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Climate change, species-area curves and the extinction crisis.

An article published in the journal Nature in January 2004-in which an international team of biologists predicted that climate change would, by 2050, doom 15-37% of the earth's species to extinction-attracted unprecedented, worldwide media attention. The predictions conflict with the conventional wisdom that habitat change and modification are the most important causes of current and future extinctions. The new extinction projections come from applying a well-known ecological pattern, the species-area relationship (SAR), to data on the current distributions and climatic requirements of 1103 species. Here, I examine the scientific basis to the claims made in the Nature article. I first highlight the potential and pitfalls of using the SAR to predict extinctions in general. I then consider the additional complications that arise when applying SAR methods specifically to climate change. I assess the extent to which these issues call into question predictions of extinctions from climate change relative to other human impacts, and highlight a danger that conservation resources will be directed away from attempts to slow and mitigate the continuing effects of habitat destruction and degradation, particularly in the tropics. I suggest that the most useful contributions of ecologists over the coming decades will be in partitioning likely extinctions among interacting causes and identifying the practical means to slow the rate of species loss.

Animals↗

Early onset of secondary extinctions in ecological communities following the loss of top predators.

The large vulnerability of top predators to human-induced disturbances on ecosystems is a matter of growing concern. Because top predators often exert strong influence on their prey populations their extinction can have far-reaching consequences for the structure and functioning of ecosystems. It has, for example, been observed that the local loss of a predator can trigger a cascade of secondary extinctions. However, the time lags involved in such secondary extinctions remain unexplored. Here we show that the loss of a top predator leads to a significantly earlier onset of secondary extinctions in model communities than does the loss of a species from other trophic levels. Moreover, in most cases time to secondary extinction increases with increasing species richness. If local secondary extinctions occur early they are less likely to be balanced by immigration of species from local communities nearby. The implications of these results for community persistence and conservation priorities are discussed.

Animals↗

Assessing the causes of late Pleistocene extinctions on the continents.

One of the great debates about extinction is whether humans or climatic change caused the demise of the Pleistocene megafauna. Evidence from paleontology, climatology, archaeology, and ecology now supports the idea that humans contributed to extinction on some continents, but human hunting was not solely responsible for the pattern of extinction everywhere. Instead, evidence suggests that the intersection of human impacts with pronounced climatic change drove the precise timing and geography of extinction in the Northern Hemisphere. The story from the Southern Hemisphere is still unfolding. New evidence from Australia supports the view that humans helped cause extinctions there, but the correlation with climate is weak or contested. Firmer chronologies, more realistic ecological models, and regional paleoecological insights still are needed to understand details of the worldwide extinction pattern and the population dynamics of the species involved.

Animals↗

Selectivity of end-Cretaceous marine bivalve extinctions.

Analyses of the end-Cretaceous or Cretaceous-Tertiary mass extinction show no selectivity of marine bivalve genera by life position (burrowing versus exposed), body size, bathymetric position on the continental shelf, or relative breadth of bathymetric range. Deposit-feeders as a group have significantly lower extinction intensities than suspension-feeders, but this pattern is due entirely to low extinction in two groups (Nuculoida and Lucinoidea), which suggests that survivorship was not simply linked to feeding mode. Geographically widespread genera have significantly lower extinction intensities than narrowly distributed genera. These results corroborate earlier work suggesting that some biotic factors that enhance survivorship during times of lesser extinction intensities are ineffectual during mass extinctions.

Animals↗

Experimental studies of extinction dynamics

Extinction of populations occurs naturally, but global extinction rates are accelerating, making understanding extinction a high priority for conservation. Extinction in experimental populations of brine shrimp (Artemia franciscana) was measured to assess hypothesized extinction processes. Greater initial population size, greater maximum population size supported by the environment, and lower variation in environmental conditions reduced the likelihood of extinction, as hypothesized. However, initial population size was less important, and maximum population size and environmental variation were more important than often hypothesized. Unexpectedly, deterministic oscillations in population size due to inherent nonlinear dynamics and overcrowding were as important or more important than hypothesized processes.

Journal Article↗

Extinction of prolactin gene expression in somatic cell hybrids is correlated with the repression of the pituitary-specific trans-activator GHF-1/Pit-1.

