In the currentwork, we used event-related electroencephalography (EEG) and functional magnetic resonanceimaging (fMRI) to determine neural correlates for differentiating contextually correct and incorrecttool use.

We discovered that exercise for 4th-6th postnatal weeks (juv-adol ELE), as well as a shorter exercise experience only during the 4th postnatal week (juv ELE) enable hippocampal-dependent spatial memory formation in male mice. This was not true for mice that exercised only during the 6th postnatal week (adol ELE), suggesting that the 4th postnatal week of development was particularly sensitive to the exercise experience with regard to enabling long-term memory function in a lasting manner.

.

adolescent exercisers when compared to sedentary controls.

Overall, these data suggest a significant impact of ELE on enhancing hippocampal long-term potenti-ation. Although this finding is in contrast to data in adult mice demonstrating lack of enhancement in CA1-LTP after chronic voluntary wheel running9, it may implicate a specific, 1-week period of juvenile exercise that can lead to lasting changes in hippocampal CA3-CA1 circuit function and plasticity.

Therefore, synaptic plasticity was examined in the CA3-CA1 Schaffer collateral pathway of the hippocampus in sedentary and ELE mice, to test the hypothesis that ELE also leads to an enhance-ment in synaptic strength in the same region involved in enabled memory performance after juv and juv-adol ELE.

These results suggest that in both sexes, exercise taking place during a specific juvenile developmental period (P21–27) is sufficient for enhancing long-term memory for an OLM acquisition trial that is usually insufficient for long-term memory in sedentary controls, and fur-thermore, juv ELE-induced enabling of long-term memory is present at least 2 weeks after the juvenile exercise period ends.

These data suggest that performance in the OLM task can be used as a robust measure of long-term memory formation in adolescent male and female mice.

We therefore tested the following hypotheses: 1) that a learning stimulus typically insufficient for long-term memory formation in sedentary wild-type mice can become sufficient after ELE (as it does after 2–3 weeks of exercise in adulthood), and 2) the early-life timing of exercise during juvenile and/or ado-lescent periods will have a lasting impact on the duration of ELE-induced improvements in long-term memory.

We next addressed the question whether there are sex differences in daily and cumulative running distances in our three ELE groups. Juv-adol ELE male and female mice gradually increased their daily running distance over the 3-week period (Fig. 1c).

We next compared daily and cumulative running distances in 1-week runners, expecting that running distance would be significantly greater in adol ELE mice when compared to juv ELE mice (regardless of sex) given their developmental stage and body mass differences when entering running cages.

Given the developmental timing of voluntary exercise in this model, we postulated that there would be important sex-specific and running group-specific differences in weight gain and distance ran across time.

In sum, all running groups and both sexes of mice gradually and significantly increased their running distances across time. The cumulative amount of voluntary running throughout the running period was dependent on when early life exercise was initiated (in the juvenile period vs in adolescence).

These findings suggest that a longer duration of ELE expo-sure (three weeks) during juvenile/adolescence significantly reduces weight gain in male mice, whereas in female mice, presence of a stationary wheel led to greater weight gain than mice in sedentary cages without running wheel and mice that ran during adolescence.

.

.

In this study we developed a model of voluntary physical activity during specific early life developmental periods in mice (early-life exercise, or ELE) to address the hypothesis that the timing of exercise during postnatal hippocampal maturation can lead to enduring benefits in cognitive function and synaptic plasticity.

.

.

hysical exercise is a powerful modulator of learning and memory. Mechanisms underlying the cognitive benefits of exercise are well documented in adult rodents. Exercise studies targeting postnatal periods of hippocampal maturation (specifically targeting periods of synaptic reorganization and plasticity) are lacking. We characterize a model of early-life exercise (ELE) in male and female mice designed with the goal of identifying critical periods by which exercise may have a lasting impact on hippocampal memory and synaptic plasticity.

Our results suggest that early-life exercise, specifically during the 4th postnatal week, can enable hippocampal memory, synaptic plasticity, and alter hippocampal excitability when occurring during postnatal periods of hippocampal maturation.

.

Again, support was found for the hypotheses that oxytocin creates intergroup bias because it motivates in-group favoritism. Put differently, oxytocin motivated in-group favoritism both when an intergroup compari- son was salient (experiments 1 and 2) and when such an intergroup comparison was substantially more implicit (experiments 3-5). Together, these results suggest that in-group favoritism emerges regardless of whether an explicit out-group comparison is ren- dered salient

.

