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Comparative analyses of extinction risk routinely apply methods that account for phylogenetic non-independence, but few analyses of extinction risk have addressed the possibility of spatial non-independence. We explored patterns of extinction risk in Banksia, a plant genus largely endemic to Australia's southwest biodiversity hotspot, using methods to partition the variance in two response variables (threat status and range size) into phylogenetic, spatial, and independent components. We then estimated the effects of a number of biological and external predictors on extinction risk independently of phylogeny and space. The models explained up to 34.2% of the variation in range size and up to 9.7% of the variation in threat status, nearly all of which was accounted for by the predictors, not by phylogeny or space. In the case of Banksia, therefore, high extinction risk can be clearly linked with biological syndromes (such as a brief flowering period) or geographic indicators of human impact (such as extensive habitat loss), but cannot be predicted from phylogenetic relatedness or geographic proximity.
Fear extinction can be viewed as an inhibitory learning process. This is supported by post-extinction phenomena demonstrating the return of fear, such as reinstatement. Recent work has questioned this account, claiming that extinction initiated immediately after fear acquisition can abolish the return of fear. In the current study, participants were fear conditioned to four different conditioned stimuli (CS) and underwent extinction either immediately or after a 24 h delay. During extinction, we manipulated CS contingency awareness by presenting two of the CSs (one CS+, one CS-) under non-masked conditions and the other two CSs under masked conditions. Compared to delayed extinction, immediate extinction of non-masked CSs promoted less extinction of fear-potentiated startle and shock expectancy ratings and less reinstatement of fear-potentiated startle without affecting shock expectancy ratings. Critically, future research should clarify how the differences between immediate and delayed extinction in within-session extinction modulate the recovery of fear.
Extinction events impact the trajectory of biological evolution significantly. They are often viewed as upheavals to the evolutionary process. In contrast, this paper supports the hypothesis that although they are unpredictably destructive, extinction events may in the long term accelerate evolution by increasing evolvability. In particular, if extinction events extinguish indiscriminately many ways of life, indirectly they may select for the ability to expand rapidly through vacated niches. Lineages with such an ability are more likely to persist through multiple extinctions. Lending computational support for this hypothesis, this paper shows how increased evolvability will result from simulated extinction events in two computational models of evolved behavior. The conclusion is that although they are destructive in the short term, extinction events may make evolution more prolific in the long term.
Various neuropsychiatric conditions, including posttraumatic stress disorder (PTSD), are characterized by deficient fear extinction, but individuals differ greatly in risk for these. While there is growing evidence that fear extinction is influenced by certain procedural variables, it is unclear how these influences might vary across individuals and subpopulations. To model individual differences in fear extinction, prior studies identified a strain of inbred mouse, 129S1/SvImJ (S1), which exhibits a profound deficit in fear extinction, as compared to other inbred strains, such as C57BL/6J (B6).
Vagus nerve stimulation (VNS) has shown promise as an adjuvant treatment for posttraumatic stress disorder (PTSD), as it enhances fear extinction and reduces anxiety symptoms in multiple rat models of this condition. Yet, identification of the optimal stimulation paradigm is needed to facilitate clinical translation of this potential therapy. Using an extinction-resistant rat model of PTSD, we tested whether varying VNS intensity and duration could maximize extinction learning while minimizing the total amount of stimulation. We confirmed that sham rats failed to extinguish after a week of extinction training. Delivery of the standard LONG VNS trains (30 s) at 0.4 mA enhanced extinction and reduced anxiety but did not prevent fear return. Increasing the intensity of LONG VNS trains to 0.8 mA prevented fear return and attenuated anxiety symptoms. Interestingly, delivering 1, 4 or 16 SHORT VNS bursts (0.5 s) at 0.8 mA during each cue presentation in extinction training also enhanced extinction. LONG VNS trains or multiple SHORT VNS bursts at 0.8 mA attenuated fear renewal and reinstatement, promoted extinction generalization and reduced generalized anxiety. Delivering 16 SHORT VNS bursts also facilitated extinction in fewer trials. This study provides the first evidence that brief bursts of VNS can enhance extinction training, reduce relapse and support symptom remission using much less VNS than previous protocols. These findings suggest that VNS parameters can be adjusted in order to minimize total charge delivery and maximize therapeutic effectiveness.
