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Attention helps us to be aware of the external world, and this may be especially important when a threat stimulus predicts an aversive outcome. Electroencephalogram (EEG) alpha-band suppression has long been considered as a neural signature of attentional engagement. The present study was designed to test whether attentional engagement, as indexed by alpha-band suppression, is increased in a sustained manner following a conditioned stimulus (CS) that is paired with an aversive (CS+) vs neutral (CS-) outcome. We tested 70 healthy young adults in aversive conditioning and extinction paradigms. One of three colored circles served as the CS+, which was paired in 50% of the trials with a noise burst (unconditioned stimulus, US). The other colored circles (CS-) were never paired with the US. For conditioning, we found greater alpha-band suppression for the CS+ compared to the CS-; this suppression was sustained through the time of the predicted US. This effect was significantly reduced for extinction. These results indicate that conditioned threat stimuli trigger an increase in attentional engagement as subjects monitor the environment for the predicted aversive stimulus. Moreover, this alpha-band suppression effect may be valuable for future studies examining normal or pathological increases in attentional monitoring following threat stimuli.

Fear extinction underlies prolonged exposure, one of the most well-studied treatments for posttraumatic stress disorder (PTSD). There has been increased interest in exploring pharmacological agents to enhance fear extinction learning in humans and their potential as adjuncts to PE. The objective of such adjuncts is to augment the clinical impact of PE on the durability and magnitude of symptom reduction. In this study, we examined whether hydrocortisone (HC), a corticosteroid, and D-Cycloserine (DCS), an N-methyl-D-aspartate receptor partial agonist, enhance fear extinction learning and consolidation in individuals with PTSD. In a double-blind placebo-controlled 3-group experimental design, 90 individuals with full or subsyndromal PTSD underwent fear conditioning with stimuli that were paired (CS+) or unpaired (CS-) with shock. Extinction learning occurred 72 h later and extinction retention was tested one week after extinction. HC 25 mg, DCS 50 mg or placebo was administered one hour prior to extinction learning. During extinction learning, the DCS and HC groups showed a reduced differential CS+/CS- skin conductance response (SCR) compared to placebo (b = -0.19, CI = -0.01 to -37, p = 0.042 and b = -0.25, CI = -08 to -0.43, p = 0.005, respectively). A nonsignificant trend for a lower differential CS+/CS- SCR in the DCS group, compared to placebo, (b = -0.25, CI = 0.04 to -0.55, p = 0.089) was observed at retention testing, one week later. A single dose of HC and DCS facilitated fear extinction learning in participants with PTSD symptoms. While clinical implications have yet to be determined, our findings suggest that glucocorticoids and NMDA agonists hold promise for facilitating extinction learning in PTSD.

Sex differences in the neurobiological mechanisms involved in fear conditioning and extinction have been suggested to contribute to differential vulnerability for the development of posttraumatic stress disorder (PTSD) in women compared with men. Reproductive hormones, such as estradiol, have been shown to facilitate fear conditioning and extinction learning and may explain some of these differences. However, the effect of commonly used hormonal contraceptives on the neurobiological mechanisms of fear conditioning and extinction is poorly understood. A laboratory study was conducted in trauma-exposed men and women with and without full or partial PTSD to examine effects of sex and use of hormonal birth control on fear conditioning, fear extinction learning, and extinction retention. Participants underwent fear conditioning with stimuli that were paired (CS+) or unpaired (CS-) with shock. Extinction learning occurred 72 h later, and extinction retention was tested 1 wk after extinction. Women on hormonal contraceptives (HCs) demonstrated enhanced acquisition of fear conditioning and enhanced extinction of fear as compared with women off hormonal birth control and men. While clinical implications have yet to be determined, these results suggest that hormonal contraceptives may facilitate learning during both fear acquisition and extinction. Understanding the impact of sex and hormones on fear conditioning and extinction processes may lead to new insights into the pathophysiology of PTSD and result in advancements in treatment that may vary by sex.

"Fungi on Mars!": a popular news heading that piques public interest and makes scientists' blood boil. While such a statement is laden with misinformation and light on evidence, the search for past and present extraterrestrial life is an ongoing scientific effort. Moreover, it is one that is increasingly gaining momentum with the recent collection of martian rock cores from Jezero Crater by NASA's Perseverance rover. Despite the increasingly sophisticated approaches guiding the search for microbial life on other planets, fungi remain relatively underexplored compared to their bacterial counterparts, highlighting a gap between the astrobiological and fungal research communities. Through a meeting in April 2021, the CIFAR Earth 4D and Fungal Kingdom research programs worked to bridge this divide by uniting experts in each field. CIFAR is a Canadian-based global research organization that convenes researchers across disciplines to address important questions facing science and humanity. The CIFAR Earth 4D: Subsurface Science & Exploration and Fungal Kingdom: Threats & Opportunities research programs were launched by CIFAR in July 2019, each made up of approximately two dozen international researchers who are experts in their fields. The Earth 4D program, led by co-directors John Mustard (Brown University, USA) and Barbara Sherwood Lollar (University of Toronto, Canada), aims to understand the complex chemical, physical, and biological interactions that occur within and between Earth's surface and subsurface to explore questions on the evolution of planets and life. The Fungal Kingdom program, led by co-directors Leah Cowen (University of Toronto, Canada) and Joseph Heitman (Duke University, USA), seeks to tackle the most pressing threats fungi pose to human health, agriculture, and biodiversity and to harness their extraordinary potential. The programs met to explore areas for synergy within four major themes: (1) the origins of life; (2) the evolution and diversification of life; (3) life in diverse and extreme environments; and (4) extinction: lessons learned and threats. This report covers the research discussed during the meeting across these four themes.

A widely held dogma in the preclinical addiction field is that females are more vulnerable than males to drug craving and relapse. Here, we first review clinical studies on sex differences in psychostimulant and opioid craving and relapse. Next, we review preclinical studies on sex differences in psychostimulant and opioid reinstatement of drug seeking after extinction of drug self-administration, and incubation of drug craving (time-dependent increase in drug seeking during abstinence). We also discuss ovarian hormones role in relapse and craving in humans and animal models and speculate on brain mechanisms underlying their role in cocaine craving and relapse in rodent models. Finally, we discuss imaging studies on brain responses to cocaine cues and stress in men and women.The results of the clinical studies reviewed do not appear to support the notion that women are more vulnerable to psychostimulant and opioid craving and relapse. However, this conclusion is tentative because most of the studies reviewed were correlational, not sufficiently powered, and not a priori designed to detect sex differences. Additionally, imaging studies suggest sex differences in brain responses to cocaine cues and stress. The results of the preclinical studies reviewed provide evidence for sex differences in stress-induced reinstatement and incubation of cocaine craving but not cue- or cocaine-induced reinstatement of cocaine seeking. These sex differences are modulated in part by ovarian hormones. In contrast, the available data do not support the notion of sex differences in craving and relapse/reinstatement for methamphetamine or opioids in rodent models. SIGNIFICANCE STATEMENT: This systematic review summarizes clinical and preclinical studies on sex differences in psychostimulant and opioid craving and relapse. Results of the clinical studies reviewed do not appear to support the notion that women are more vulnerable to psychostimulant and opioid craving and relapse. Results of preclinical studies reviewed provide evidence for sex differences in reinstatement and incubation of cocaine seeking but not for reinstatement or incubation of methamphetamine or opioid seeking.

