Limbic system

A study that provided evidence for basic principles of Primal Therapy

gettingwell4 5+ stars Premium, Cerebrum, Epigenetics, Glutamate, Hippocampus, Limbic system, Memory, Neurochemicals, Primal Therapy, Stress , , , , , ,

This 2015 Northwestern University rodent study found:

“Fear-inducing memories can be state dependent, meaning that they can best be retrieved if the brain states at encoding and retrieval are similar.

Memories formed in a particular mood, arousal or drug-induced state can best be retrieved when the brain is back in that state.

‘It’s difficult for therapists to help these patients,’ Radulovic said, ‘because the patients themselves can’t remember their traumatic experiences that are the root cause of their symptoms.’

The best way to access the memories in this system is to return the brain to the same state of consciousness as when the memory was encoded.”

The study demonstrated one method of activating neurobiological pathways with a drug to remove a hippocampal memory’s protection, which played a part in enabling subjects to relive their remembered experiences. This rodent study’s methods weren’t designed to therapeutically access similarly protected memories with humans.

From the Northwestern press release:

“There are two kinds of GABA [gamma-Aminobutyric acid] receptors. One kind, synaptic GABA receptors, works in tandem with glutamate receptors to balance the excitation of the brain in response to external events such as stress.

The other population, extra-synaptic GABA receptors, are independent agents.

If a traumatic event occurs when these extra-synaptic GABA receptors are activated, the memory of this event cannot be accessed unless these receptors are activated once again.

‘It’s an entirely different system even at the genetic and molecular level than the one that encodes normal memories,’ said lead study author Vladimir Jovasevic, who worked on the study when he was a postdoctoral fellow in Radulovic’s lab.

This different system is regulated by a small microRNA, miR-33, and may be the brain’s protective mechanism when an experience is overwhelmingly stressful.

The findings imply that in response to traumatic stress, some individuals, instead of activating the glutamate system to store memories, activate the extra-synaptic GABA system and form inaccessible traumatic memories.”

I’d point out that “can’t remember” and “inaccessible traumatic memories” phrases used above were in reference to what’s usually called “memory” i.e., a recall initiated by the cerebrum.

The study’s findings should inform memory-study researchers if they care to understand how emotional memories can be formed and re-experienced.

The study provided evidence for fundamentals of Dr. Arthur Janov’s Primal Therapy, such as:

  • Experiences associated with pain can be remembered below our conscious awareness.
  • The retrieval and re-experiencing of emotional memories can engage our lower-level brain areas without our higher-level brain areas’ participation.

The obvious nature of this study’s straightforward experimental methods made me wonder why other researchers hadn’t used the same methods decades ago.

Use of this study’s methodology could have resulted in dozens of informative follow-on study variations by now, and subsequently found whether subjects’ physiological, behavioral, and epigenetic measurements differed from control group subjects, as in:

“miR-33 is downregulated in response to gaboxadol [the drug used to change subjects’ brain state] and modulates its effects on state-dependent fear.”

See Resiliency in stress responses for abstracts of three follow-on papers by these researchers.

http://www.nature.com/neuro/journal/v18/n9/full/nn.4084.html “GABAergic mechanisms regulated by miR-33 encode state-dependent fear”

MP3 with lead researcher Dr. Jelena Radulovic: http://www.thenakedscientists.com/HTML/specials/show/20150825/

Leaky gates, anxiety, and grocery store trips without buying list items

gettingwell4 4-5 stars Advanced knowledge, Brain development, Brainstem, Cerebrum, Cortisol, Dopamine, Epigenetics, Limbic system, Lower brain, Memory, Neurochemicals, Oxytocin, Primal Therapy, Serotonin, Stress , , , , , , , ,

An interview with Jeff Link, the editor of Dr. Arthur Janov’s 2011 book “Life Before Birth: The Hidden Script that Rules Our Lives” with Ken Rose:

“Even further confirmation for some of the views of Janov, that maybe weren’t widely accepted for a time, it’s new research now being done into memory and what a lot of scientist are seeing, a lot of different studies is that memory reactivates the same neuroimpulses that were initially firing off when the event happened.

