Certain regions of the brain activate when viewing or interacting with tools, suggesting the existence of a tool use brain network. Neural activation appears to be the same for tool observation and tool use, so tool observation may induce simulations of tool use.

Just because I won't get the chance to ask about it in class: what is a fiber volley amplitude?

CA1-LTP significantly increased for juv-adol ELE mice but not for juv ELE or adol ELE mice when compared to controls. Hippocampal excitability properties were significantly modulated in juv ELE and juv-adol ELE mice. Modulation of hippocampal excitability properties as well as enhanced OLM function lasted for two weeks after stopping exercise in juv ELE mice.

Paired-pulse facilitation did not yield significant differences between groups.

Input/output curve plotting EPSP slope against presynaptic fiber volleys. fEPSP slopes were significantly different for the juv-adol ELE and adol ELE mice but not for the juv ELE mice when compared to controls.

input/output curve plotting presynaptic fiber volleys against stimulus intensity showed a main effect of ELE group, main effect of stimulus intensity, and significant interaction between ELE group and stimulus intensity.

input/output curve plotting EPSP slope against stimulus intensity showed a main effect of ELE group, effect of stimulus intensity, and significant interaction between ELE group and stimulus intensity. fEPSP slopes were significantly higher for the juv ELE and juv-adol ELE mice but not for the adol ELE mice when compared to controls.

LTP significantly increased in response to theta burst stimulation for juv-adol ELE mice, but not for juv ELE or adol ELE mice in comparison with controls.

Enhanced LTP in juv-adol ELE mice lasted for 50-60 minutes following the theta burst stimulation, significantly more than it did for controls.

What is the stimulus being referred to here? Is it the theta bursts? Is it basically saying that the fEPSP intensity (the slope) in response to theta burst intensity is being recorded? I had a very difficult time interpreting this paragraph because I wasn't sure what the stimulus being discussed here was. Does anyone who is more knowledgeable about this type of research understand what is meant by stimulus?

A form of short-term, activity-dependent synaptic plasticity common to most chemically transmitting synapses, manifested as an enhancement in the amplitude of the second of two rapidly evoked excitatory postsynaptic potentials (EPSPs).

Needs definition.

EPSPs that are generated by transient imbalances in ion concentrations in the spaces outside the cells, that result from cellular electrical activity.

Axon collaterals given off by CA3 pyramidal cells in the hippocampus.

short bursts of stimulation that more closely mimic the natural rhythms of activity in the neurons of the brain at high frequencies, with the bursts themselves being applied 5 times per second.

There were no significant differences between any groups of male and female mice in terms of total time spent exploring objects.

In male mice, juv-adol ELE mice and juv ELE mice showed a significantly higher preference for the object placed in the novel location when compared to no ELE mice and adol ELE mice. In female mice, juv ELE mice showed a significantly higher preference for the object placed in the novel location when compared to no ELE mice, juv ELE mice, and juv-adol ELE mice. All male ELE mice demonstrated significant object preference from acquisition to testing when compared with male no ELE mice. Female juv ELE and juv-adol ELE mice demonstrated significant object preference from acquisition to testing when compared with female adol ELE mice and no ELE mice.

The 3 min OLM acquisition task did not result in significant object discrimination (object preference) in any groups of mice, regardless of sex. 3 min-trained, sedentary male and female mice demonstrated significantly lower object discrimination than 10 min-trained, ELE male and female mice.

There were no significant differences between any groups of male and female mice in terms of total time spent exploring objects.

For all groups of male and female mice, a 5 min OLM testing task 24 h after the 10 min OLM acquisition task resulted in significant object discrimination (object preference) for the object placed in the novel location. No group demonstrated discrimination for the novel object significantly more than any other group.

The 10 min OLM acquisition task did not result in significant object discrimination (object preference) in any groups of mice, regardless of sex.

For both male and female mice, distance traveled significantly decreased over the six OLM trials, indicating that the mice were habituated to the OLM chambers.

Two groups of mice did an object location memory (OLM) task for either 3 or 10 minutes, and then all mice did that same task again for 5 minutes 24 hours later with one of the objects moved to a different location.

What exactly is a stationary wheel, and how is it different from a regular running wheel? Why would the presence of such a thing cause the mice to gain a significant amount of weight? I looked up the definition of "stationary wheel" and it just seems like an alternative name for a running wheel, but that's clearly not what it is given the differential effects it had on weight gain in female mice.

