Amygdala

People who donated a kidney to a stranger have a larger amygdala

gettingwell4 2-3 stars Required further work, Amygdala, Brain hemispheres, Cerebrum, Epigenetics, Limbic system ,

This 2014 Georgetown study was of people who had donated a kidney to a stranger. The study found that the subjects had a larger right amygdala part of their limbic systems:

“Our results support the possibility of a neural basis for extraordinary altruism.

In sum, our findings suggest that individuals who have performed an act of extraordinary altruism can be distinguished from healthy controls by increased right amygdala volume, as well as heightened responsiveness in right amygdala to fearful facial expressions, which may support enhanced recognition of these expressions.”

The researchers stopped short of causal explanations. They stated in the study’s abstract that:

“Individual variation in altruistic tendencies may be genetically mediated”

but didn’t develop any evidence to support this statement.

It would have been within the scope of the study had the researchers continued on to examine:

  • What may have happened in the subjects’ lives to possibly cause their neurobiological and psychological attributes?
  • What were the causes for the subjects’ extreme altruistic behavior?
  • Were these the same causes for their larger, more sensitive amygdala?

An accompanying PNAS commentary from a Harvard researcher made other points. However, the author showed his biases that the cerebrum rules human behavior with an out-of-left-field question at the end of a paragraph in which he developed specious reasoning.

The commentator was completely off base when he stated:

“Could it be that extraordinary altruists such as Maupin [a study participant] and the 19 individuals studied by Marsh et al. [the researchers] are special, not only because of how they feel when they see people in distress, but because of how they think?”

I don’t imagine that the brilliant commentator’s attempt to upstage the study’s subjects and put the spotlight on himself for some brilliant idea was much appreciated by anyone involved.

The amygdala is the central hub of a person’s limbic system. The study’s findings had very little to say about the subjects’ cerebral activity – thinking.

To postulate that the researchers missed that there was something different about the subjects’ thinking was out of touch with the realities of both the researchers’ scientific bases and the subjects. It’s another example of the current research mindset/social meme of cerebral dominance.

http://www.pnas.org/content/111/42/15036.full “Neural and cognitive characteristics of extraordinary altruists”

A missed opportunity to research the oxytocin receptor gene and autism

gettingwell4 2-3 stars Required further work, Amygdala, Brain development, Epigenetics, Hypothalamus, Limbic system, Neurochemicals, Oxytocin, Vasopressin ,

This 2013 study:

“Examined whether genetic variants of the OXTR [oxytocin receptor] affect face recognition memory in families with an autistic child.

We investigated whether common polymorphisms in the genes encoding the oxytocin and vasopressin 1a receptors influence social memory for faces.”

I feel that the researchers missed an opportunity to improve their assessment of the autism-related genetic contribution to the study’s findings by separating the degree of environmental influence on the oxytocin receptor gene expression, as did the How epigenetic DNA methylation of the oxytocin receptor gene affects the perception of anger and fear study.

An assessment of epigenetic DNA methylation of the oxytocin receptor gene may have been even more compelling because the researchers genetically sampled one non-autistic sibling in each of the autistic children’s families. I hope the study’s samples are still available, because they may offer the possibility of evaluating the contribution of the autistic children’s historical environment with potential confirmation from their siblings.

Both studies gave their subjects similar facial emotion recognition tests, with the current one deriving from findings about autism, and the second from findings about the amygdala. The studies also had common references, such as a 2010 study, A common allele in the oxytocin receptor gene (OXTR) impacts prosocial temperament and human hypothalamic-limbic structure and function.

http://www.pnas.org/content/111/5/1987.full “Common polymorphism in the oxytocin receptor gene (OXTR) is associated with human social recognition skills”

Translating PTSD research findings from animals to humans

gettingwell4 0-1 star Wasted resources, Amygdala, Cortisol, Hippocampus, Limbic system, Neurochemicals, Stress

This 2014 rodent study stressed the animals, measured their stress responses, then killed them and sampled genes in their amygdala, hippocampus, and blood. The researchers found that glucocorticoid receptor signaling genes were the primary pathway associated with “exposure-related individual differences“ in stress responses for the amygdala and blood. This pathway also placed first for the hippocampus in female rats (glucocorticoid receptor was second in male rats and prostate cancer signaling was first).