Historical and long-term environmental datasets are imperative to understanding how natural systems respond to our changing world. Although immensely valuable, these data are at risk of being lost unless actively curated and archived in data repositories. The practice of data rescue, which we define as identifying, preserving, and sharing valuable data and associated metadata at risk of loss, is an important means of ensuring the long-term viability and accessibility of such datasets. Improvements in policies and best practices around data management will hopefully limit future need for data rescue; these changes, however, do not apply retroactively. While rescuing data is not new, the term lacks formal definition, is often conflated with other terms (i.e. data reuse), and lacks general recommendations. Here, we outline seven key guidelines for effective rescue of historically collected and unmanaged datasets. We discuss prioritization of datasets to rescue, forming effective data rescue teams, preparing the data and associated metadata, and archiving and sharing the rescued materials. In an era of rapid environmental change, the best policy solutions will require evidence from both contemporary and historical sources. It is, therefore, imperative that we identify and preserve valuable, at-risk environmental data before they are lost to science.
There has been a longstanding debate on whether original fear memory is inhibited or erased after extinction. One possibility that reconciles this uncertainty is that the inhibition and erasure mechanisms are engaged in different phases (early or late) of extinction. In this study, using single-session extinction training and its repetition (multiple-session extinction training), we investigated the inhibition and erasure mechanisms in the prefrontal cortex and amygdala of rats, where neural circuits underlying extinction reside. The inhibition mechanism was prevalent with single-session extinction training but faded when single-session extinction training was repeated. In contrast, the erasure mechanism became prevalent when single-session extinction training was repeated. Moreover, ablating the intercalated neurons of amygdala, which are responsible for maintaining extinction-induced inhibition, was no longer effective in multiple-session extinction training. We propose that the inhibition mechanism operates primarily in the early phase of extinction training, and the erasure mechanism takes over after that.
Spatial structure across fragmented landscapes can enhance regional population persistence by promoting local "rescue effects." In small, vulnerable populations, where chance or random events between individuals may have disproportionately large effects on species interactions, such local processes are particularly important. However, existing theory often only describes the dynamics of metapopulations at regional scales, neglecting the role of multispecies population dynamics within habitat patches.
The extinction of species can destabilize ecological processes. A way to assess the ecological consequences of species loss is by examining changes in functional diversity. The preservation of functional diversity depends on the range of ecological roles performed by species, or functional richness, and the number of species per role, or functional redundancy. However, current knowledge is based on short timescales and an understanding of how functional diversity responds to long-term biodiversity dynamics has been limited by the availability of deep-time, trait-based data. Here, we compile an exceptional trait dataset of fossil molluscs from a 23-million-year interval in the Caribbean Sea (34 011 records, 4422 species) and develop a novel Bayesian model of multi-trait-dependent diversification to reconstruct mollusc (i) diversity dynamics, (ii) changes in functional diversity, and (iii) extinction selectivity over the last 23 Myr. Our results identify high diversification between 23-5 Mya, leading to increases in both functional richness and redundancy. Conversely, over the last three million years, a period of high extinction rates resulted in the loss of 49% of species but only 3% of functional richness. Extinction rates were significantly higher in small, functionally redundant species suggesting that competition mediated the response of species to environmental change. Taken together, our results identify long-term diversification and selective extinction against redundant species that allowed functional diversity to grow over time, ultimately buffering the ecological functions of biological communities against extinction.
Canine distemper virus (CDV) has recently emerged as an extinction threat for the endangered Amur tiger (Panthera tigris altaica). CDV is vaccine-preventable, and control strategies could require vaccination of domestic dogs and/or wildlife populations. However, vaccination of endangered wildlife remains controversial, which has led to a focus on interventions in domestic dogs, often assumed to be the source of infection. Effective decision making requires an understanding of the true reservoir dynamics, which poses substantial challenges in remote areas with diverse host communities. We carried out serological, demographic, and phylogenetic studies of dog and wildlife populations in the Russian Far East to show that a number of wildlife species are more important than dogs, both in maintaining CDV and as sources of infection for tigers. Critically, therefore, because CDV circulates among multiple wildlife sources, dog vaccination alone would not be effective at protecting tigers. We show, however, that low-coverage vaccination of tigers themselves is feasible and would produce substantive reductions in extinction risks. Vaccination of endangered wildlife provides a valuable component of conservation strategies for endangered species.
