment, variation in available food was experimentally manipulated in 281 laboratory populations of Daphnia magna to test hypothesized effects of environmental variation on population persistence. Here, half of those data were used to select and fit a stochastic model of population growth to predict extinctions of populations in the other half. When density-dependent demographic stochasticity was detected and incorporated in simple stochastic models, rates of population extinction were accurately predicted or only slightly biased. However, when density-dependent demographic stochasticity was not accounted for, as is usual when forecasting extinction of threatened and endangered species, predicted extinction rates were severely biased. Thus, an experimental demonstration shows that reliable estimates of extinction risk may be obtained for populations in variable environments if high-quality data are available for model selection and if density-dependent demographic stochasticity is accounted for. These results suggest that further consideration of density-dependent demographic stochasticity is required if predicted extinction rates are to be relied upon for conservation planning.

Animals↗

Extinction times in experimental populations.

Predicting population extinctions is a key element of quantitative conservation biology and population ecology. Although stochastic population theories have long been used to obtain theoretical distributions of population extinction times, model-based predictions have rarely been tested. Here I report results from a quantitative analysis of extinction time in 281 experimental populations of water fleas (Daphnia magna) in variable environments. To my knowledge, this is the first quantitative estimate of the shape of the distribution of population extinction times based on extinction data for any species. The finding that the distribution of population extinction times was extraordinarily peaked is consistent with theoretical predictions for density-independent populations, but inconsistent with predictions for density-dependent populations. The tail of the extinction time distribution was not exponential. These results imply that our current theories of extinction are inadequate. Future work should focus on how demographic stochasticity scales with population size and effects of nonrandom variable environments on population growth and decline.

Animals↗

Resistance to extinction following variable-interval reinforcement: reinforcer rate and amount.

Rats obtained food-pellet reinforcers by nose poking a lighted key. Experiment 1 examined resistance to extinction following single-schedule training with different variable-interval schedules, ranging from a mean interval of 16 min to 0.25 min. That is, for each schedule, the rats received 20 consecutive daily baseline sessions and then a session of extinction (i.e., no reinforcers). Resistance to extinction (decline in response rate relative to baseline) was negatively related to the rate of reinforcers obtained during baseline, a relation analogous to the partial-reinforcement-extinction effect. A positive relation between these variables emerged, however, when the unit of extinction was taken as the mean interreinforcer interval that had been in effect during training (i.e., as an omitted reinforcer during extinction). In a second experiment, rats received blocks of training sessions, all with the same variable-interval schedule but with a reinforcer of four pellets for some blocks and one pellet for others. Resistance to extinction was greater following training with the larger (four pellets) than with the smaller (one pellet) reinforcer. Taken together, these results support the principle that greater reinforcement during training (e.g., higher rate or larger amount) engenders greater resistance to extinction even when the different conditions of reinforcement are varied between blocks of sessions.

Animals↗

Extinction of fear-potentiated startle: blockade by infusion of an NMDA antagonist into the amygdala.

Data derived from in vitro preparations indicate that NMDA receptors play a critical role in synaptic plasticity in the CNS. More recently, in vivo pharmacological manipulations have suggested that an NMDA-dependent process may be involved in specific forms of behavioral plasticity. All of the work thus far has focused on the possible role of NMDA receptors in the acquisition of responses. However, there are many examples in the behavioral literature of learning-induced changes that involve the reduction or elimination of a previously acquired response. Experimental extinction is a primary example of the elimination of a learned response. Experimental extinction is well described in the behavioral literature, but has not received the same attention in the neurobiological literature. As a result, the neural mechanisms that underlie this important form of learning are not at all understood. In the present experiments, the fear-potentiated startle paradigm was employed to begin to investigate neural mechanisms of extinction. The results show that infusion of the NMDA antagonist D,L-2-amino-5-phosphonovaleric acid (AP5) into the amygdala, a limbic structure known to be important for fear conditioning, dose-dependently blocked extinction of conditioned fear. Control experiments showed that the blockade of extinction was neither the result of the permanent disruption of amygdaloid function nor the result of decreased sensitivity of the animals to the conditioned stimulus. Infusion of AP5 into the interpositus nucleus of the cerebellum, a control site, did not block extinction. Finally, intra-amygdala infusion of a selected dose of the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione did not block extinction of conditioned fear. These results, together with a previous report from our laboratory (Miserendino et al., 1990), demonstrate the importance of the amygdala in the elaboration of conditioned fear and suggest that an NMDA-dependent process might underlie the extinction of conditioned fear.

2-Amino-5-phosphonovalerate↗

The influence of limb crossing on left tactile extinction.