I’ll quote one press article’s coverage to show where the researchers wanted to go with the study’s findings:

“We found that most of the genes and pathways that are different in PTSD [post-traumatic stress disorder]-like animals compared to resilient animals are related to the glucocorticoid receptor, which suggests we might have identified a therapeutic target for treatment of PTSD.”

How about this lead sentence:

“There may some day be a blood test to determine whether someone suffers from Post-Traumatic Stress Disorder or is at risk for the psychiatric condition.”

Here’s another article’s paraphrase of a different researcher:

“Those are genes that become activated in the presence of stress. Like a key fitting into a lock, the hormone corticosterone, produced naturally by the body, connects to the receptor and has a calming effect.

In some rodents, and apparently in some people, the pathway appears to be defective, and this puts them at higher risk for PTSD.”

Also, from the study’s abstract:

“Corticosterone treatment 1 h[our] after PSS [predator-scent-stress]-exposure prevented anxiety and hyperarousal 7 d[ays] later in both sexes, confirming the GR [glucocorticoid receptor] involvement in the PSS behavioral response.”

Like other researchers continue to do, they stopped this study short of finding causes for the effects:

  1. What were the causes for genes in the glucocorticoid receptor signaling pathway being differentially expressed? “Exposure-related individual differences” isn’t a causal finding.
  2. If this pathway is “defective,” what exactly happened to make it that way?
  3. Did dampening the effects of stress with a shot of cortisol one hour after the stress treat the cause such that the rats were cured? Since the readers of the study and associated articles were led to infer that this treatment was a cure, why destroy the treated animals afterwards before the proofs of long-term efficacy were thoroughly documented and tested?

When studies like this are carried forward with humans, researchers should try to find the causes for these effects. It isn’t sufficient to pretend that there aren’t early-life causes for these effects. Such a pretense leads to the follow-on pretense that later-life consequences are mysteries such as “exposure-related individual differences” and not effects.

Researchers should act like the subjects are feeling human beings who can participate in treatments of both the causes and effects. They should remember that humans are not lab rats who need to be fixed.

http://www.pnas.org/content/111/37/13529.full “Expression profiling associates blood and brain glucocorticoid receptor signaling with trauma-related individual differences in both sexes”

Can a Romanian orphan give informed consent to be an experimental subject?

gettingwell4 < 0 Detracted from science, Amygdala, Brain development, Cerebrum, Cortisol, Hypothalamus, Limbic system, Neurochemicals, Stress , ,

This 2015 study used Romanian orphans as lab rats for findings of which I failed to see the value. The world didn’t really need any further research to demonstrate that foster care would be better for a child than staying in an orphanage.

The researchers placed the orphans in five separate stressful situations, and measured their cortisol and DHEA-S levels, along with their electrocardiograph and impedance cardiograph activity. The findings were:

“Children who were removed from the Romanian institutions and placed with foster parents before the age of 24 months had stress system responses similar to those of children being raised by families in the community.

The children raised in institutions showed blunted responses in the sympathetic nervous system, associated with the flight or fight response, and in the HPA axis, which regulates cortisol.”

One unsupported assertion from the researchers was:

“We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.”

The researchers stated that rodent studies have converged to find:

“Early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis.”

It’s baloney that the same results from early life adversity in rodents haven’t also been present in humans. Even the lead researcher herself said in a news article:

“More significantly, McLaughlin said, their [the orphans] stress response systems might have been initially hyperactive at earlier points in development, then adapted to high levels of stress hormones.”

The difference was that the rodents were monitored 24/7 until researchers killed and dissected them. The children’s periods of adversity likely started while in the womb, and their lives had been monitored for research purposes sporadically after their births.

Everybody knows that just because adverse events and effects in these children’s lives weren’t recorded by researchers didn’t mean these effects weren’t present at some point.