The tissue-specific expression of the PRL and GH genes is dependent on the presence of a pituitary-specific trans-activator, GHF-1/Pit-1. Previous studies indicate that somatic cell hybridization of rat pituitary GH3 cells with LB82 mouse fibroblasts frequently results in the extinction of GH and PRL expression. The extinction of the GH gene occurs at the transcriptional level, and is accompanied by repression of GHF-1/Pit-1 synthesis. To elucidate the mechanism of PRL extinction we further characterized these same somatic cell hybrid lines as well as the parental GH3 and LB82 cells. The pattern of PRL extinction and reexpression paralleled that of GH in the three hybrid lines that were examined. Two of these lines extinguished both GH and PRL synthesis, while a third displayed reexpression of both genes, apparently due to the loss of mouse chromosomal material. These studies revealed that the extinction of PRL expression in these hybrid lines occurs at the level of mRNA accumulation and is strongly correlated with the loss of GHF-1/Pit-1 mRNA and protein synthesis. These data suggest that in pituitary x fibroblast hybrids repression of the trans-activator GHF-1/Pit-1 is a primary mechanism for the extinction of PRL and GH gene expression.

Animals↗

Aerosol extinction models based on measurements at two sites in Sweden.

Two aerosol extinction models have been developed using statistical analysis of long-term optical transmission measurements in Sweden performed at two locations from July 1977 to June 1982. The aerosol volume extinction coefficient for infrared (IR) radiation is calculated by the models with visibility, temperature, and air pressure as input parameters. As in the MODTRAN model, the IR extinction coefficient is proportional to the coefficient at 550 nm, which depends on the visibility. In the new models, the wavelength dependence of the extinction also depends on the visibility. The models predict significantly higher attenuation in the IR than does the Rural aerosol model from MODTRAN, which is commonly used. Comparison with the Maritime model shows that the new models predict lower extinction values in the 3-5 microm region and higher values in the 8-12 microm region. The uncertainties in terms of variance levels are calculated by the models. The properties of aerosols, and thereby the extinction coefficient, are partly correlated to local meteorological parameters, which enables the calculation of a mean predicted value. A substantial part of the variation is, however, caused by conditions in the source area and along the trajectory path of the aerosols. They are not correlated to the local meteorological parameters and therefore cause the variance in the models.

Journal Article↗

De-extinction technology and its application to conservation.

De-extinction, once the realm of science fiction, has evolved into a tangible scientific endeavor thanks to breakthroughs in genome sequencing, engineering, advanced assisted reproductive technologies, and stem cell biology. Alongside this work are innovations in reintroduction science and artificial intelligence, which are refining strategies for species translocations, rewilding, and long-term ecosystem monitoring of de-extinct species and populations. While the primary motivation for de-extinction is restoring lost ecological functions to eroded ecosystems, each of these technologies can also be applied to conservation biology for de-endangerment, offering new solutions for biodiversity preservation. This review synthesizes the technological advancements emerging from de-extinction science and explores their broad applications in conservation, demonstrating how de-extinction is both about resurrecting lost species and about expanding the conservation toolkit to sustain and rebuild biodiversity in the face of accelerating environmental change.

Conservation of Natural Resources↗

PUS7-dependent Ψ reshapes specific synaptic gene exons to facilitate fear extinction memory formation.

RNA modifications serve as dynamic regulators of neural plasticity through their ability to fine-tune transcript stability and splicing. Pseudouridine (Ψ), an evolutionarily conserved RNA modification catalyzed by pseudouridine synthases, plays established roles in neurodevelopment, yet its functional significance in activity-dependent behavioral adaptation remains poorly defined. Here, we investigate Ψ-mediated epitranscriptomic regulation within the infralimbic prefrontal cortex (ILPFC), a brain region requiring precise synaptic remodeling for the clinically relevant form of fear extinction memory. Combining transcriptome-wide pseudouridylation profiling with behavioral analysis in mice, we identified selective Ψ enrichment at exons of synaptic regulatory genes within ILPFC during fear extinction learning. Fear extinction in the ILPFC drives concomitant exonic Ψ deposition and upregulation of synaptogenic transcripts, processes that involve pseudouridine synthase PUS7. Crucially, PUS7 knockdown in the ILPFC selectively impaired fear extinction memory formation without altering baseline fear expression, establishing a causal link between Ψ-dependent RNA processing and activity-dependent synaptic structural remodeling in this microcircuit. Our findings demonstrate that PUS7-mediated Ψ modification spatiotemporally regulates activity-dependent RNA dynamics in the ILPFC, providing the evidence that epitranscriptomic mechanisms precisely coordinate synaptic gene expression within behaviorally defined brain sub-region. This work bridges molecular RNA biology with systems neuroscience, revealing a novel mechanism for activity-dependent regulation of fear extinction in ILPFC.