Identifying the early warning signals of catastrophic extinctions has recently become a central focus for ecologists, but species' functional responses to environmental changes remain an untapped source for the sharpening of such warning signals. Telomere length (TL) analysis represents a promising molecular tool with which to raise the alarm regarding early population decline, since telomere attrition is associated with aging processes and accelerates after a recurrent exposure to environmental stressors. In the southern margin of their range, populations of the common lizard (Zootoca vivipara) recently became extinct at lowest elevations due to changes in climate conditions. However, the proximal signals involved in these demographic declines are still unknown. Here, we sampled 100 yearling lizards from 10 natural populations (n = 10 per population) along an extinction risk gradient. Relative lizard abundance dramatically dropped over 12 years in low-altitude populations characterized by warmer ambient temperatures and higher body growth of lizards early in life. A non-linear relationship was found between TL and population extinction risk, with shorter telomeres in populations facing high risk of extinction when compared to non-threatened ones. Our results identify TL as a promising biomarker and imply that population extinctions might be preceded by a loop of physiological aging.
Here, we use optogenetics and chemogenetics to investigate the contribution of the paraventricular thalamus (PVT) to nucleus accumbens (NAc) pathway in aversion and heroin relapse in two different heroin self-administration models in rats. In one model, rats undergo forced abstinence in the home cage prior to relapse testing, and in the other, they undergo extinction training, a procedure that is likened to cognitive behavioral therapy. We find that the PVT→NAc pathway is both sufficient and necessary to drive aversion and heroin seeking after abstinence, but not extinction. The ability of extinction to reduce this pathway's contribution to heroin relapse is accompanied by a loss of synaptic plasticity in PVT inputs onto a specific subset of NAc neurons. Thus, extinction may exert therapeutic reductions in opioid seeking by altering synaptic plasticity within the PVT→NAc pathway, resulting in reduced aversion during opioid withdrawal as well as reduced relapse propensity.
Accurately predicting an outcome requires that animals learn supporting and conflicting evidence from sequential experience. In mammals and invertebrates, learned fear responses can be suppressed by experiencing predictive cues without punishment, a process called memory extinction. Here, we show that extinction of aversive memories in Drosophila requires specific dopaminergic neurons, which indicate that omission of punishment is remembered as a positive experience. Functional imaging revealed co-existence of intracellular calcium traces in different places in the mushroom body output neuron network for both the original aversive memory and a new appetitive extinction memory. Light and ultrastructural anatomy are consistent with parallel competing memories being combined within mushroom body output neurons that direct avoidance. Indeed, extinction-evoked plasticity in a pair of these neurons neutralizes the potentiated odor response imposed in the network by aversive learning. Therefore, flies track the accuracy of learned expectations by accumulating and integrating memories of conflicting events.
The mammalian brain contains dedicated circuits for both the learned expression and suppression of fear. These circuits require precise coordination to facilitate the appropriate expression of fear behavior, but the mechanisms underlying this coordination remain unclear. Using a combination of chemogenetics, activity-based neuronal-ensemble labeling and in vivo electrophysiology, we found that fear extinction learning confers on parvalbumin-expressing (PV) interneurons in the basolateral amygdala (BLA) a dedicated role in the selective suppression of a previously encoded fear memory and BLA fear-encoding neurons. In addition, following extinction learning, PV interneurons enable a competing interaction between a 6-12 Hz oscillation and a fear-associated 3-6 Hz oscillation within the BLA. Loss of this competition increases a 3-6 Hz oscillatory signature, with BLA→medial prefrontal cortex directionality signaling the recurrence of fear expression. The discovery of cellular and oscillatory substrates of fear extinction learning that critically depend on BLA PV interneurons could inform therapies aimed at preventing the pathological recurrence of fear following extinction learning.
Current neurocircuitry models of anxiety disorders posit a lack of inhibitory tone in the amygdala during acquisition of Pavlovian fear responses and deficient encoding of extinction responses in amygdala-medial prefrontal cortex circuits. Competition between these two responses often results in a return of fear, limiting control over anxiety. However, one hypothesis holds that a pharmacologic strategy aimed at reducing amygdala activity while simultaneously augmenting medial prefrontal cortex function could facilitate the extinction of conditioned fear.