Particularly irksome was another unsupported assertion from the lead reviewer:

“The children involved in the study are now about 16 years old, and researchers next plan to investigate whether puberty has an impact on their stress responses. It could have a positive effect, McLaughlin said, since puberty might represent another sensitive period when stress response systems are particularly tuned to environmental inputs. “It’s possible that the environment during that period could reverse the impacts of early adversity on the system,” she said.”

No, this is NOT possible. We may as well expect an apple to fall upward.

The impacts of early adversity persist with enduring physiological changes as shown in experimental studies. Studies have NOT provided evidence that the subjects’ environment can cause the effects of complete reversal of all these changes, no matter the stage of life of the subjects.

This point was addressed in The effects of early-life stress are permanent alterations in the child’s brain circuitry and function rodent study:

“The current study manipulates the type and timing of a stressor and the specific task and age of testing to parallel early-life stress in humans reared in orphanages.

The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress.

These effects are not reversed when the stressor is removed nor diminished with the development of prefrontal regulation regions.”

That study had the same reviewer as the current study. The current study’s lead researcher knew or should have known of this and other relevant research. She knew or should have known of the irreversibility of critical periods, during which developments either occurred or were forever missed.

Did the lead researcher make assertions not supported by the study or relevant research – assertions made counter to her scientific knowledge – show her unease about treating the orphans as lab rats? Was there was some other agenda in play?

The larger problem was the study’s informed consent with this group of Romanian orphans. If you were in contact with a damaged person, and implicitly gave them hope that you would improve their life, then who are you as a feeling human being when you don’t personally carry through? Does the legal documentation matter?

Also, I’ve noticed problems with several studies that had this particular reviewer:

Add the current study to the list.

http://www.pnas.org/content/112/18/5637.full “Causal effects of the early caregiving environment on development of stress response systems in children”

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The amygdala part of the limbic system doesn’t process beliefs

gettingwell4 0-1 star Wasted resources, Amygdala, Beliefs, Cerebrum, Limbic system

Does your desk light switch on or off when other people in the office switch their desk lights on or off? Something in the wiring would probably be wrong if it did.

And wouldn’t you expect that other desk lights would still operate normally if your desk light’s bulb burned out, although everyone may be plugged into the same electrical circuit?

It surprised the researchers of this 2015 CalTech/MIT study when:

“Two patients with bilateral amygdala lesions performed a belief reasoning test.

Both patients showed typical test performance and cortical activity when compared with nearly 500 healthy controls.”

The study’s overall frame of reference was expressed as:

“Humans use a so-called “theory-of-mind” to reason about the beliefs of others. Neuroimaging studies of belief reasoning suggest it activates a specific cortical network. The amygdala is interconnected with this network and plays a fundamental role in social behavior.”

The experimental test:

“Was designed to optimize functional contrast in those brain regions thought to be involved in attempts, be they successful or unsuccessful, to evaluate the veracity of another person’s belief about the world.”

A “belief reasoning test..to reason about the beliefs of others” is a cerebral exercise. The amygdala, in contrast, is an emotional center of a person’s limbic system.

The logic by which the study may be viewed is:

  1. The “belief reasoning test” had no emotional content to activate the subjects’ amygdalae.
  2. fMRI scans confirmed that limbic system areas in the 2 lesioned subjects weren’t activated during the test.
  3. Apply the logic of Occam’s razor, and we arrive at the findings of “typical test performance and cortical activity.”

Task performance and beliefs about task responses are solely cerebral exercises had a similar methodology and result in that those subjects’ limbic systems were monitored during fMRI scans and subsequent reporting, but the subjects’ limbic system areas weren’t activated during any of the experiments.

The researchers stated the results:

“Suggest a reevaluation of the role of the amygdala and its cortical interactions in human social cognition.”

But per the beginning analogy – if your desk light’s bulb burned out, would you be surprised that it didn’t affect the normal operations of desk lights in other offices, although they all may be plugged into the same circuit?