BackgroundDisruption of the Neurobeachin gene is a rare genetic mutation that has been implicated in the development of autism and enhanced long-term potentiation of the hippocampal CA1 region, causing a heightened conditioned fear response and impaired fear extinction. Prazosin, an alpha-1 receptor antagonist, has been used in patients with posttraumatic stress disorder to mitigate the increased alpha-1 activity involved in fear and startle responses. Here we report a case of a patient with a rare Neurobeachin gene deletion, who demonstrated marked and sustained improvement in paranoid behavior within days of prazosin initiation.Case presentationThe patient is a 27-year-old White male with autism spectrum disorder, obsessive-compulsive disorder, and schizophrenia, with a chromosome 13q12 deletion including deletion of the Neurobeachin gene, who presented to the emergency department due to worsening functional status and profound weight loss as a result of only eating prepackaged foods. He had not showered or changed clothes in several months prior to presentation. He was hospitalized in the inpatient psychiatric unit for 2 months before prazosin was initiated. During that time, he demonstrated paranoia as evidenced by heightened sensitivity to doors opening, guarded interactions, and limited communication with providers and other patients. He also exhibited poor grooming habits, with aversion to showering, shaving, and changing clothes. Since initiating prazosin, he has demonstrated a brighter affect, initiates and maintains conversations, showers and changes clothes on a regular basis, and eats a variety of foods. At the time of this report, the patient was discharged to live in an apartment with a caregiver after a 7-month inpatient hospitalization.ConclusionsLow-dose prazosin shows rapid and sustained improvement in paranoid behavior in a patient with a rare Neurobeachin gene deletion. Prazosin has a relatively favorable side effect profile with once-daily dosing and low cost. Prazosin may provide clinical improvement in patients with Neurobeachin gene deletions due to its theoretical attenuation in fear response through alpha-1 antagonism.

Few studies have examined threat generalization across development and no developmental studies have compared the generalization of social versus nonsocial threat, making it difficult to identify contextual factors that contribute to threat learning across development. The present study assessed youth and adults multivoxel neural representations of social versus nonsocial threat stimuli. Twenty adults (Mage  = 25.7 ± 4.9) and 16 youth (Mage  = 14.1 ± 1.7) completed two conditioning and extinction recall paradigms: one social and one nonsocial paradigm. Three weeks after conditioning, participants underwent a functional magnetic resonance imaging extinction recall task that presented the extinguished threat cue (CS+), a safety cue (CS-), and generalization stimuli (GS) consisting of CS-/CS+ blends. Across age groups, neural activity patterns and self-reported fear and memory ratings followed a linear generalization gradient for social threat stimuli and a quadratic generalization gradient for nonsocial threat stimuli, indicating enhanced threat/safety discrimination for social relative to nonsocial threat stimuli. The amygdala and ventromedial prefrontal cortex displayed the greatest neural pattern differentiation between the CS+ and GS/CS-, reinforcing their role in threat learning and extinction recall. Contrary to predictions, age did not influence threat representations. These findings highlight the importance of the social relevance of threat on generalization across development.

IntroductionPoor sleep is prevalent among individuals with social anxiety disorder (SAD) and may negatively affect exposure therapy outcomes. Poor sleep may impair memory and learning, and thus compromise fear extinction learning thought to take place in exposure therapy. We examined poor sleep as a predictor of exposure therapy outcomes for SAD and the moderating role of d-cycloserine (DCS) on this relationship.MethodsParticipants were 152 individuals with a primary diagnosis of SAD. As part of a randomized clinical trial evaluating the efficacy of DCS for enhancing the effects of exposure therapy, they completed self-report baseline measure of sleep quality, and self-report sleep diaries assessing sleep duration (total sleep time [TST]) and sleep quality the nights before and after treatment sessions.ResultsPoorer baseline sleep quality was significantly associated with slower improvement over time and worse symptom outcomes at the end of treatment and follow-up after controlling for baseline symptoms of depression and social anxiety. Greater TST the night before treatment predicted lower SAD symptoms at the next session, after controlling for symptoms at the previous session. There was no relation between prior or subsequent night sleep quality on symptoms at the next session. No associations were moderated by DCS.ConclusionsWe replicated and extended findings indicating that poor sleep quality is associated with poorer exposure therapy outcomes for SAD. Assessing for sleep difficulties before treatment initiation and incorporating sleep interventions into treatment may enhance exposure therapy outcomes for SAD.

Posttraumatic stress disorder (PTSD) is associated with lower gray matter volume (GMV) in brain regions critical for extinction of learned threat. However, relationships among volume, extinction learning, and PTSD symptom development remain unclear. We investigated subcortical brain volumes in regions supporting extinction learning and fear-potentiated startle (FPS) to understand brain-behavior interactions that may impact PTSD symptom development in recently traumatized individuals. Participants (N = 99) completed magnetic resonance imaging and threat conditioning two weeks following trauma exposure as part of a multisite observational study to understand the neuropsychiatric effects of trauma (AURORA Study). Participants completed self-assessments of PTSD (PTSD Checklist for DSM-5; PCL-5), dissociation, and depression symptoms two- and eight-weeks post-trauma. We completed multiple regressions to investigate relationships between FPS during late extinction, GMV, and PTSD symptom development. The interaction between thalamic GMV and FPS during late extinction at two weeks post-trauma predicted PCL-5 scores eight weeks (t (75) = 2.49, β = 0.28, p = 0.015) post-trauma. Higher FPS predicted higher PCL-5 scores in the setting of increased thalamic GMV. Meanwhile, lower FPS also predicted higher PCL-5 scores in the setting of decreased thalamic GMV. Thalamic GMV and FPS interactions also predicted posttraumatic dissociative and depressive symptoms. Amygdala and hippocampus GMV by FPS interactions were not associated with posttraumatic symptom development. Taken together, thalamic GMV and FPS during late extinction interact to contribute to adverse posttraumatic neuropsychiatric outcomes. Multimodal assessments soon after trauma have the potential to distinguish key phenotypes vulnerable to posttraumatic neuropsychiatric outcomes.