All mice in the juv-adol ELE group, juv ELE group, and adol ELE group significantly increased their running distances during the three week exercise period.

In the juv-adol ELE group, the juv ELE group, and the adol ELE group, there were no significant differences in distance ran between male and female mice.

In male mice, the juv ELE group gained significantly more weight than the juv-adol ELE group. In female mice, the stationary group gained significantly more weight than the sedentary group, the juv-adol ELE group, and the adol ELE group.

Young male and female mice were split into four groups over a period of three weeks. One group of mice was sedentary from the first to the third week (sed), one exercised for the first week (juv ELE), one exercised from the first to the third week (juv-adol ELE), and one group of mice exercised for the third week (adol ELE). After this, all mice were either tested for object location memory or sacrificed for electrophysiology.

In rodents, the hippocampus develops milestone learning and memory functions by about the 3rd to 4th postnatal week. At this time, brain development via synaptic plasticity is especially sensitive to environmental experiences. For that reason, it makes sense to see whether exercise during this period modulates hippocampal development.

This was very confusing for me. I THINK what it's saying is that the gene expression that controls cell function in specific brain circuits is influenced by certain environmental experiences and activities engaged in, and that gene expression is what drives brain development. Essentially, brain development happens via synaptic plasticity, and that synaptic plasticity is very sensitive to the environment. I could be totally off here but I THINK that's what I think it means.

This reminds me of the childhood sensitive periods during which synaptic plasticity being higher allows for the acquisition of different languages. Based on the content of this article, it seems like early life plasticity in general allows experiences to seriously alter how the brain develops, so something like exercise has much longer lasting or more permanent positive impact. I wonder if this works the other way, as well. Like, could trauma experienced during early life have a longer-lasting or more permanent negative impact than trauma experienced during adulthood?

Both male and female mice that underwent exercise during the juvenile period showed enhanced hippocampal memory and synaptic plasticity. The results of this study could be used to investigate the time-sensitive molecular mechanisms underlying the long-lasting effects of early life exercise on neuronal function and behavior.

A maze task that measures spatial memory and learning in rats.

The effects of exercise on synaptic plasticity and memory formation are not long-lasting in exercise is done in adulthood, but may be longer lasting if exercise is done during development. The time frame of when exercise should be done to promote long-lasting changes to synaptic plasticity and memory formation, however, are not known.

In humans, exercise promotes synaptic plasticity mechanisms and enhances cognition, especially during childhood. In rodents, exercise similarly promotes synaptic plasticity mechanisms and enhances cognition, although it has only been studied in adults and not in juveniles.

The process of growing blood vessels into a tissue to improve oxygen and nutrient supply.

Oxytocin may indirectly contribute to the development of out-group and intergroup bias derogation by promoting in-group favoritism. This challenges the view that oxytocin is purely prosocial, since that prosociality may only apply to members of the in group and may also motivate exclusion and negativity towards the out-group.

In experiments 1, 2, and 3, in-group vs. out-group target presentation order did not effect whether or not in-group favoritism emerged. Experiments 4 and 5 evaluated in-group favoritism and out-group derogation in the absence of inter-group comparison. It can't be known for whether oxytocin motivates in-group favoritism in the absence of inter-group comparisons, so future research should investigate this.

It may be that oxytocin creates intergroup bias primarily by promoting in-group favoritism, and not so much by promoting out-group derogation. Oxytocin strongly promoting in-group favoritism and weakly promoting out-group derogation is adaptive, because in-group favoritism is much more important for survival and within-group coordination.

The results of this study showed that oxytocin system activation underlies the phenomenon of in group bias and, in some cases, the phenomenon of out-group derogation. Oxytocin has the same effects on in-group favoritism, regardless of what the compared out-group is.

The group that was administered oxytocin was significantly less likely to sacrifice an in-group member than an out-group member when compared with the group that was administered placebo.

The group that was administered oxytocin was significantly less likely to sacrifice an in-group member than an out-group member when compared with the group that was administered placebo.

Both groups associated uniquely human emotions with in-group members more frequently than with outgroup members, but the oxytocin group associated uniquely human emotions with in-group members more frequently than with outgroup members significantly more than the placebo group.

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In experiment 1, both in-group regard and out-group disregard were significantly higher for the group administered oxytocin than for the group administered placebo.

In experiment 2, in-group regard was significantly higher for the group administered oxytocin than for the group administered placebo. Out-group disregard was not significantly different between groups.