This study informed us that the amygdala isn’t slaved to the cerebrum. It’s hard to change the current research mindset/social meme of cerebral dominance, though, so maybe this information will be overlooked.

http://www.pnas.org/content/112/15/4827.full “Amygdala lesions do not compromise the cortical network for false-belief reasoning”

Epigenetic DNA methylation of the oxytocin receptor gene affected the perception of anger and fear

gettingwell4 2-3 stars Required further work, Amygdala, Anterior cingulate cortex, Brain development, Brain hemispheres, Cerebrum, Epigenetics, Hippocampus, Limbic system, Neurochemicals, Oxytocin, Thalamus ,

This 2015 Virginia human study:

“Reveals how epigenetic variability in the endogenous oxytocin system impacts brain systems supporting social cognition and is an important step to better characterize relationships between genes, brain, and behavior.”

The researchers did a lot of things right:

  • They studied a priori selected brain areas, followed by whole brain analyses;
  • Their subjects were carefully selected

    “Because methylation levels have been shown to differ as a function of race, we restricted our sample to Caucasians of European descent”

    but they didn’t restrict subjects to the same gender;

  • They acknowledged as a limitation:

    “A lack of behavioral evidence to reveal how these epigenetic and neural markers impact the overt social phenotype.”

One thing on which I disagree with the researchers is their assessment of what needs to be done next. Their news release stated:

“When imagining the future possibilities and implications this DNA methylation and oxytocin receptor research may have, the investigators think a blood test could be developed in order to predict how an individual may behave in social situations.”

Nice idea, but the next step should be to complete the research. The next step is to develop evidence for how the oxytocin receptor gene became methylated.

The subjects had a wide range of DNA methylation at the studied gene site – from 33% to 72% methylated!

Why?

At the same gene site:

“There was a significant effect of sex such that females have a higher level of methylation than males.”

Why?

Given these significant effects, why was there no research into likely causes?

Aren’t early periods in people’s lives the most likely times when the “Epigenetic modification of the oxytocin receptor gene” that “influences the perception of anger and fear in the human brain” takes place?

Wouldn’t findings from research on the subjects’ histories potentially help other people?

http://www.pnas.org/content/112/11/3308.full “Epigenetic modification of the oxytocin receptor gene influences the perception of anger and fear in the human brain”

If you had a disease, would you agree to treatment where you became a lab rat?

gettingwell4 2-3 stars Required further work, Amygdala, Limbic system, Thalamus ,

This 2015 Czech research studied individual neurons in an area of the limbic system of Parkinson’s disease patients. The findings corroborated several findings of previous research, such as:

“We confirm the importance of the subthalamic nucleus as a hub within the limbic circuitry involved in both emotional valence and arousal processing as in two functionally and spatially segregated systems.”

This statement summed up the study for me:

“Several factors could affect our results and reduce the inferences that can be drawn with regards to the physiology of emotional processing and the role of the subthalamic nucleus in the limbic circuits.

One such factor is that the study was conducted with Parkinson’s disease patients, who are known to have a widespread central nervous system pathology and to experience problems in emotional processing.”

The current study referenced The amygdala is where we integrate our perception of human facial emotion study, which similarly used the opportunity of patients with electrodes implanted for deep-brain stimulation to study individual neurons in the amygdala. However, a design difference was that the amygdala study had healthy control subjects in addition to patients, which led to fewer potential limitations on their findings.

Also referenced was a summary study entitled Exploring emotions using invasive methods: review of 60 years of human intracranial electrophysiology. Despite excluding studies of decision making, reward processing, learning, mood disorders, and pain experiences, it didn’t demonstrate that 60 years of experiments using implanted electrodes in the brains of people with epilepsy had substantially advanced science, other than confirming what fMRI and animal research had shown.