Childhood exposure to violence is strongly associated with psychopathology. High resting respiratory sinus arrhythmia (RSA) is associated with lower levels of psychopathology in children exposed to violence. High RSA may help to protect against psychopathology by facilitating fear extinction learning, allowing more flexible autonomic responses to learned threat and safety cues. In this study, 165 youth (79 female, aged 9-17; 86 exposed to violence) completed assessments of violence exposure, RSA, and psychopathology, and a fear extinction learning task; 134 participants returned and completed psychopathology assessments 2 years later. Resting RSA moderated the longitudinal association of violence exposure with post-traumatic stress disorder (PTSD) symptoms and externalizing psychopathology, such that the association was weaker among youths with higher RSA. Higher skin conductance responses (SCR) during extinction learning to the threat cue (CS+) was associated with higher internalizing symptoms at follow-up and greater SCR to the safety cue (CS-) was associated with higher PTSD, internalizing, and externalizing symptoms, as well as the p-factor, controlling for baseline symptoms. Findings suggest that higher RSA may protect against emergence of psychopathology among children exposed to violence. Moreover, difficulty extinguishing learned threat responses and elevated autonomic responses to safety cues may be associated with risk for future psychopathology.

Adaptive reward-related decision making requires accurate prospective consideration of the specific outcome of each option and its current desirability. Often this information must be inferred based on the presence of predictive environmental events. The basolateral amygdala (BLA) and medial orbitofrontal cortex (mOFC) are two key nodes in the circuitry supporting such outcome expectations, but very little is known about the function of direct connections between these regions. Here, in male rats, we first anatomically confirmed the existence of bidirectional, direct projections between the mOFC and BLA and found that BLA projections to mOFC are largely distinct from those to lateral OFC (lOFC). Next, using pathway-specific chemogenetic inhibition and the outcome-selective Pavlovian-to-instrumental transfer and devaluation tests, we interrogated the function of the bidirectional mOFC-BLA connections in reward-directed behavior. We found evidence that the mOFC→BLA pathway mediates the use of environmental cues to understand which specific reward is predicted, information needed to infer which action to choose, and how desirable that reward is to ensure adaptive responses to the cue. By contrast, the BLA→mOFC pathway is not needed to use the identity of an expected reward to guide choice but does mediate adaptive responses to cues based on the current desirability of the reward they predict. These functions differ from those we previously identified for the lOFC-BLA circuit. Collectively, the data reveal the mOFC-BLA circuit as critical for the cue-dependent reward outcome expectations that influence adaptive behavior and decision making.SIGNIFICANCE STATEMENT To make good decisions we evaluate how advantageous a particular course of action would be. This requires understanding what rewarding outcomes can be expected and how desirable they currently are. Such prospective considerations are critical for adaptive decision making but disrupted in many psychiatric diseases. Here, we reveal that direct connections between the medial orbitofrontal cortex and basolateral amygdala mediate these functions. These findings are especially important in light of evidence of dysfunction in this circuit in substance use disorder and mental illnesses marked by poor decision making.

Dimensional models of anxiety and depression highlight common and distinct symptom clusters that are thought to reflect disruptions in underlying functional processes. The current study investigated how functioning of threat neurocircuitry relates to symptom dimensions of anxiety and depression. Participants were aged 18-19 years (n = 229, 158 female) and were selected to ensure a range of scores on symptom measures. Symptom dimensions of "General Distress" (common to anxiety disorders and depression), "Fears" (more specific to anxiety disorders), and "Anhedonia-apprehension" (more specific to depression) were evaluated. Participants underwent functional magnetic resonance imaging during a Pavlovian fear conditioning paradigm. Multilevel modeling analyses estimated relationships between symptom dimensions and activation in threat neural circuitry. Exploratory whole brain analyses were also conducted. Threat-related neural activity was not associated with General Distress or Fears. Anhedonia-apprehension was associated with activation of bilateral amygdala, anterior insula and dACC during late extinction. We found no evidence to support an association between symptom dimensions of General Distress or Fears with threat circuitry activation in a large sample of young adults. We did, however, find that the symptom dimension of Anhedonia-apprehension was significantly associated with threat-related neural activation during fear extinction. This effect requires replication in future work but may reflect anhedonic impairments in learning when contingencies are altered, possibly linked to the rewarding relief of an unexpectedly absent threat.

Deficits in associative and Pavlovian learning are thought to lie at the center of anxiety-related disorders. However, the majority of studies have been carried out in adult populations. The aim of this review was to critically examine the behavioral and neuroimaging literature on Pavlovian learning in pediatric anxiety disorders. We conclude that although there is evidence for deficits in Pavlovian processes (e.g., heightened reactivity to safety cues in anxious samples), the extant literature suffers from key methodological and theoretical issues. We conclude with theoretical and methodological recommendations for future research in order to further elucidate the role of Pavlovian learning in the etiology, maintenance, and treatment of pediatric anxiety disorders.

The upstream causes of the COVID-19 pandemic have received little attention so far in public health and clinical medicine, as opposed to the downstream effects of mass morbidity and mortality. To resolve this pandemic and to prevent even more severe future pandemics, a focus on upstream causation is essential. Convincing evidence shows that this and every other important viral epidemic emerging in the recent past and predictably into the future comes from the same upstream causes: capitalist agriculture, its destruction of natural habitat, and the industrial production of meat. International and national health organizations have obscured the upstream causes of emerging viral epidemics. These organizations have suffered cutbacks in public funding but have received increased support from international financial institutions and private philanthropies that emphasize the downstream effects rather than upstream causes of infectious diseases. Conflicts of interest also have impacted public health policies. A worldwide shift has begun toward peasant agricultural practices: Research so far has shown that peasant agriculture is safer and more efficient than capitalist industrial agricultural practices. Without such a transformation of agriculture, even more devastating pandemics will result from the same upstream causes.

BackgroundRegenerative therapies to mitigate Alzheimer's disease (AD) neuropathology have shown very limited success. In the recent era, extracellular vesicles (EVs) derived from multipotent and pluripotent stem cells have shown considerable promise for the treatment of dementia and many neurodegenerative conditions.MethodsUsing the 5xFAD accelerated transgenic mouse model of AD, we now show the regenerative potential of human neural stem cell (hNSC)-derived EVs on the neurocognitive and neuropathologic hallmarks in the AD brain. Two- or 6-month-old 5xFAD mice received single or two intra-venous (retro-orbital vein, RO) injections of hNSC-derived EVs, respectively.ResultsRO treatment using hNSC-derived EVs restored fear extinction memory consolidation and reduced anxiety-related behaviors 4-6 weeks post-injection. EV treatment also significantly reduced dense core amyloid-beta plaque accumulation and microglial activation in both age groups. These results correlated with partial restoration of homeostatic levels of circulating pro-inflammatory cytokines in the AD mice. Importantly, EV treatment protected against synaptic loss in the AD brain that paralleled improved cognition. MiRNA analysis of the EV cargo revealed promising candidates targeting neuroinflammation and synaptic function.ConclusionsCollectively, these data demonstrate the neuroprotective effects of systemic administration of stem cell-derived EVs for remediation of behavioral and molecular AD neuropathologies.