Animals↗

Exposure to estradiol before but not during acquisition of LiCl-induced conditioned taste avoidance accelerates extinction.

Estradiol accelerates extinction of LiCl-induced conditioned taste avoidance when it is present continuously before and during acquisition. We have suggested that the effect of estradiol on extinction is due to its illness-associated, rather than learning-associated, properties. If this were the case, then one would expect estradiol to act before but not during acquisition. This expectation is based on previous work showing attenuation of learned taste avoidance when rats are given distal preexposure (greater than 24 h before conditioning) or proximal preexposure (less than 24 h before conditioning) to the illness-inducing agent LiCl before acquisition of a LiCl-induced conditioned taste avoidance. In three separate experiments, estradiol was administered during three different time periods via subcutaneous implantation of a 10-mm estradiol-filled capsule. In each experiment, the extinction of estradiol-treated females was compared to that of females implanted with empty capsules. In the first experiment, female rats were given distal exposure to estradiol before acquisition. Capsules were implanted 11 days before acquisition and were removed 2 days before acquisition. In the second experiment, female rats were given proximal exposure to estradiol before acquisition. Capsules were implanted 2.5 h before LiCl was paired with a sucrose solution and were removed 16.5 h later. In the third experiment, female rats were given exposure to estradiol during acquisition. Capsules were implanted at the same time as LiCl administration and were removed 18 h later. The only estradiol-treated females to show accelerated extinction were those given distal preexposure to estradiol in Experiment 1. These data do not support a learning-associated hypothesis and only partially support an illness-associated hypothesis. The failure to find accelerated extinction following proximal preexposure may reflect an inappropriate choice of the parameters used in the experiment or a difference in the stimulus properties of LiCl and estradiol that allow each to serve as conditioning and preexposure agents in conditioned taste avoidance paradigms [corrected].

Animals↗

Extinction of conditioned odor potentiation of startle.

Several recent studies with rats (Sprague-Dawley strain) have documented that an odor previously paired with shock potentiates the acoustic startle response, a phenomenon referred to as conditioned odor potentiation of startle (OPS). A surprising finding in these studies was that OPS did not extinguish even though the odor was present throughout the 25-min test session. Therefore, the present study more fully examined extinction of OPS. The results of Experiment 1, which employed both within-subject and between-group comparisons, showed that extinction of OPS occurred in adult rats only after several days of testing. Experiment 2 used the between-group procedure and found similar results with 23-day-old rats, the youngest age that exhibits the OPS effect. Experiment 2 also showed that giving rats 15 odor-shock pairings at 16 days of age, an age where they acquire the odor-shock association but cannot express it via OPS, does not increase subsequent resistance to extinction following odor-shock pairings at 23 days of age. Taken together, the results of this study show that (1) although OPS is somewhat resistant to extinction, it does extinguish with repeated tests and (2) suggests that there are no age differences in the rate of extinction of OPS.

Animals↗

Conditioned behavioural responses to apomorphine: extinction and haloperidol-induced inhibition.

In previous studies it was established that stereotypies (sniffing, licking, gnawing) produced by apomorphine can be conditioned and after repeated pairings with defined conditioned stimuli (auditory, tactile + olfactory) these stereotypies can be observed in the presence of the conditioned stimuli alone. In the present experiments, the extinction of these conditioned stereotypies was studied in one series; in another series, the possible inhibition of conditioned stereotypies by the blocker of dopamine receptors, haloperidol, was measured. The rats were conditioned (or the controls pseudoconditioned, respectively) for either 3 or 10 days with 2.0 mg/kg s.c. apomorphine or 6 days with 0.5 mg/kg s.c. of the drug and by placing them into particular cages in the presence of an auditory and an olfactory stimulus. Under all these conditions, episodes of conditioned stereotypies were observed, when solvent + conditioned stimuli instead of apomorphine was applied 1 day after the last conditioning session (first session of extinction). The conditioned responses seemed to be on the highest level after conditioning with 2.0 mg/kg apomorphine 3 days, lower after conditioning with the same dose on 10 days, and even lower after conditioning for 6 days with 0.5 mg/kg. Under all these conditions, the stereotypies summed up and averaged for the total observation period of 60 min rapidly decreased during the extinction period, so that on day 4 of the extinction period, no further significant differences between conditioned and pseudoconditioned animals were observed, although a short initial period was still observed on the fourth day. On day 3 of extinction, not only an early, but also a late episode of conditioned stereotypies was manifest, interrupted by an almost silent period. The acute (unconditioned) stereotypies produced by 0.5 mg/kg s.c. apomorphine were almost completely suppressed by pretreatment with 0.1 mg/kg i.p. haloperidol. In contrast, the same dose of haloperidol produced a much less pronounced inhibition of conditioned stereotypies after conditioning with the same dose of apomorphine for 6 times. These results, together with previous findings, suggest that the conditioned behavioural effects are not due to an activation of dopaminergic mechanisms during conditioning with apomorphine.