I’m not sure how I would feel if I had a disease where the physicians treated my symptoms in such a way that I became a lab rat for research that wasn’t groundbreaking. Do people with epilepsy and Parkinson’s disease have treatments available that factually resolve the underlying causes?

http://www.pnas.org/content/112/10/3116.full “Distinct populations of neurons respond to emotional valence and arousal in the human subthalamic nucleus”

Research on brain areas involved when we imagine people, places, and pleasantness

gettingwell4 2-3 stars Required further work, Amygdala, Beliefs, Brain hemispheres, Cerebrum, Hippocampus, Limbic system, Thalamus ,

This highly jargoned 2014 Harvard study was on how people imagine that they’ll feel in the future.

One of the researchers was an author of:

I was surprised that this study also didn’t ignore the limbic system to the point to where the researchers wouldn’t even bother to measure important areas.

Limbic system areas that process people were different than those that process places. For example, the data in Table S4 showed that the subjects’ left amygdala and hippocampus were more activated when simulating future familiar people, whereas their right hippocampus was more activated when simulating future familiar places.

The researchers may have improved the study’s findings if they were informed by studies such as the Hippocampus replays memories and preplays to extend memories into future scenarios, which found that “place” cells in the CA1 segment of the hippocampus preplay events that imagine future scenarios of:

“Novel spatial experiences of similar distinctiveness and complexity.”

Such information may have helped to disambiguate one of the study’s findings in Table S5, that both sides of the subjects’ hippocampus were more activated than other brain regions when simulating both familiar people and places.

The researchers got a little carried away in broadly attributing most of the study’s findings to the ventromedial prefrontal cortex. For example, the data in Table S6 showed that the thalamus was more activated when the subjects anticipated positive pleasantness, but not when negative effects were anticipated.

We know from Thalamus gating and control of the limbic system and cerebrum is a form of memory that this is normally how the thalamus part of the limbic system actively controls and gates information to and from the cerebrum. Their data showed thalamic gating in operation:

  • Active when passing along pleasantness to cerebral areas, and
  • Passive when blocking unpleasantness from cerebral areas.

Also, I didn’t see how the researchers differentiated some of their findings from a placebo effect. For example, Using expectations of oxytocin to induce positive placebo effects of touching is a cerebral exercise found:

“Pain reduction dampened sensory processing in the brain, whereas increased touch pleasantness increased sensory processing.”

This was very similar to the above finding involving the thalamus.

http://www.pnas.org/content/111/46/16550.full “Ventromedial prefrontal cortex supports affective future simulation by integrating distributed knowledge”

Fear extinction is the learned inhibition of retrieval of previously acquired responses

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Cerebrum, Epigenetics, Hippocampus, Limbic system, Memory

This 2014 rodent study showed that fear extinction doesn’t depend on memory retrieval:

“These results show that extinction and retrieval are separate processes and strongly suggest that extinction is triggered or gated by the conditioned stimulus even in the absence of retrieval.”

Key to my understanding this finding came from a definition in another summary study by the authors, The learning of fear extinction, where they stated:

“Extinction is the learned inhibition of retrieval of previously acquired responses.”

These two studies and Hippocampal mechanisms involved in the enhancement of fear extinction caused by exposure to novelty should inform researchers of studies such as If rodent training has beneficial epigenetic effects, how can the next step be human gene therapy? of desirable alternative treatments, rather than proceeding from rodent training directly to human gene therapy.

http://www.pnas.org/content/112/2/E230.full “Extinction learning, which consists of the inhibition of retrieval, can be learned without retrieval”

What is the purpose of music? A review of evolutionary and pleasurable research findings

gettingwell4 2-3 stars Required further work, Amygdala, Anterior cingulate cortex, Cerebrum, Dopamine, Hippocampus, Hypothalamus, Limbic system, Lower brain, Neurochemicals

Ever wonder what happens in your brain and body when you get chills from a musical performance?

This 2013 summary review of 126 studies provided details of brain areas that contribute to our enjoyment of music.

Much of the review addressed Darwin’s observation that music had no readily apparent functional consequence and no clear-cut adaptive function. The researchers noted that:

“There is scant evidence that other species possess the mental machinery to decode music in the way humans do, or to derive enjoyment from it.”

The reasons why different types of music affect us differently are similar to the findings of the Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards study.