The Zoonomia Project is investigating the genomics of shared and specialized traits in eutherian mammals. Here we provide genome assemblies for 131 species, of which all but 9 are previously uncharacterized, and describe a whole-genome alignment of 240 species of considerable phylogenetic diversity, comprising representatives from more than 80% of mammalian families. We find that regions of reduced genetic diversity are more abundant in species at a high risk of extinction, discern signals of evolutionary selection at high resolution and provide insights from individual reference genomes. By prioritizing phylogenetic diversity and making data available quickly and without restriction, the Zoonomia Project aims to support biological discovery, medical research and the conservation of biodiversity.

The Zoonomia Project is investigating the genomics of shared and specialized traits in eutherian mammals. Here we provide genome assemblies for 131 species, of which all but 9 are previously uncharacterized, and describe a whole-genome alignment of 240 species of considerable phylogenetic diversity, comprising representatives from more than 80% of mammalian families. We find that regions of reduced genetic diversity are more abundant in species at a high risk of extinction, discern signals of evolutionary selection at high resolution and provide insights from individual reference genomes. By prioritizing phylogenetic diversity and making data available quickly and without restriction, the Zoonomia Project aims to support biological discovery, medical research and the conservation of biodiversity.

Comparing distributional information derived from fossils with the modern distribution of species, we summarize the changing bird communities of the Bahamian Archipelago across deep ecological time. While our entire dataset consists of 7,600+ identified fossils from 32 sites on 15 islands (recording 137 species of resident and migratory birds), we focus on the landbirds from four islands with the best fossil records, three from the Late Pleistocene (∼25 to 10 ka [1,000 y ago]) and one from the Holocene (∼10 to 0 ka). The Late Pleistocene sites feature 51 resident species that have lost one or more Bahamian populations; 29 of these species do not occur in any of the younger Holocene sites (or in the Bahamas today). Of these 29 species, 17 have their closest affinities to species now or formerly living in Cuba and/or North America. A set of 27 species of landbirds, most of them extant somewhere today, was more widespread in the Bahamas in the prehistoric Holocene (∼10 to 0.5 ka) than they are today; 16 of these 27 species were recorded as Pleistocene fossils as well. No single site adequately captures the entire landbird fauna of the combined focal islands. Information from all sites is required to assess changes in Bahamian biodiversity (including endemism) since the Late Pleistocene. The Bahamian islands are smaller, flatter, lower, and more biotically depauperate than the Greater Antilles, resulting in more vulnerable bird communities.

BackgroundIn rodents, context specificity of Pavlovian extinction is attenuated by manipulations that impair hippocampal function, including systemic administration of scopolamine, a muscarinic-cholinergic receptor antagonist. Context renewal translates into return of fear following exposure therapy to feared situations. We evaluated the effectiveness of scopolamine for attenuating context renewal of phobic fear in humans.MethodsA total of 60 participants (35 female, 22 male, 1 transgender, 2 undeclared) with social anxiety disorder and fear of public speaking were randomized to placebo, 0.5 mg scopolamine, or 0.6 mg scopolamine. They completed seven exposure sessions in an exposure context and subsequently tested in the exposure context (extinction retest) versus a different context (context renewal test), which were counterbalanced. Testing 1 month later occurred in the exposure context (long-term extinction retest). Fear measures included skin conductance and self-reported distress during speeches. Hippocampus-dependent cognitive tasks were completed as well.ResultsScopolamine augmented extinction across exposure sessions on skin conductance response and skin conductance level. Lower skin conductance response at context renewal in scopolamine groups relative to the placebo group was constrained to simple effects and complicated by unexpected outcomes within placebo and on self-reported fear. Scopolamine led to lower skin conductance response at long-term extinction retest. Scopolamine impaired performance on a cognitive task of hippocampal function.ConclusionsNoninvasive and well-tolerated scopolamine impaired hippocampal processes and augmented extinction during exposure. Drug-free effects persisted 1 month later. Findings at context renewal were limited and suggestive only. Further investigation is warranted with varying scopolamine dosages.

The great auk was once abundant and distributed across the North Atlantic. It is now extinct, having been heavily exploited for its eggs, meat, and feathers. We investigated the impact of human hunting on its demise by integrating genetic data, GPS-based ocean current data, and analyses of population viability. We sequenced complete mitochondrial genomes of 41 individuals from across the species' geographic range and reconstructed population structure and population dynamics throughout the Holocene. Taken together, our data do not provide any evidence that great auks were at risk of extinction prior to the onset of intensive human hunting in the early 16th century. In addition, our population viability analyses reveal that even if the great auk had not been under threat by environmental change, human hunting alone could have been sufficient to cause its extinction. Our results emphasise the vulnerability of even abundant and widespread species to intense and localised exploitation.

Occasion setting refers to the ability of 1 stimulus, an occasion setter, to modulate the efficacy of the association between another, conditioned stimulus (CS) and an unconditioned stimulus (US) or reinforcer. Occasion setters and simple CSs are readily distinguished. For example, occasion setters are relatively immune to extinction and counterconditioning, and their combination and transfer functions differ substantially from those of simple CSs. Similarly, the acquisition of occasion setting is favored when stimuli are separated by longer intervals, by empty trace intervals, and are of different modalities, whereas the opposite conditions typically favor the acquisition of simple associations. Furthermore, the simple conditioning and occasion setting properties of a single stimulus can be independent, for example, that stimulus may simultaneously predict the occurrence of a reinforcer and indicate that another stimulus will not be reinforced. Many behavioral phenomena that are intractable to simple associative analysis are better understood within an occasion setting framework. Besides capturing the distinction between direct and modulatory control common to many arenas in neuroscience, occasion setting provides a model for the hierarchical organization of memory for events and event relations, and for contextual control more broadly. Although early lesion studies further differentiated between occasion setting and simple conditioning functions, little is known about the neurobiology of occasion setting. Modern techniques for precise manipulation and monitoring of neuronal activity in multiple brain regions are ideally suited for disentangling contributions of simple conditioning and occasion setting in associative learning. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Social Reticence (SR) is a temperament construct identified in early childhood that is expressed as shy, anxiously avoidant behavior and, particularly when stable, robustly associated with risk for anxiety disorders. Threat circuit function may develop differently for children high on SR than low on SR. We compared brain function and behavior during extinction recall in a sample of 11-to-15-year-old children characterized in early childhood on a continuum of SR. Three weeks after undergoing fear conditioning and extinction, participants completed a functional magnetic resonance imaging extinction recall task assessing memory and threat differentiation for conditioned stimuli. Whereas self-report and psychophysiological measures of differential conditioning, extinction, and extinction recall were largely similar across participants, SR-related differences in brain function emerged during extinction recall. Specifically, childhood SR was associated with a distinct pattern of hemodynamic-autonomic covariation in the brain when recalling extinguished threat and safety cues. SR and attention focus impacted associations between trial-by-trial variation in autonomic responding and in brain activation. These interactions occurred in three main brain areas: the anterior insular cortex (AIC), the anterior subdivision of the medial cingulate cortex (aMCC), and the dorsolateral prefrontal cortex (dlPFC). This pattern of SCR-BOLD coupling may reflect selective difficulty tracking safety in a temperamentally at-risk population.