BACKGROUND: Previous research on patients with left tactile extinction has shown that crossing of hands, so that each hand is on the opposite side of the body midline relative to the other, improves detection of stimuli given to the left hand. OBJECTIVES: To study the influence of the spatial position of limbs on left tactile extinction, and its relations with left visual neglect. METHODS: Normal participants and patients with right cerebral hemisphere damage and left tactile extinction were asked to detect single or double light touch stimuli applied to their cheeks, hands, or knees with their arm and legs either in anatomical or in crossed position, increasing the attentional load of the task. RESULTS: In patients with left extinction, limb crossing caused a deterioration in performance for stimuli applied to right body parts, with only a tendency to an improvement in detection for left body parts (only two of 24 patients showed substantial (>20%) improvement in left extinction after limb crossing). After crossing, left limb detections of double stimuli decreased with increasing degrees of visual neglect. CONCLUSIONS: In conditions of high attentional load, limb crossing may impair tactile detection in most patients with left extinction, and particularly in those showing signs of left visual neglect. These results underline the importance of general attentional capacity in determining tactile extinction. Attentional and somatotopic mechanisms of extinction may assume different weights in different patients.

Aged↗

The effects of haloperidol on the partial reinforcement extinction effect (PREE): implications for neuroleptic drug action on reinforcement and nonreinforcement.

The effects of haloperidol 0.1 mg/kg on the partial reinforcement extinction effect (PREE) paradigm 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 quasi-random 50% schedule. All animals were then tested in extinction. Haloperidol 0.1 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 of partially reinforced as compared to continuously reinforced animals, was obtained in all four drug conditions. The administration of haloperidol in acquisition increased markedly resistance to extinction in CRF animals. The administration of the drug in extinction decreased resistance to extinction in both CRF and PRF animals. The results are explained in terms of two independent actions of haloperidol: the well-known effect of reduction in the effectiveness of reinforcement as well as enhancement of the effectiveness of nonreinforcement.

Animals↗

The effects of intrahippocampal ibotenate on resistance to extinction after continuous or partial reinforcement.

Intracerebral injections of ibotenate were used to produce, in rats, extensive cell loss in the hippocampus and dentate gyrus (complete hippocampal, CH), in the CH plus subiculum (SUB + CH), or in the subiculum plus entorhinal cortex (SUB + EC). These rats and sham-operated controls were trained to run in a straight alley for food reward delivered on a continuous (CR) or partial (PR) reinforcement schedule. In controls PR training gave rise to the well-known partial reinforcement extinction effect (PREE), i.e., greater resistance to extinction than that observed in CR-trained animals. Previous work had shown that large aspiration lesions of the hippocampal formation eliminate the PREE by increasing resistance to extinction in CR-trained animals and decreasing resistance to extinction in PR-trained animals. In the present experiments the PREE survived CH lesions, which increased resistance to extinction in both CR and PR training conditions; these effects were observed in the start and run (but not goal) sections of the alley. In contrast, subicular cell loss (in both SUB + CH and SUB + EC groups) abolished the PREE (but in the goal section only) by increasing resistance to extinction in the CR condition and decreasing resistance to extinction in the PR condition. In addition, some of the effects of PR training on start and run speeds during acquisition were altered by the CH and SUB + CH lesions. These results confirm previous data showing that the hippocampal formation plays a role in mediating the behavioural effects of PR training, but require modification of the model previously proposed to account for these data.

Animals↗

Hormonal influences of the extinction of conditioned taste aversion.

Conditioned taste aversion for a 5% glucose solution (sugar water) was induced in rats by an i.p. injection of LiCl 30 min after the first presentation of sugar water. Extinction of conditioned taste aversion was measured either in the forced-drinking test or in the preference-drinking test. In the forced-drinking test sugar water was the only fluid presented to the animals during extinction sessions. In the preference-drinking test the animals had the choice of tap water or sugar water. The rate of extinction was much slower in the preference test. The ACTH-analogues, ACTH 4-10 and ACTH 4-10 7d Phe, and alpha-MSH delayed extinction in the preference test but not extinction in the forced-drinking test. ACTH 11-24 was without any effect. MSH-release inhibiting factor (MIF) facilitated extinction in the forced-drinking test but did not alter extinction in the preference test. The peptides did not affect intake of tap water of preference of sugar water over tap water by control rats.

Adrenocorticotropic Hormone↗

Nicotine vs. ethanol discrimination: extinction and spontaneous recovery of responding.