Here are the “We seek limbic system rewards” similarities:

“The nucleus accumbens played an important role with both familiar and novel music. In the case of familiar music, hemodynamic activity in the nucleus accumbens was associated with increasing pleasure, and maximally expressed during the experience of chills, which represent the peak emotional response; these were the same regions that showed dopamine release. The nucleus accumbens is tightly connected with subcortical limbic areas of the brain, implicated in processing, detecting, and expressing emotions, including the amygdala and hippocampus. It is also connected to the hypothalamus, insula, and anterior cingulate cortex, all of which are implicated in controlling the autonomic nervous system, and may be responsible for the psychophysiological phenomena associated with listening to music and emotional arousal.”

Here is the “We seek cerebral rewards” part.

“Finally, the nucleus accumbens is tightly integrated with cortical areas implicated in “high-level” processing of emotions that integrate information from various sources, including the orbital and ventromedial frontal lobe. These areas are largely implicated in assigning and maintaining reward value to stimuli and may be critical in evaluating the significance of abstract stimuli that we consider pleasurable.”

http://www.pnas.org/content/110/Supplement_2/10430.full “From perception to pleasure: Music and its neural substrates”

Using expectations of oxytocin to induce positive placebo effects of touching

gettingwell4 2-3 stars Required further work, Amygdala, Beliefs, Brain hemispheres, Limbic system, Neurochemicals, Oxytocin, Thalamus

This 2013 Scandinavian study detailed which brain structures were involved when fooling oneself about actual sensations in favor of expected sensations.

It was hilarious how the researchers used studies of oxytocin to create expectations in the subjects:

“To induce expectation of intranasal oxytocin’s beneficial effects on painful and pleasant touch experience, participants viewed a 6-min locally developed video documentary about oxytocin’s putative prosocial effects such as involvement in bonding, love, grooming, affective touch, and healing. As all of the material was based on published research, there was no deception. The video concluded that a nasal spray of oxytocin might enhance the pleasantness of:

  • (i) stroking and
  • (ii) warm touch, and
  • (iii) reduce the unpleasantness of pain.”

Other items:

  • Only the placebo effects for the warm and pain-reducing touches were statistically significant, not the stroking touch;
  • The a priori brain areas monitored in the “sensory circuitry” included the thalamus and were all in the right brain hemisphere;
  • The a priori brain areas monitored in the “emotional appraisal circuitry” included the amygdala.

One way the researchers summarized the study was:

“Pain reduction dampened sensory processing in the brain, whereas increased touch pleasantness increased sensory processing.”

This finding demonstrated how the thalamus part of the limbic system actively controls and gates information to and from the cerebrum, similar to the Thalamus gating and control of the limbic system and cerebrum is a form of memory study.

There was a terminology problem in the study, evidenced by statements such as:

“We induced placebo improvement of both negative and positive feelings (painful and pleasant touch).”

Touch is a sensation, not a feeling or emotion. This placebo study created expectations of sensations in the subjects’ cerebrums, not expectations of emotions.

Also, including parts of the limbic system such as the amygdala in the “emotional appraisal circuitry” didn’t mean that the researchers studied feelings or emotions. We know from research summarized in the Conscious mental states should not be the first-choice explanation of behavior study that:

“Neither amygdala activity nor amygdala-controlled responses are telltale signatures of fearful feelings.“

The current study cast additional light on the dubious Problematic research on human happiness study. Those researchers were fooled by a positive placebo effect!

http://www.pnas.org/content/110/44/17993.full “Placebo improves pleasure and pain through opposite modulation of sensory processing”

Are stress-induced epigenetic changes to DNA inherited across generations?

gettingwell4 0-1 star Wasted resources, Amygdala, Brain development, Cortisol, Epigenetics, Limbic system, Memory, Neurochemicals, Stress , , , , ,

This 2014 Geneva/Cambridge plant study ended by stating:

“The unequivocal demonstration of transgenerational transmission of environmentally-induced epigenetic traits remains a significant challenge.

One of the critical activities erasing stress memories is conserved between plants and mammals.”