This article's researchers did experiments to determine whether oxytocin had an effect on in-group favoritism and out-group derogation. Of two groups, one was administered oxytocin and the other was administered placebo. Both groups had to engage in a task that measured in-group favoritism and out-group derogation.

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Ethnocentrism is the tendency to view one's own group as superior to others. It manifests itself as the valuation of members of the in-group as good and superior, and members of out-groups as bad and inferior. It is a survival mechanism because it builds cooperation between in-group members and avoids harm from out-group members.

Oxytocin has been shown to motivate in-group favoritism. Because in-group favoritism can sometimes manifest itself as out-group derogation, oxytocin may also motivate out-group derogation.

Pleasure derived by someone from another person's misfortune.

This article's researchers hypothesized that human ethnocentrism is motivated by oxytocin. Oxytocin is a neurotransmitter/peptide hormone that has various effects in different brain areas. Oxytocin promotes trust and cooperation in humans, but this effect may apply to in-group members only. If that is the case, then humans given oxytocin should show more in-group favoritism than humans given a placebo in an experiment.

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The tacitly held belief that one's ingroup is more human than an outgroup, which is less human.

The perception or treatment of someone or something as being of little worth.

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Seems like the control group attenuated to anxiety more effectively than the PI group. Could this maybe be related to habituation? I.e., the controls being in a less stressful environment than the PI group allows them to habituate to negative feelings like anxiety more effectively than the PI group.

IVs: previously institutionalized children, biologically raised children. DVs: brain activity, trait anxiety.

So, the aversive noise is the US. Am I correct in interpreting the CS as the shape border becoming thicker? Also, this is the terminology used in classical conditioning, but this seems more like operant conditioning, since the participants actually have to do a specific behavior in order for the aversive stimulus to be removed.

H1: aversive learning will be supported by a more distributed, adult-like set of brain regions in PI youth relative to comparison youth.

H2: altered amygdala-hippocampal-mPFC function during aversive learning will predict reduced anxiety among PI youth.

RQ2: do differences in aversive learning partially explain the association between early institutionalization and anxiety?

RQ1: does early adversity, in the form of prior institutionalization, alter neurobiology of aversive learning during human development?

As an adult with an anxiety disorder...yeah, this is pretty accurate. It's weird to think of anxiety as affording benefits when it's seemingly so maladaptive, but I guess it does make it easier for us to detect potentially harmful situations and avoid them. The problem is really when you begin to experience anxiety when you shouldn't, in response to nonthreatening or neutral stimuli.

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This study looking into how stress experienced by orphaned children effects structure and function of mPFC and limbic structures made me curious about how children who go through foster care differ from children who grow up with their biological parents in terms of brain development, since the U.S. foster care system is notorious for child maltreatment. Looking into it, it seems that children who grow up in the foster care system significantly differ from children who grow up with their biological parents in terms of inhibitory control neurocircuitry (Bruce et al., 2013), although it isn't clear to me from skimming the article whether inhibitory control is more robust in foster care children or controls.

Is it possible that the mPFC, in a sense, "learns" to exert a greater amount of top-down control over the amygdala and hippocampus in individuals with high trait anxiety, since they appear to be overly active in said individuals (particularly the amygdala)? Could it be that spending time in an aversive environment early in development "conditions" these limbic structures to be hyperactive, which in turn leads to strengthened connections with the PFC, since it needs to exert a greater amount of top-down control over them in order to inhibit their overactivity?

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Previous research has found that barrel cortex NMDAR activation was required to initiate plasticity after learning a somatosensory task, but that barrel cortex mGluR activation was required to initiate plasticity after re-practicing that same task. The current study hypothesized that a similar phenomenon occurred with plasticity after learning a fear task in the hippocampus, and its results support this assertion.

A region of the somatosensory cortex that is identifiable in some rodents.

Previous research has found that piriform cortex NMDAR activation was required for initial learning of an olfactory discrimination task, but piriform cortex neuron intrinsic excitability increase and synaptic NMDAR subunit composition alteration was required for subsequent learning of the same task. The current study hypothesized that a similar phenomenon occurred in the hippocampus with spatial/contextual learning, and its results support this assertion.

Blocking neuronal excitability or the reactivation of excitable neurons may reduce NMDAR-independent learning, and NMDAR-independent learning may persist over time before eventually disappearing. Recent study results support these assertions.

Two conditions must be met to conclude that hippocampal NMDAR activation is not required for subsequent memory formation: animals must form a new memory during training and not simply generalize from previous experiences, and NMDAR-independent memories must depend on the hippocampus. The current study found that both of these conditions were met, suggesting that hippocampal NMDAR activation is in fact not required for subsequent memory formation.