Studies regarding extinction and spontaneous recovery of the discriminative stimulus effects of drugs are limited. Eight rats were initially trained to discriminate nicotine (0.4 mg/kg) vs. ethanol (800 mg/kg). For four rats, itraperitaneal (IP) administrations of nicotine fifteen minutes prior to fifteen-minute training sessions served as a discriminative stimulus (SD) for predicting food-reinforced lever pressing (VI-1 min). On other sessions ethanol functioned in predicting nonreinforcement (SA). The stimulus roles of the drugs were counterbalanced for the remaining four rats. SA and SD sessions alternated quasi-randomly with two daily sessions at 1000 and 1400 hours. Discriminative control was not disrupted following ten extinction sessions under a non-drug/saline condition, but was disrupted following extinction sessions under the original training drugs. Instances of spontaneous recovery (SR) occurred throughout extinction under the drug condtions. There was no evidence for SR two weeks following extinction, but partial recovery four weeks following the final extinction phase. Contextual status (context renewal) had neither a restorative or disruptive impact on extinguished or discriminated responding, respectively. These results support and extend the limited number of other studies by demonstrating extinction and spontaneous recovery of responding discriminated by two distinct drugs. Some theoretical interpretations regarding history effects and training in the context of drug discrimination are entertained.

Animals↗

Disruption of CB(1) receptor signaling impairs extinction of spatial memory in mice.

RATIONALE: A growing body of in vitro and in vivo evidence indicates that a central endocannabinoid system, consisting of CB(1) receptors and endogenous cannabinoids, modulates specific aspects of mnemonic processes. Previous research has demonstrated that either permanent or drug-induced disruption of CB(1) receptor signaling interferes with the extinction of a conditioned fear response. OBJECTIVES: In the present study, we evaluated whether the endocannabinoid system also plays a role in extinguishing learned escape behavior in a Morris water maze task. METHODS: CB(1) (-/-) mice and mice repeatedly treated with 3 mg/kg of the CB(1) receptor antagonist SR 141716 (Rimonabant) were trained to locate a hidden platform in the Morris water maze. Following acquisition, the platform was removed and subjects were assigned to either a massed (i.e., five consecutive sessions consisting of four 2-min trials/session) or a spaced (a single, 1-min trial every 2-4 weeks) extinction protocol. RESULTS: Strikingly, both 3 mg/kg SR 141716-treated mice and CB(1) (-/-) mice continued to return to the target location across all five trials in the spaced extinction procedure, while the control mice underwent extinction by the third or fourth trial. In contrast, both the 3-mg/kg SR 141716-treated and CB(1) (-/-) mice exhibited extinction in the massed extinction trial procedure. CONCLUSIONS: These findings indicate that disruption of CB(1) receptor signaling impairs extinction processes in the Morris water maze, thus lending further support to the hypothesis that the endocannabinoid system plays an integral role in the suppression of non-reinforced learned behaviors.

Animals↗

The cannabinoid receptor agonist WIN 55,212-2 facilitates the extinction of contextual fear memory and spatial memory in rats.

RATIONALE: Previous studies demonstrated that pharmacological blockade of CB1 cannabinoid receptors decreases the extinction of conditioned fear and spatial memory in rodents. However, the effects of CB1 cannabinoid receptor activation in this response remain unclear. OBJECTIVES: To evaluate the effects of the cannabinoid agonist WIN 55,212-2 (WIN) and the cannabinoid antagonist SR 147778 (SR) on the extinction of contextual fear memory in rats 24 h or 30 days after fear conditioning. METHODS: For fear conditioning, rats were placed in the conditioning chamber for 3 min and received a 1-s electric foot shock (1.5 mA). Retrieval testing consisted of a 3-min exposure to the conditioning chamber and extinction training consisted of successive 9-min exposures at 24-h intervals. Rats were also evaluated in the open field and water maze reversal task. RESULTS: The administration of SR (1.0 mg/kg, i.p.) and WIN (0.25 mg/kg, i.p.) before extinction training disrupted and facilitated, respectively, the extinction of 24 h contextual fear memory. These effects were not related to any disturbance in memory retrieval, unconditioned freezing expression, or locomotor activity. WIN (0.25 mg/kg, i.p.) also facilitated the extinction of 30-day-old contextual fear memory, while the prior administration of SR (0.2 mg/kg, i.p.) antagonized this response. The facilitative effect of WIN on memory extinction does not seem to be specific for contextual fear memory because it was also observed in the water maze reversal task. CONCLUSIONS: These results suggest cannabinoid receptor agonists as potential drugs to treat anxiety disorders related to the retrieval of aversive memories.