Addiction is a chronic relapsing disorder, in that most addicted individuals who choose to quit taking drugs fail to maintain abstinence in the long-term. Relapse is especially likely when recovering addicts encounter risk factors like small "priming" doses of drug, stress, or drug-associated cues and locations. In rodents, these same factors reinstate cocaine seeking after a period of abstinence, and extensive preclinical work has used priming, stress, or cue reinstatement models to uncover brain circuits underlying cocaine reinstatement. Here, we review common rat models of cocaine relapse, and discuss how specific features of each model influence the neural circuits recruited during reinstated drug seeking. To illustrate this point, we highlight the surprisingly specific roles played by ventral pallidum subcircuits in cocaine seeking reinstated by either cocaine-associated cues, or cocaine itself. One goal of such studies is to identify, and eventually to reverse the specific circuit activity that underlies the inability of some humans to control their drug use. Based on preclinical findings, we posit that circuit activity in humans also differs based on the triggers that precipitate craving and relapse, and that associated neural responses could help predict the triggers most likely to elicit relapse in a given person. If so, examining circuit activity could facilitate diagnosis of subgroups of addicted people, allowing individualized treatment based on the most problematic risk factors.

Chitin, one of the most abundant biopolymers on Earth, is bound and degraded by chitinases, specialized enzymes that are similarly widespread in nature. Chitin catabolism affects global carbon and nitrogen cycles through a host of diverse biological processes, but recent work has focused attention on systems of chitin recognition and degradation conserved in mammals, connecting an ancient pathway of polysaccharide processing to human diseases influenced by persistent immune triggering. Here we review current advances in our understanding of how chitin-chitinase interactions affect mucosal immune feedback mechanisms essential to maintaining homeostasis and organ health.

Transcutaneous stimulation of the auricular branch of the vagus nerve (tVNS) may accelerate fear extinction in healthy humans. Here, we aimed to investigate this hypothesis in healthy young participants in a prepared learning paradigm, using spider pictures as conditioned stimuli. After a fear conditioning phase, participants were randomly allocated to receive tVNS (final N = 42) or sham stimulation (final N = 43) during an extinction phase. Conditioned fear was assessed using US expectancy ratings, skin conductance and fear potentiated startle responses. After successful fear acquisition, participants in both groups showed a reduction of fear over the course of the extinction phase. There were no between-group differences in extinction rates for physiological indices of fear. Contrary to previous findings, participants in the tVNS condition also did not show accelerated declarative extinction learning. Participants in the tVNS condition did have lower initial US expectancy ratings for the CS- trials than those who received sham stimulation, which may indicate an enhanced processing of safety cues due to tVNS. In conclusion, the expected accelerated extinction due to tVNS was not observed. The results from this study call for more research on the optimal tVNS stimulation intensity settings.

Increasing predictability of animal models of posttraumatic stress disorder (PTSD) has required active collaboration between clinical and preclinical scientists. Modeling PTSD is challenging, as it is a heterogeneous disorder with ≥20 symptoms. Clinical research increasingly utilizes objective biological measures (e.g., imaging, peripheral biomarkers) or nonverbal behaviors and/or physiological responses to complement verbally reported symptoms. This shift toward more-objectively measurable phenotypes enables refinement of current animal models of PTSD, and it supports the incorporation of homologous measures across species. We reviewed >600 articles to examine the ability of current rodent models to probe biological phenotypes of PTSD (e.g., sleep disturbances, hippocampal and fear-circuit dysfunction, inflammation, glucocorticoid receptor hypersensitivity) in addition to behavioral phenotypes. Most models reliably produced enduring generalized anxiety-like or depression-like behaviors, as well as hyperactive fear circuits, glucocorticoid receptor hypersensitivity, and response to long-term selective serotonin reuptake inhibitors. Although a few paradigms probed fear conditioning/extinction or utilized peripheral immune, sleep, and noninvasive imaging measures, we argue that these should be incorporated more to enhance translation. Data on female subjects, on subjects at different ages across the life span, or on temporal trajectories of phenotypes after stress that can inform model validity and treatment study design are needed. Overall, preclinical (and clinical) PTSD researchers are increasingly incorporating homologous biological measures to assess markers of risk, response, and treatment outcome. This shift is exciting, as we and many others hope it not only will support translation of drug efficacy from animal models to clinical trials but also will potentially improve predictability of stage II for stage III clinical trials.

Background and objectivesAlthough exposure therapy is an effective treatment for anxiety disorders, fear sometimes returns following successful therapy. Recent literature in animal models indicates that incorporating some aversive events into extinction training may offset these return of fear effects.MethodsThe effect of occasional reinforced extinction trials was investigated in a sample of thirty-nine participants using a fear conditioning and extinction paradigm. Participants either underwent traditional extinction procedures during which the conditional stimulus which had been paired with the unconditional stimulus (US) during acquisition training (CS+) was presented alone with no presentations of the US or partially reinforced extinction during which there were several unpredicted CS+/US pairings.ResultsAs measured by skin conductance responses, physiological fear responding remained elevated during extinction for participants who experienced partially reinforced extinction; however, these participants demonstrated protection from rapid reacquisition effects. Results from the subjective US-expectancy ratings did not provide evidence of protection against rapid reacquisition in the partially reinforced extinction group; however, there was evidence of protection from spontaneous recovery effects. Lastly, as measured by valence ratings, it was unclear whether partially reinforced extinction provided protection from fear recovery effects.LimitationsAlthough participants who experienced partially reinforced extinction demonstrated protection from rapid reacquisition as measured by skin conductance responses, they also demonstrated significantly higher levels of physiological fear responding during extinction which made the results of the spontaneous recovery test more difficult to interpret.ConclusionsOccasional CS-US pairings during extinction may protect against return of fear effects. Clinical implications are discussed.