Post-synaptic NMDAR activation is believed to be necessary for LTP to occur and for memories to be formed.

Hippocampal NMDAR activation is only required for initial memories to be formed, since subsequent memories can be formed in the presence of hippocampal NMDAR antagonists. Prior NMDAR-dependent learning has to be of a similar task for later NMDAR-independent learning to occur.

Indirect, slowly acting (metabotropic) excitatory (glutamate) receptors that have some sort of effect on LTP. Needs explanation.

This procedure was done to determine whether mGluR activation occurring as a result of intrinsic excitability increase is the plasticity mechanism by which subsequent learning following initial learning happens in the absence of NMDAR activation.

CA1 sub-region of the hippocampus.

Some forms of hippocampal LTP that do not require NMDAR activation require the activation of metabotropic glutamate receptors (mGluRs) instead. The current study aimed to see if that was the case through the use of bioassays of animal models.

Needs explanation.

CA3 sub-region of the hippocampus.

LTP that occurs at the so-called "mossy fiber synapses" of the hippocampus, which is a specific group of synapses that is involved with encoding short-term memory.

This procedure was done to determine whether the intrinsic excitability of hippocampal neurons increases when learning subsequent information that builds on initially learned information. The point of this was to see whether plasticity mechanisms other than NMDA receptor activation are involved in subsequent learning that follows initial learning.

It is possible that initial learning increases intrinsic excitability, which allows subsequently learned information to be encoded by plasticity mechanisms that don't involve the activation of NMDARs. The current study aimed to see if this was the case using bioassays of animal models.

We know from psychology that previous experiences impact how individuals learn, but we don't know much about the neurobiological mechanisms underlying this process. This is because we've only been able to experiment in lab settings that may not accurately reflect nature.

In various animal models, NMDA receptors have been found to activate when something is initially being learned, but not when it is subsequently being practiced or built upon.

Memory of past experiences interfering with an individual's ability to hold new information in working memory.

A change in the physiological or biochemical state of neurons such that the ability to generate synaptic plasticity is altered.

Electrical excitability of a particular neuron.

Receptors important for learning and memory.

FBOE is a reliable correlate, but not predictor, of same sex attraction in men (more older brothers, but not more older sisters).

Many questions remain about how sexual orientation develops, despite how much research has been done into the topic. These studies cannot infer causality between the phenomena studied and the development of sexual orientation, however, this does not erase the possibility that they may contribute to the development of sexual orientation in some way (albeit indirectly). Overall, it seems like biology and prenatal hormone exposure do play a significant role in the development of sexual orientation in both men and women.

A study that examined the co-occurrence of sexual orientation biomarkers in adult men found that they don't significantly co-occur, but that the FBOE is the most accurate predictor of homosexuality in men.

The study that supports FBOE also supports that a maternal immune mechanism underlies FBOE. In addition, it provides evidence that a male specific protein may be important in the development of sexual orientation and in neurological functioning associated with forming social connections (including sexual ones).

a family of presynaptic cell adhesion proteins that have roles in connecting neurons at the synapse.

A study found that mothers of gay sons had higher rates of antibodies to male-specific proteins expressed in the fetal brain than mothers of heterosexual sons, suggesting that the immune response to these proteins during pregnancy was greater in mothers of gay sons than in mothers of heterosexual sons (supports FBOE).

The study that supports FBOE had reliable methods, so the significance of its results should be trusted.

FBOE is biological in nature (non-biological older brothers do not contribute to the effect). Basically, male fetuses have proteins on the Y chromosome called HY antigens that mothers develop more antibodies to with each subsequent pregnancy. These antibodies are theorized to alter the function of proteins in areas of the brain that are relevant to the development of sexual attraction, leading to the incidence of homosexuality. So, the more sons a mother has (and the more antibodies she has), the more likely she is to have a son who is homosexual.

A study supported the idea that sexual orientation was a polygenic (controlled by multiple genes) characteristic in male and female homosexuals, as it was associated with the location of multiple specific SNPs. In homosexual men, one of these SNPs was located near a gene that regulates olfactory functioning (which may be tied to sexuality/sexual orientation), and one of them was located near a gene that regulates reproductive functioning and development. The study had a flawed methodology.

A study showed that male homosexuality may be associated with the location of specific SNPs, but the study's sample size wasn't large enough to make any definitive conclusions.