Animals↗

The role of serum testosterone in the accelerated extinction of a conditioned taste aversion in fluid deprived male rats.

Fluid deprivation decreases serum testosterone (T) levels and increases the rate of extinction of a conditioned taste aversion in Sprague-Dawley male rats. It has been suggested that the decreased serum levels may be the primary factor responsible for the accelerated extinction rates during fluid deprivation. To test the generality of this hypothesis, the effect of fluid deprivation on T levels and extinction rate was investigated in Fischer 344 male rats. Extinction rates were accelerated in Fischer 344 rats but T levels were not decreased. In a second study, the behavioral and hormonal responses of Fischer 344 and Sprague-Dawley males to fluid deprivation were compared. Extinction rates were increased in both strains of rat by fluid deprivation, but serum T levels were decreased in fluid-deprived Sprague-Dawley males and not Fischer 344 males. It was suggested that the accelerated extinction in fluid-deprived Sprague-Dawley males was primarily due to decreases in serum T levels, while the faster extinction in deprived Fisher 344 males could be accounted for by decreases in sensitivity to T.

Animals↗

Cognitive factors and CS-UCS interval effects in the differential conditioning and extinction of skin conductance responses.

Mandel and Bridger (1967) found resistance to extinction of differentially conditioned skin conductance responses by subjects, who, according to a post-conditioning questionnaire, believed pre-extinction instructions that the shock-UCS would no longer be administered. The present study was intended to: (1) determine whether or not an extraordinarily noxious shock-UCS is required to produce such results; (2) eliminate possible retrospective falsification effects associated with the use of a post-conditioning questionnaire by monitoring subjects' UCS expectancies continuously throughout extinction as well as acquisition trials; (3) attempt to confirm that resistance to extinction is stronger with a 0.5 sec CS-UCS interval than with an 8 sec interval; and (4) test several predictions regarding UCS expectancies during the intertrial intervals of acquisition. After receiving 16 instructed acquisition trials, two groups (N = 20 in each) exposed to either a 0.5 sec or 8 sec CS-UCS interval were fully instructed regarding discontinuation of the UCS during the pending 20 extinction trials. Reliable differential conditioning was obtained during the first extinction trial block for subjects who, according to the expectancy monitoring measure as well as a post-conditioning questionnaire, did not expect UCS administration. The extent of resistance to extinction did not differ between the two groups. Consistent with predictions from a cognitive viewpoint, the expectancy monitoring data of the two groups differed significantly during the intertrial intervals of acquisition.

Adolescent↗

Effects of post-session injections of anisomycin on the extinction of a spatial preference and on the acquisition of a spatial reversal preference.

Four experiments with C57BL/6 mice examined the effects of protein synthesis inhibition on extinction of spatial preferences in the Morris water maze. The protein synthesis inhibitor anisomycin was injected systemically immediately after spatial reversal sessions, which consisted of eight, two, or one reversal trials. Anisomycin had no effect on extinction of a spatial preference with eight reversal trials per session. When only two reversal trials were administered per session, anisomycin slowed extinction initially, although full extinction occurred with further training even in the presence of anisomycin. In both cases, anisomycin blocked acquisition of the reversal preference. When anisomycin injections followed a single simple extinction trial, performance was not disrupted. These findings suggest that acquisition and extinction may involve different molecular processes, and they do not support the idea that brief extinction trials induce a protein synthesis-dependent reconsolidation phase of spatial memory.

Animals↗

Return of fear in a human differential conditioning paradigm caused by a stimulus change after extinction.

In a human fear conditioning experiment, 32 participants were trained in a differential conditioning procedure with geometrical shapes as CS+ and CS- (four presentations each), and an electric shock as US. Measures of conditioned responding were skin conductance response (SCR) and retrospective US-expectancy ratings. For half of the participants (Generalization Group, GG), the subsequent extinction phase consisted of four nonreinforced presentations of generalization stimuli (GS+ and GS-). Participants from the Extinction control Group received an equal amount of nonreinforced presentations of the CSs. Finally, all participants were tested with the original CSs. The results from both measures clearly show an increase in the size of the discrimination upon the stimulus change after extinction in the GG. Because this pattern is not observed in the Extinction control Group, extinction performance appears to be somehow restricted to the perceptual characteristics of the extinction stimulus. Interestingly, the size of the conditioned SCR discrimination in the GG is not influenced by the stimulus change after acquisition. This observation points to a differential impact of stimulus change after acquisition vs. extinction treatment. The findings are discussed from the theoretical perspective of renewal and the clinical perspective of Return of Fear.

Analysis of Variance↗

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

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

Adolescent↗