Animals↗

Different effects of haloperidol and extinction on instrumental behaviours.

The effects of 0.1 mg/kg haloperidol (HP) and extinction following FR20 training in rats were compared. Animals under extinction responded at higher rates at the beginning of the session than rats treated with HP, but slower than HP-treated animals at the end of the session. Extinction subjects also emitted proportionately more ratios that were faster than the previous baseline response rate when compared to HP subjects. In a second experiment, animals were reinforced under an FI30-s schedule for merely being on one floor panel of a chamber which also measured locomotor activity. Comparison of the effects of 0.4 mg/kg HP and extinction revealed that both manipulations reduced locomotor activity, while only extinction reduced time on the reinforced panel. The results of these experiments were viewed as contrary to the hypothesis that dopamine antagonist drugs reduce the primary reinforcing impact of food. However, they were seen as consistent with the notion that HP reduced incentive-related motor activity.

Animals↗

Sensory extinction: a procedure form eliminating self-stimulatory behavior in developmentally disabled children.

This study was designed to investigate the role of sensory reinforcement in the motivation of self-stimulation. If self-stimulatory behavior is maintained by its sensory consequences, such as the proprioceptive, auditory, or visual stimulation it produces, then such behavior should extinguish when those sensory consequences are not permitted. The present study introduces a new procedure, Sensory Extinction, in which certain sensory consequences are masked or removed, to examine whether self-stimulation is operant behavior maintained by sensory reinforcement. The effectiveness of Sensory Extinction was assessed by a reversal design for each of three autistic children, and the results showed the following. First, self-stimulation reliably extinguished when a certain sensory consequence was removed, then increased when that consequence was permitted. This was replicable within and across children. Second, different Sensory Extinction procedures were required for different self-stimulatory behaviors, since the sensory reinforcers supporting them were idiosyncratic across children. Finally, regarding clinical gains, the data suggest that Sensory Extinction may be a relatively convenient and rapid alternative for the treatment of self-stimulation. The present findings extend the efficacy of extinction as a behavior-modification technique to instances in which the reinforcer is purely sensory. The implications of these results for the treatment of other forms of deviant behavior are discussed.

Autistic Disorder↗

Extinction and reacquisition of differential responding in rats trained to discriminate between chlordiazepoxide and saline.

In order to assess the resistance of drug discriminative responding to prolonged reinforcement omission, rats were trained to discriminate between either 6.0 mg/kg PO or 30.0 mg/kg PO. CDP and saline, using a food reinforced (V140-FR10) operant procedure. Dose generalization tests were conducted for both groups. Sessions were then run without reinforcement while drug (D) and saline (S) administrations were continued (extinction phase). After a maximum of 30 sessions without reinforcement, or when the rats emitted less than ten responses on either lever during three successive sessions (extinction criterion), reinforcement was reinstated. Finally, additional dose generalization tests with CDP were run. The discriminative responding controlled by the D and S administrations was not affected significantly by prolonged reinforcement omission in either group. For both groups, response rates were decreased and latencies to initiate responding were increased during the extinction phase. Response rate reduction occurred more rapidly for the drug condition in the high training dose group. This group also reached the extinction criterion sooner than the low training dose group. The reacquisition process occurred very rapidly. Response rates increased substantially after the first reinforcement had been obtained. After ten reacquisition sessions, response rates and latencies had reached values similar to those observed before extinction was initiated. Data revealed no differences between groups and the course of reacquisition did not differ between the S and D conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cocaine- but not food-seeking behavior is reinstated by stress after extinction.