PTSD has been associated consistently with abnormalities in fear acquisition and extinction learning and retention. Fear acquisition refers to learning to discriminate between threat and safety cues. Extinction learning reflects the formation of a new inhibitory-memory that competes with a previously learned threat-related memory. Adjudicating the competition between threat memory and the new inhibitory memory during extinction may rely, in part, on cognitive processes such as working memory (WM). Despite significant shared neural circuits and signaling pathways the relationship between WM, fear acquisition, and extinction is poorly understood. Here, we analyzed data from a large sample of healthy Marines who underwent an assessment battery including tests of fear acquisition, extinction learning, and WM (N-back). Fear potentiated startle (FPS), fear expectancy ratings, and self-reported anxiety served as the primary dependent variables. High WM ability (N = 192) was associated with greater CS + fear inhibition during the late block of extinction and greater US expectancy change during extinction learning compared to individuals with low WM ability (N = 204). WM ability was not associated with magnitude of fear conditioning/expression. Attention ability was unrelated to fear acquisition or extinction supporting specificity of WM associations with extinction. These results support the conclusion that individual differences in WM may contribute to regulating fear responses.

A diagnostic criterion for drug addiction, persistent drug-craving continues to be the most treatment-resistant aspect of addiction that maintains the chronic, relapsing, nature of this disease. Despite the high prevalence of psychomotor stimulant addiction, there currently exists no FDA-approved medication for craving reduction. In good part, this reflects our lack of understanding of the neurobiological underpinnings of drug-craving. In humans, cue-elicited drug-craving is associated with the hyperexcitability of prefrontal cortical regions. Rodent models of cocaine addiction indicate that a history of excessive cocaine-taking impacts excitatory glutamate signaling within the prefrontal cortex to drive drug-seeking behavior during protracted withdrawal. This review summarizes evidence that the capacity of cocaine-associated cues to augment craving in highly drug-experienced rats relates to a withdrawal-dependent incubation of glutamate release within prelimbic cortex. We discuss how stimulation of mGlu1/5 receptors increases the activational state of both canonical and noncanonical intracellular signaling pathways and present a theoretical molecular model in which the activation of several kinase effectors, including protein kinase C, extracellular signal-regulated kinase and phosphoinositide 3-kinase (PI3K) might lead to receptor desensitization to account for persistent cocaine-craving during protracted withdrawal. Finally, this review discusses the potential for existing, FDA-approved, pharmacotherapeutic agents that target kinase function as a novel approach to craving intervention in cocaine addiction.

The eco-evolutionary dynamics of species are fundamentally linked to the energetic constraints of their constituent individuals. Of particular importance is the interplay between reproduction and the dynamics of starvation and recovery. To elucidate this interplay, here we introduce a nutritional state-structured model that incorporates two classes of consumers: nutritionally replete, reproducing consumers, and undernourished, nonreproducing consumers. We obtain strong constraints on starvation and recovery rates by deriving allometric scaling relationships and find that population dynamics are typically driven to a steady state. Moreover, these rates fall within a "refuge" in parameter space, where the probability of population extinction is minimized. We also show that our model provides a natural framework to predict steady state population abundances known as Damuth's law, and maximum mammalian body size. By determining the relative stability of an otherwise homogeneous population to a competing population with altered percent body fat, this framework provides a principled mechanism for a selective driver of Cope's rule.

BackgroundRisk for posttraumatic stress disorder (PTSD) is thought to be mediated by gene × environment (G × E) interactions that affect core cognitive processes such as fear learning. The catechol-O-methyltransferase (COMT) val158met polymorphism has been associated with risk for PTSD and impaired fear inhibition. We used a large, relatively homogenous population to (1) replicate previous findings of poor fear inhibition in COMT Met/Met carriers with PTSD; (2) determine if COMT association with fear inhibition is moderated by childhood trauma (CT), an environmental risk factor for PTSD; and (3) determine if COMT is associated with altered fear processes after recent exposure to combat trauma.MethodsMale Marines and Navy Corpsmen of European-American ancestry were assessed prior to (n = 714) and 4-6 months after deployment to Afghanistan (n = 452). Acquisition and extinction of fear-potentiated startle, childhood and combat trauma history, and PTSD diagnosis were assessed at both time points.ResultsBefore deployment, Met/Met genotype was associated with fear inhibition deficits in participants with current PTSD; however, this association was dependent on CT exposure. After deployment, combat trauma was associated with a modest reduction in fear extinction in Met/Met compared with Val/Val carriers. There were no associations of COMT genotype with fear extinction within healthy and non-traumatized individuals.ConclusionsThese findings support the hypothesis that G × E interactions underlie associations of COMT val158met with fear inhibition deficits. These studies confirm that Met/Met carriers with PTSD have poor fear inhibition, and support further research in understanding how this polymorphism might impact response to extinction-based therapies.

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Global biodiversity loss is disproportionately rapid on islands, where invasive species are a major driver of extinctions. To inform conservation planning aimed at preventing extinctions, we identify the distribution and biogeographic patterns of highly threatened terrestrial vertebrates (classified by the International Union for Conservation of Nature) and invasive vertebrates on ~465,000 islands worldwide by conducting a comprehensive literature review and interviews with more than 500 experts. We found that 1189 highly threatened vertebrate species (319 amphibians, 282 reptiles, 296 birds, and 292 mammals) breed on 1288 islands. These taxa represent only 5% of Earths terrestrial vertebrates and 41% of all highly threatened terrestrial vertebrates, which occur in

Conservation of species and ecosystems is increasingly difficult because anthropogenic impacts are pervasive and accelerating. Under this rapid global change, maximizing conservation success requires a paradigm shift from maintaining ecosystems in idealized past states toward facilitating their adaptive and functional capacities, even as species ebb and flow individually. Developing effective strategies under this new paradigm will require deeper understanding of the long-term dynamics that govern ecosystem persistence and reconciliation of conflicts among approaches to conserving historical versus novel ecosystems. Integrating emerging information from conservation biology, paleobiology, and the Earth sciences is an important step forward on the path to success. Maintaining nature in all its aspects will also entail immediately addressing the overarching threats of growing human population, overconsumption, pollution, and climate change.

Social support is associated with positive health outcomes, and research has demonstrated that the presence, or even just a reminder, of a social-support figure can reduce psychological and physiological responses to threats. However, the mechanisms underlying this effect are unclear, and no previous work has examined the impact of social support on basic fear learning processes, which have implications for threat responding. This study examined whether social support inhibits the formation of fear associations. After conducting a fear-conditioning procedure in which social-support stimuli were paired with conditional stimuli during fear acquisition, we found that the threat of shock was not associated with conditional stimuli paired with images of social-support figures, but was associated with stimuli paired with images of strangers. These findings indicate that social support prevents the formation of fear associations, reducing the amount of learned fears people acquire as they navigate the world, consequently reducing threat-related stress.

By virtue of adopting the core symptomatic fear (i.e., a fear of weight gain) as a primary treatment target, the treatment of AN centrally involves exposure-driven processes. However, exposure trials targeting the fear of weight gain in AN have been sparse, yielding mixed results to date. In translating extinction theory to the treatment of AN, it is likely that the absence of a clear distinction between what constitutes the core feared cue and the core feared outcome has stymied the application of exposure treatments in AN. This review considers several configurations of the core fear association in AN, noting distinct therapeutic strategies which may allow for more precise efforts in violating fear-based expectancies. Specific guidance is offered in the clinical decision making process as to which strategies might best promote inhibitory learning, and a clinical case is discussed, in which treatment was adjusted to specifically violate the core underlying fear association.