.

.

Results show that oxytocin creates intergroup bias because it motivates in-group favoritism and, in some cases, out-group der- ogation.

Together, these results provide additional support for the hypothesis that (/) oxytocin creates intergroup bias because (ii) oxytocin promotes in-group favoritism. There was no support for the hypothesis that (Hi) oxytocin promotes out-group derogation.

Experiment 3 thus supports the hy- pothesis that .(/) oxytocin creates intergroup bias because (ii) oxytocin promotes in-group favoritism. There was no support for the hypothesis that (Hi) oxytocin promotes out-group derogation.

Thus, there is support for the hypothesis that (/) oxytocin creates in- tergroup bias because (//) oxytocin promotes in-group favoritism. Mixed support was obtained for the hypothesis (Hi) that oxytocin promotes out-group derogation.

.

In-group favoritism and out-group derogation conspire to create intergroup bias: the unfair response toward another group that devalues or disadvantages the other group and its members by valuing or privileging members of one's in-group (29). Here we predicted that (/) oxytocin creates such intergroup bias because (ii) oxytocin promotes in-group favoritism and, possibly, (///) out- group derogation.

.

.

.

If in-group favoritism and out-group derogation have adaptive value and sustain in-group functioning, coordination, and co- operation, it follows that (/) throughout evolution those individ- uals who displayed in-group favoritism and out-group derogation and who detected such tendencies in others were more likely to spread than individuals lacking these capacities (5-8) and (ii) the human brain may have evolved to sustain ethnocentrism through yet-unknown neurobiological systems.

Human ethnocentrism - the tendency to view one's group as cen- trally important and superior to other groups- creates intergroup bias that fuels prejudice, xenophobia, and intergroup violence. Grounded in the idea that ethnocentrism also facilitates within- group trust cooperation, and coordination, we conjecture that eth- nocentrism may be modulated by brain oxytocin, a peptide shown to promote cooperation among in-group members.

Results show that oxytocin creates intergroup bias be- cause oxytocin motivates in-group favoritism and, to a lesser ex- tent, out-group derogation. These findings call into question the view of oxytocin as an indiscriminate "love drug" or "cuddle chem- ical" and suggest that oxytocin has a role in the emergence of in- tergroup conflict and violence.

The present results ought to be considered alongside the lim-itations of this study.

recruitment of prefrontal and subcortical circuitry. Beyond estab-lishing these basic differences between PI and comparison youth,thepresentstudyidentifiedaneuraladaptationamongPIyouththatpredicted greater resilience over time. Specifically, stronger hip-pocampal–prefrontal coupling prospectively predicted a reductionin anxiety symptomology over a 2 year period. This suggests thatgreater integration of information across brain systems involved inaversive learning and regulation is a protective factor for individualswho have experienced adversity.

The present study revealed that PI and comparison youth arecapable of amygdala-based aversive learning. However, aversivelearning following institutionalization was associated with a broader

caregiving adversity.

Specifically, individual differences in hip-pocampal–vmPFC connectivity during aversive learning predictanxiety outcomes among individuals who have experienced early

Theseresults suggest that greater prefrontal–hippocampal communi-cation during development may protect against a pathologicalcourse of anxiety for individuals who have experienced caregiv-ing adversity.

Together withthe present findings, this suggests that adversity-induced altera-tions in hippocampal function may facilitate adaptive learning, atleast in the short term, about threats in one’s environment.

Together with the present findings, this suggests that earlycaregiving adversity changes the pacing of amygdala–hippo-campus–vmPFC circuit development and, in doing so, alters theway that aversive learning is represented in the brain.

These resultssuggest that age-atypical hippocampal–vmPFC connectivitymay be an important source of resilience for youth with ahistory of caregiving adversity.

The current study examined this rearing aberration in human development.Eighty-nine children and adolescents who were either previously institutionalized (PI youth; N46; 33 females and 13 males; age range,7–16 years) or were raised by their biological parents from birth (N43; 22 females and 21 males; age range, 7–16 years) completed anaversive-learning paradigm while undergoing functional neuroimaging, wherein visual cues were paired with either an aversive sound(CS) or no sound (CS).