However, the researchers didn’t demonstrate that their findings were broadly applicable for mammals or organisms other than the specific plant variety they studied. Possible reasons for these limited findings were given in a 2015 Australian study referenced by Mechanisms of stress memories in plants:

“The majority of DNA methylation analyses performed in plants to date have focused on Arabidopsis, despite being relatively depleted of TEs [transposable elements] (15–20% of the genome) and being poorly methylated compared to other plant genomes.

These studies have lacked the resolution to provide the specific context and genomic location of the changes in DNA methylation.”

There are also significant differences in how epigenetic inheritance across generations may operate among different species per Epigenetic reprogramming in plant and animal development.

Neither the current study nor the above review addressed the behavioral aspect of stress-induced epigenetic inheritance across generations. For example, the behavior of a mother whose DNA was epigenetically changed by stress can induce the same epigenetic changes to her child’s DNA when her child is stressed per One way that mothers cause fear and emotional trauma in their infants:

“Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

http://www.pnas.org/content/111/23/8547.full “Identification of genes preventing transgenerational transmission of stress-induced epigenetic states”

Is oxytocin why more women than men like horror movies?

gettingwell4 2-3 stars Required further work, Amygdala, Brain hemispheres, Limbic system, Neurochemicals, Oxytocin, Serotonin

This 2014 human study showed how oxytocin regulates serotonin with the involvement of the right part of the amygdala.

The following passage caught my eye as a possible explanation of why more women than men prefer horror movies: oxytocin?

“We have chosen to enroll male subjects only to avoid the confounding effects linked to sex and a possible interaction with gonadal steroids. Indeed, as shown by previous studies, oxytocin modulates brain activity differently in male and female subjects.

For instance, oxytocin suppresses amygdala response to emotionally threatening stimuli in males but enhances the same response in females.“

http://www.pnas.org/content/111/23/8637.full “Switching brain serotonin with oxytocin”

Can psychologists exclude the limbic system and adequately study awareness and social cognition?

gettingwell4 < 0 Detracted from science, Amygdala, Cerebrum, Limbic system, Lower brain, Memory , , , ,

This 2014 Princeton human study was proof that cognitive researchers are stuck in the cerebrum. That and gadgets.

The researchers didn’t measure limbic system or lower brain areas, yet from their use of cartoon faces and magnetically zapping their subjects’ brains they proclaimed:

“The findings suggest a fundamental connection between private awareness and social cognition.”

For just one example of the gross omissions of the study’s design, look at the limbic system’s part in “social cognition” for The amygdala is where we integrate our perception of human facial emotion.

And it’s a very limited scope of “private awareness” that excludes conscious awareness of what’s in our own feeling, instinctual, and impulsive levels of consciousness.

http://www.pnas.org/content/111/13/5012.full “Attributing awareness to oneself and to others”

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The amygdala is where we integrate our perception of human facial emotion

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Hippocampus, Limbic system ,

We all have specialized brain circuits for recognizing faces.

Each person has their own historical judgment of the emotion in a human face, which may or may not be the emotion objectively displayed by the face.

The amygdala, not the hippocampus, was found to be where we integrate our perception of human facial emotion.

The facial information conveyed by the eyes, not the mouth, was primarily how the amygdala perceived emotion.

This 2014 study was performed on seven neurology patients who had deep-brain electrodes implanted for other purposes of diagnosis or treatment, including epilepsy and autism, and six healthy control subjects. With the electrodes, the researchers were able to measure individual neurons instead of functional MRI aggregate results.

This increased measuring capability enabled the researchers to develop other findings, such as:

“Neuronal selectivity for fear faces in the amygdala comes mainly from a suppression of activity in happy-face trials, whereas selectivity for happy faces is mainly due to an increase in activity for happy-face trials.”

Also:

“The long latency of the amygdala responses we observed already argues for considerable synthesis, consistent with the integration of face input from temporal cortex with signals from other brain regions, as well as substantial processing internal to the amygdala.”

http://www.pnas.org/content/111/30/E3110.full “Neurons in the human amygdala selective for perceived emotion”