According to Epstein (1985), extinction is one of the main processes for creative problem solving. To test this assertion, we present an experiment in which we manipulated extinction in a problem situation using the computer game Portal 2®. Three groups of participants were exposed to the same problem (i.e., get out of a chamber) under two different conditions. Two groups of participants learned the prerequisite behavior to solve the problem (NOEXT and EXT), but one group did not receive this training (BL). Under one condition, the problem could be solved in two ways: either by emitting a new flexible behavior (innovative) or by doing all of the previously learned behaviors (not innovative). Under the second condition, the problem had to be solved by emitting the innovative behavior, and the learned behaviors were under operational extinction. NOEXT was exposed to the first condition and EXT and LB groups to the second. Results showed that all participants from EXT and NOEXT, but fewer than half of LB groups, solved the problem, corroborating previous data that showed that creative problem solving is a function of previous learning. All but two participants from the NOEXT group solved the problem by emitting the learned behaviors; thus, extinction increased the likelihood of emitting new and flexible problem-solving behaviors. The results also showed that the EXT group spent more time solving the problem, emitted a higher frequency of behaviors other than E1, and interacted more often with objects than the NOEXT group. Therefore, even if the problem-solving behavior of EXT and NOEXT groups was equally effective for obtaining the solution, it was not equally efficient. We discuss that the constraints (i.e., extinction vs. no extinction) of each problem imposed different learning conditions during problem solving. New learning was necessary to produce the new and flexible problem solving of the EXT group, and this process demands more time and effort than solving the problem by just performing what was learned in the past, as the NOEXT group did. Finally, results also suggested a modulatory effect of gaming experience of the effects of experimental training on creative problem solving, because the participants from LB who solved the problem were those with more experience with different types of games. [ABSTRACT FROM AUTHOR]

Invasive mammals on islands pose severe, ongoing threats to global biodiversity. However, the severity of threats from different mammals, and the role of interacting biotic and abiotic factors in driving extinctions, remain poorly understood at a global scale. Here we model global extirpation patterns for island populations of threatened and extinct vertebrates. Extirpations are driven by interacting factors including invasive rats, cats, pigs, mustelids and mongooses, native species taxonomic class and volancy, island size, precipitation and human presence. We show that controlling or eradicating the relevant invasive mammals could prevent 41-75% of predicted future extirpations. The magnitude of benefits varies across species and environments; for example, managing invasive mammals on small, dry islands could halve the extirpation risk for highly threatened birds and mammals, while doing so on large, wet islands may have little benefit. Our results provide quantitative estimates of conservation benefits and, when combined with costs in a return-on-investment framework, can guide efficient conservation strategies.

Although the temporal overlap between human dispersal across Australia and the disappearance of its largest animals is well established, the lack of unambiguous evidence for human-megafauna interactions has led some to question a human role in megafaunal extinction. Here we show that diagnostic burn patterns on eggshell fragments of the megafaunal bird Genyornis newtoni, found at >200 sites across Australia, were created by humans discarding eggshell in and around transient fires, presumably made to cook the eggs. Dating by three methods restricts their occurrence to between 53.9 and 43.4 ka, and likely before 47 ka. Dromaius (emu) eggshell occur frequently in deposits from >100 ka to present; burnt Dromaius eggshell first appear in deposits the same age as those with burnt Genyornis eggshell, and then continually to modern time. Harvesting of their eggs by humans would have decreased Genyornis reproductive success, contributing to the bird's extinction by ∼47 ka.

The late Pleistocene extinction of so many large-bodied vertebrates has been variously attributed to two general causes: rapid climate change and the effects of humans as they spread from the Old World to previously uninhabited continents and islands. Many large-bodied vertebrates, especially large apex predators, maintain their associated ecosystems through top-down forcing processes, especially trophic cascades, and megaherbivores also exert an array of strong indirect effects on their communities. Thus, a third possibility for at least some of the Pleistocene extinctions is that they occurred through habitat changes resulting from the loss of these other keystone species. Here we explore the plausibility of this mechanism, using information on sea otters, kelp forests, and the recent extinction of Stellers sea cows from the Commander Islands. Large numbers of sea cows occurred in the Commander Islands at the time of their discovery by Europeans in 1741. Although extinction of these last remaining sea cows during early years of the Pacific maritime fur trade is widely thought to be a consequence of direct human overkill, we show that it is also a probable consequence of the loss of sea otters and the co-occurring loss of kelp, even if not a single sea cow had been killed directly by humans. This example supports the hypothesis that the directly caused extinctions of a few large vertebrates in the late Pleistocene may have resulted in the coextinction of numerous other species.

The use of quantitative, laboratory-based measures of threat in humans for proof-of-concept studies and target development for novel drug discovery has grown tremendously in the last 2 decades. In particular, in the field of posttraumatic stress disorder (PTSD), human models of fear conditioning have been critical in shaping our theoretical understanding of fear processes and importantly, validating findings from animal models of the neural substrates and signaling pathways required for these complex processes. Here, we will review the use of laboratory-based measures of fear processes in humans including cued and contextual conditioning, generalization, extinction, reconsolidation, and reinstatement to develop novel drug treatments for PTSD. We will primarily focus on recent advances in using behavioral and physiological measures of fear, discussing their sensitivity as biobehavioral markers of PTSD symptoms, their response to known and novel PTSD treatments, and in the case of d-cycloserine, how well these findings have translated to outcomes in clinical trials. We will highlight some gaps in the literature and needs for future research, discuss benefits and limitations of these outcome measures in designing proof-of-concept trials, and offer practical guidelines on design and interpretation when using these fear models for drug discovery.

The role of theory within ecology has changed dramatically in recent decades. Once primarily a source of qualitative conceptual framing, ecological theories and models are now often used to develop quantitative explanations of empirical patterns and to project future dynamics of specific ecological systems. In this essay, I recount my own experience of this transformation, in which accelerating computing power and the widespread incorporation of stochastic processes into ecological theory combined to create some novel integration of mathematical and statistical models. This stronger integration drives theory towards incorporating more biological realism, and I explore ways in which we can grapple with that realism to generate new general theoretical insights. This enhanced realism, in turn, may lead to frameworks for projecting ecological responses to anthropogenic change, which is, arguably, the central challenge for 21st-century ecology. In an era of big data and synthesis, ecologists are increasingly seeking to infer causality from observational data; but conventional biometry provides few tools for this project. This is a realm where theorists can and should play an important role, and I close by pointing towards some analytical and philosophical approaches developed in our sister discipline of economics that address this very problem. While I make no grand prognostications about the likely discoveries of ecological theory over the coming century, you will find in this essay a scattering of more or less far-fetched ideas that I, at least, think are interesting and (possibly) fruitful directions for our field.