Reinstatement of drug-seeking behavior after extinction constitutes a potential animal model of relapse to drug abuse. In a typical reinstatement experiment, previously drug-trained rats undergo extinction during which responding is no longer followed by drug delivery. After significant extinction is observed, rats are then exposed to an event expected to reinstate drug-seeking behavior. Using this procedure, it has been recently reported that footshock stress leads to reinstatement of drug-seeking in heroin-trained, presently drug-free rats. The purpose of the present study was to assess the generality of this effect of stress. Here we report that 15 min of intermittent footshock (0.86 mA; 0.5 s on, with a mean off period of 40 s) reinstated selectively cocaine-seeking behavior after 14 extinction sessions (rats were previously trained on a FR1 TO 20 s to obtain cocaine at a dose of 0.25 mg/infusion). In contrast, under similar experimental conditions, the same stressor did not reinstate food-seeking in food-trained rats after seven extinction sessions (rats were previously trained on a FR1 TO 20 s to obtain six food pellets). Rather, when the basal level of responding was sufficiently high, footshock stress induced a significant suppression of the instrumental performance. These data are discussed in light of several behavioral mechanisms which may explain the specificity of stress in reinstating drug-seeking behavior and not food-seeking behavior.

Animals↗

Extinction of ethanol-induced conditioned place preference and conditioned place aversion: effects of naloxone.

Four experiments examined the effect of naloxone pretreatment on the expression and extinction of ethanol-induced conditioned place preference (experiments 1, 2, 4) or conditioned place aversion (experiments 1, 3). DBA/2 J mice received four pairings of a distinctive tactile (floor) stimulus (CS) with injection of ethanol (2 g/kg) given either immediately before or after 5-min exposure to the CS. A different stimulus was paired with injection of saline. Pre-CS injection of ethanol produced conditioned place preference, whereas post-CS injection of ethanol produced conditioned place aversion. Both behaviors extinguished partially during repeated choice testing after vehicle injection. Naloxone (10 mg/kg) had little effect on the initial expression of conditioned place preference, but facilitated its extinction. Moreover, repeated naloxone testing resulted in the expression of a weak conditioned place aversion to the CS that initially elicited a place preference. In contrast, naloxone (1.5 or 10 mg/kg) enhanced expression of conditioned place aversion, thereby increasing its resistance to extinction. A control experiment (experiment 4) indicated that repeated testing with a different aversive drug, lithium chloride, did not affect rate of extinction or produce an aversion to the CS previously paired with ethanol. These findings do not support the suggestion that naloxone facilitates the general processes that underlie extinction of associative learning. Also, these data are not readily explained by the conditioning of place aversion at the time of testing. Rather, naloxone's effects appear to reflect a selective influence on maintenance of ethanol's conditioned rewarding effect, an effect that may be mediated by release of endogenous opioids. Overall, these findings encourage further consideration of the use of opiate antagonists in the treatment of alcoholism.

Alcohol Deterrents↗

Time-dependent changes in extinction behavior and stress-induced reinstatement of drug seeking following withdrawal from heroin in rats.

RATIONALE AND OBJECTIVES: Footshock stress reliably reinstates heroin seeking in rats, but the time course of the development of this effect following drug withdrawal is not known. Here we studied the effect of intermittent footshock stress on reinstatement of heroin seeking following different withdrawal periods (1-66 days). We also studied whether changes in corticotropin-releasing factor (CRF) mRNA in the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST) are correlated with this reinstatement after 1 day and 6 days of heroin withdrawal. METHODS: Rats were trained to self-administer heroin (9 h/day; 0.1 mg/kg per infusion) for 10 days. Tests for extinction behavior and footshock-induced reinstatement of heroin seeking were then conducted after 1, 6, 12, 25, or 66 days of heroin withdrawal. On the test day, rats were given five to ten 60-min extinction sessions until they reached the extinction criterion of less than 15 responses per 60 min on the lever previously associated with heroin. Rats were then exposed to intermittent foot-shock (0.8 mA; 10 min), and lever-pressing behavior was recorded for 120 min. RESULTS: Reinstatement of lever-pressing behavior by footshock followed an inverted U-shaped curve with maximal responding after 6 days and 12 days of heroin withdrawal. Surprisingly, foot-shock did not reinstate lever-pressing behavior on day 1 of withdrawal. Lever pressing during extinction, prior to exposure to footshock, also followed an inverted U-shaped curve, with higher responding after 6, 12, and 25 days of heroin withdrawal. Finally, compared with control groups not exposed to shock, CRF mRNA levels in response to footshock were increased in the CeA (day 1 of withdrawal) and the dorsal BNST (day 1 and day 6), but not in the ventral BNST. CONCLUSIONS: The duration of the heroin withdrawal period is an important factor in the manifestation of (1) footshock stress-induced reinstatement of heroin seeking and (2) extinction of the heroin-reinforced behavior. Finally, the time-dependent changes in footshock stress-induced reinstatement following withdrawal from heroin were not correlated with alterations in CRF mRNA in the CeA and BNST.

Animals↗