Given evidence from animal models that early caregiving adver-sity accelerates amygdala, hippocampal, and medial prefrontaldevelopment (Callaghan et al., 2014), we hypothesized that aver-sive learning would be supported by a more distributed, adult-like set of brain regions in PI youth relative to comparison youth.

Given evidence thatneural adaptations to caregiving adversity can be anxiolytic (Geeet al., 2013), it was hypothesized that altered amygdala–hip-pocampal–mPFC function during aversive learning would pre-dict reduced anxiety among PI youth.

The second question that the current study addressed waswhether differences in aversive learning might partially explainthe association between early institutionalization and anxiety.

The first question the present study addressed was whetherearly adversity, in the form of prior institutionalization, alters theneurobiology of aversive learning during human development.

For the PI youth, better aversive learning was associated with higher concurrent trait anxiety. Both groupsshowed robust learning and amygdala activation for CSversus CStrials. However, PI youth also exhibited broader recruitment ofseveral regions and increased hippocampal connectivity with prefrontal cortex. Stronger connectivity between the hippocampus andventromedialPFCpredictedsignificantimprovementsinfutureanxiety(measured2yearslater),andthiswasparticularlytruewithinthePI group.

Juvenile animals rely exclu-sively on the amygdala for aversive learning (Kim et al., 2012; Li etal., 2012). During adolescence, striking changes in amygdala–hippocampal–mPFC connectivity are observed (Pattwell et al.,2011), and, by adulthood, aversive learning is supported bystrong interconnections among the amygdala, hippocampus, andmPFC in nonhuman animals (LeDoux et al., 1990; Corcoran andQuirk, 2007; Sierra-Mercado et al., 2011) and human adults (Ful-lana et al., 2016; Greco and Liberzon, 2016). Rodent models haverevealed that maternal separation leads to precocious prefrontaland hippocampal maturation (Huang et al., 2005; Muhammad etal., 2012), and adult-like aversive learning and anxiety duringdevelopment (Moriceau and Sullivan, 2006; Ono et al., 2008;Callaghan and Richardson, 2011).

Gorka et al., 2014), little is known about how it impacts aversivelearning during human development. This limits our under-standing of how early adversity begets adult anxiety.

Although it is known that early adversityalters the neural bases of aversive learning and predicts anxiety inadults (Bremner et al., 2005; Bagot et al., 2009; Kessler et al., 2010;

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

And racial discrimination doesn’t exist just within the military rank-and-file. Every year, civilians working in the financial, technical and support sectors of the Army, Air Force and Navy file hundreds of complaints alleging race and skin color discrimination, according to an AP analysis of U.S. Equal Employment Opportunity Commission data.

“For Blacks and minorities, when we initially experience racism or discrimination in the military, we feel blindsided,” Davis said. “We’re taught to believe that it’s the one place where everybody has a level playing field and that we can make it to the top with work that’s based on merit.”

Social Anxiety and Academic AchievementTo the best of our knowledge, only two research groupshave tested the hypothesis that social anxiety is directly and

chlenker and Leary hypothesizedthat individuals likely become socially anxious when theywish to make a good impression on others but anticipate thatthey will be unsuccessful. Leary (2010) further proposed thatsocially anxious individuals perceive most relationships tobe unbalanced by default, through a predisposing fear thatothers will not value the relationship as highly as they do.The consequence of this ‘‘relationship devaluation’’ is aninability for socially anxious individuals to obtain their ownparticular interpersonal objectives through their relation-ships with others

From this perspective, indi-viduals who are socially anxious might perceive the uni-versity/college social environment as somewhatthreatening, which, in turn, would restrict their openness tochange

How-ever, thoughts of engaging or interacting with others mightfoster the social fears that are central to social anxiety, hin-dering any attempt to participate in the classroom, join inconversations, or ask for help in order to successfully ma-neuver through the university/college system

The goal of the present study was to test whether socialanxiety is directly associated with academic achievementover time among university/college students, and second,to investigate a proposed indirect mechanism throughwhich social anxiety might be linked to lower academicachievement—that is, through the restricted formation ofnew social ties in university/college

In fact,Russell and Topham (2012) propose that social anxietymay have a negative impact on university/college students’academic achievement