Childhood obesity is associated with medical and psychological comorbidities, and interventions targeting overeating could be pragmatic and have a significant impact on weight. Calorically dense foods are easily available, variable, and tasty which allows for effective opportunities to learn to associate behaviors and cues in the environment with food through fundamental conditioning processes, resulting in measurable psychological and physiological food cue reactivity in vulnerable children. Basic research suggests that initial learning is difficult to erase, and that it is vulnerable to a number of phenomena that will allow the original learning to re-emerge after it is suppressed or replaced. These processes may help explain why it may be difficult to change food cue reactivity and overeating over the long term. Extinction theory may be used to develop effective cue-exposure treatments to decrease food cue reactivity through inhibitory learning, although these processes are complex and require an integral understanding of the theory and individual differences. Additionally, learning theory can be used to develop other interventions that may prove to be useful. Through an integration of learning theory, basic and translational research, it may be possible to develop interventions that can decrease the urges to overeat, and improve the weight status of children.

Remembering a past event elicits distributed neural patterns that can be distinguished from patterns elicited when encountering novel information. These differing patterns can be decoded with relatively high diagnostic accuracy for individual memories using multivoxel pattern analysis (MVPA) of fMRI data. Brain-based memory detection--if valid and reliable--would have clear utility beyond the domain of cognitive neuroscience, in the realm of law, marketing, and beyond. However, a significant boundary condition on memory decoding validity may be the deployment of "countermeasures": strategies used to mask memory signals. Here we tested the vulnerability of fMRI-based memory detection to countermeasures, using a paradigm that bears resemblance to eyewitness identification. Participants were scanned while performing two tasks on previously studied and novel faces: (1) a standard recognition memory task; and (2) a task wherein they attempted to conceal their true memory state. Univariate analyses revealed that participants were able to strategically modulate neural responses, averaged across trials, in regions implicated in memory retrieval, including the hippocampus and angular gyrus. Moreover, regions associated with goal-directed shifts of attention and thought substitution supported memory concealment, and those associated with memory generation supported novelty concealment. Critically, whereas MVPA enabled reliable classification of memory states when participants reported memory truthfully, the ability to decode memory on individual trials was compromised, even reversing, during attempts to conceal memory. Together, these findings demonstrate that strategic goal states can be deployed to mask memory-related neural patterns and foil memory decoding technology, placing a significant boundary condition on their real-world utility.

Anthropogenic impacts are endangering many long-lived species and lineages, possibly leading to a disproportionate loss of existing evolutionary history (EH) in the future. However, surprisingly little is known about the loss of EH during major extinctions in the geological past, and thus we do not know whether human impacts are pruning the tree of life in a manner that is unique in the history of life. A major impediment to comparing the loss of EH during past and current extinctions is the conceptual difference in how ages are estimated from paleontological data versus molecular phylogenies. In the former case the age of a taxon is its entire stratigraphic range, regardless of how many daughter taxa it may have produced; for the latter it is the time to the most recent common ancestor shared with another extant taxon. To explore this issue, we use simulations to understand how the loss of EH is manifested in the two data types. We also present empirical analyses of the marine bivalve clade Pectinidae (scallops) during a major Plio-Pleistocene extinction in California that involved a preferential loss of younger species. Overall, our results show that the conceptual difference in how ages are estimated from the stratigraphic record versus molecular phylogenies does not preclude comparisons of age selectivities of past and present extinctions. Such comparisons not only provide fundamental insights into the nature of the extinction process but should also help improve evolutionarily informed models of conservation prioritization.

Obese individuals develop heightened reactivity to environmental cues associated with hedonic foods through Pavlovian conditioning. This study examined differences between overweight (n = 16) and lean (n = 17) 18-26 year-olds in their acquisition of a swallowing response to visual cues paired with chocolate milk, tasteless water and no taste stimulus. We hypothesized that, compared to lean participants, overweight participants would demonstrate a heightened conditioned swallowing response to the visual cue paired with chocolate milk as well as a resistance to extinction of this response. Results showed that overweight participants swallowed more in response to the visual cue previously paired with chocolate than the cue previously paired with tasteless water (t(15) = -3.057, p = .008) while lean participants showed no cue discrimination (t(16) = -1.027, p = .320). The results evaluating the extinction hypothesis could not be evaluated, as the lean participants did not acquire a conditioned response. In evaluating the conditioned swallow response of overweight participants only, results indicated that there was not a significant decrease in swallowing to cues paired with chocolate milk or water, but overall, overweight participants swallowed more to cues paired with chocolate than cues paired with water. These are the first results to show differential acquisition of Pavlovian conditioned responding in overweight individuals compared to lean individuals, as well as differential conditioning to cues paired with hedonic food stimuli compared to cues paired with neutral stimuli.

Obsessive-compulsive disorder (OCD), like other illnesses with prominent anxiety, may involve abnormal fear regulation and consolidation of safety memories. Impaired fear extinction memory (extinction recall, ER) has been shown in individuals with current symptoms of OCD [1]. However, contrary to expectations, the only previous study investigating this phenomenon showed a positive correlation between extinction recall abilities and OCD symptomology (i.e., as OCD symptoms worsened, extinction memory improved). The purpose of the current study was to determine if patients with a lifetime diagnosis of OCD (not necessarily currently symptomatic) also demonstrate impairments in extinction memory, and the relationship between OCD symptomology and extinction memory in this type of sample. In addition, we also examined fear renewal, which has never been investigated in an OCD sample. We enrolled 37 patients with OCD, the majority of whom were on serotonin reuptake inhibitors, and 18 healthy control participants in a 2-day paradigm assessing fear conditioning and extinction (Day 1) and extinction retention and renewal (Day 2). Skin conductance responses (SCRs) were the dependent measure. Results, as in the prior study, indicated that the only between-group difference was impaired ER in OCD patients relative to controls. Contrary to our prediction, OCD symptom severity was not correlated with the magnitude of extinction recall. There were no differences in fear renewal between OCD patients and controls.

Marine defaunation, or human-caused animal loss in the oceans, emerged forcefully only hundreds of years ago, whereas terrestrial defaunation has been occurring far longer. Though humans have caused few global marine extinctions, we have profoundly affected marine wildlife, altering the functioning and provisioning of services in every ocean. Current ocean trends, coupled with terrestrial defaunation lessons, suggest that marine defaunation rates will rapidly intensify as human use of the oceans industrializes. Though protected areas are a powerful tool to harness ocean productivity, especially when designed with future climate in mind, additional management strategies will be required. Overall, habitat degradation is likely to intensify as a major driver of marine wildlife loss. Proactive intervention can avert a marine defaunation disaster of the magnitude observed on land.