Attentional bias for threat is an adaptive feature of human psychology, but may become maladaptive in anxiety-related disorders, causing distress, distraction, and distorted perception of danger. Reaction time measures have revealed automatic, covert attention biases to threat, whereas eye tracking has revealed voluntary biases over a larger timescale, with monitoring or avoidance depending on context. Recently, attentional bias for threat has been studied as a conditioned fear response, providing new insight into how attentional biases are acquired and inhibited through learning experiences. However, very few studies have examined voluntary gaze biases during fear learning. In a novel eye tracking paradigm (N = 78), we examine the overt components of attentional bias to threat and safety cues. We found that threat cues, but not safety cues, elicited an initial orienting bias, as well as sustained monitoring bias across 10-second trials. This collective "vigilance" response to threat cues was insensitive to extinction, whereas condition fear responding revealed by pupil size and self-report ratings showed marked extinction. Vigilance may be less prone to extinction, compared to autonomic arousal, because eye movements require less energy than preparing the body for defensive behavior. Implications for understanding vigilance in PTSD are considered.
Multicellular organisms have co-evolved with complex consortia of viruses, bacteria, fungi and parasites, collectively referred to as the microbiota1. In mammals, changes in the composition of the microbiota can influence many physiologic processes (including development, metabolism and immune cell function) and are associated with susceptibility to multiple diseases2. Alterations in the microbiota can also modulate host behaviours-such as social activity, stress, and anxiety-related responses-that are linked to diverse neuropsychiatric disorders3. However, the mechanisms by which the microbiota influence neuronal activity and host behaviour remain poorly defined. Here we show that manipulation of the microbiota in antibiotic-treated or germ-free adult mice results in significant deficits in fear extinction learning. Single-nucleus RNA sequencing of the medial prefrontal cortex of the brain revealed significant alterations in gene expression in excitatory neurons, glia and other cell types. Transcranial two-photon imaging showed that deficits in extinction learning after manipulation of the microbiota in adult mice were associated with defective learning-related remodelling of postsynaptic dendritic spines and reduced activity in cue-encoding neurons in the medial prefrontal cortex. In addition, selective re-establishment of the microbiota revealed a limited neonatal developmental window in which microbiota-derived signals can restore normal extinction learning in adulthood. Finally, unbiased metabolomic analysis identified four metabolites that were significantly downregulated in germ-free mice and have been reported to be related to neuropsychiatric disorders in humans and mouse models, suggesting that microbiota-derived compounds may directly affect brain function and behaviour. Together, these data indicate that fear extinction learning requires microbiota-derived signals both during early postnatal neurodevelopment and in adult mice, with implications for our understanding of how diet, infection, and lifestyle influence brain health and subsequent susceptibility to neuropsychiatric disorders.
Animal fear conditioning studies have illuminated neuronal mechanisms of learned associations between sensory stimuli and fear responses. In rats, brief electrical stimulation of the infralimbic cortex has been shown to reduce conditioned freezing during recall of extinction memory. Here, we translated this finding to humans with magnetic resonance imaging-navigated transcranial magnetic stimulation (TMS).
Fear extinction diminishes conditioned fear responses and impaired fear extinction has been reported to be related to anxiety disorders such as post-traumatic stress disorder (PTSD). We and others have reported that 129S1/SvImJ (129S1) strain of mice showed selective impairments in fear extinction following successful auditory or contextual fear conditioning. To investigate brain regions involved in the impaired fear extinction of 129S1 mice, we systemically analyzed c-Fos expression patterns before and after contextual fear conditioning and extinction. After fear conditioning, 129S1 mice showed significantly increased c-Fos expression in the medial division of the central amygdala (CEm), prelimbic (PL) cortex of the medial prefrontal cortex (mPFC), and dorsal CA3 of the hippocampus, compared to that of control C57BL/6 mice. Following fear extinction, 129S1 mice exhibited significantly more c-Fos-positive cells in the CEm, PL, and paraventricular nucleus of the thalamus (PVT) than did C57BL/6 mice. These results reveal the dynamic circuitry involved in different steps of fear memory formation and extinction, thus providing candidate brain regions to study the etiology and pathophysiology underlying impaired fear extinction.
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