So a traumatic event when you remember it, the act of remembering it is actually creating a neuromirror of what went on initially.

In a lot of ways that is what Primal Therapy is attempting to do; is to go back to that place and reconnect, or as it’s sometimes referred to, reconsolidate the brain state so that real healing can take place.”

Transcript (part 4 of 6): http://cigognenews.blogspot.com/2015/09/ken-rose-on-life-before-birth-part-46.html

MP3: http://www.pantedmonkey.org/podcastgen/download.php?filename=2011-12-15_1300_what_now_jeff_link.mp3

A hippocampal protein that increases when stress increases

gettingwell4 2-3 stars Required further work, Epigenetics, Hippocampus, Limbic system, Stress

This 2015 Michigan human/rodent study found:

“Gene expression profiling in postmortem human brain and studies using animal models have implicated the fibroblast growth factor (FGF) family in affect regulation and suggest a potential role in the pathophysiology of major depressive disorder (MDD).

We show that FGF9 expression is up-regulated in the hippocampus of individuals with MDD, and that FGF9 expression is inversely related to the expression of FGF2.”

The researchers went down the evolutionary scale from human findings to replicate many of the findings with rodents:

“We found that chronic social defeat stress, an animal model recapitulating some aspects of MDD, leads to a significant increase in hippocampal FGF9 expression.

Collectively, these results suggest that high levels of hippocampal FGF9 play an important role in the development or expression of mood and anxiety disorders.”

http://www.pnas.org/content/112/38/11953.full “Fibroblast growth factor 9 is a novel modulator of negative affect”

Adverse effects of inflammation and stress on hippocampal synapses

gettingwell4 2-3 stars Required further work, Hippocampus, Immune system, Limbic system, Memory, Neurochemicals, Stress , , ,

This dense and highly-jargoned 2015 rodent study found:

“The suppression of BDNF [brain-derived neurotrophic factor] signaling, LTP [long-term potentiation], and memory may be driven by an increased sensitivity to IL-1β [the proinflammatory cytokine interleukin 1β] that occurs directly at synapses.”

The researchers reversed the adverse effects of IL-1β after they induced stress and inflammation. Blocking IL-1β when there wasn’t stress or inflammation, however, also caused adverse effects:

“Interestingly, administration of AS1 [the compound that blocked the proinflammatory responses] in the absence of LPS [the bacterial compound used to stress the subjects’ immune systems] treatment also impaired OLM [the object location memory test where control group rodents exhibited a preference for a novel location over a familiar location].

This finding is consistent with the notion that endogenous IL-1β at physiologically low levels may be essential for hippocampal memory function.”

The researchers asserted:

“Our data reveal a previously unidentified mechanism that explains the age-related vulnerability of hippocampal function to impairment by inflammation.”

Instead of couching their findings with a non-causal “age-related” term, could the researchers have specifically identified causes?

“IL-1β activates different pathways via AcP (proinflammatory) or AcPb (prosurvival) IL-1 receptor subunits.

This study demonstrates that the IL-1 receptor subunit system undergoes an age-dependent reconfiguration in hippocampal synapses.

This previously undescribed reconfiguration, characterized by an increase in the AcP/AcPb ratio, is responsible for potentiating impairments of synaptic plasticity and memory by IL-1β.”

What were the underlying causes for the relatively increased AcP activation over AcPb activation? The researchers didn’t say. Their explanations were left hanging at a correlated-but-not-causal “age-dependent” level rather than a “mechanism that explains.”

http://www.pnas.org/content/112/36/E5078.full “Synapse-specific IL-1 receptor subunit reconfiguration augments vulnerability to IL-1β in the aged hippocampus”

A mechanistic study of neurotransmitters in the hippocampus

gettingwell4 4-5 stars Advanced knowledge, Cerebrum, Dopamine, Glutamate, Hippocampus, Limbic system, Neurochemicals ,

This 2015 UK rodent study found:

“A mechanistic understanding of how alterations in dopamine and NMDAR [a type of glutamate receptor that participates in excitatory neurotransmission] function can lead to the disruption of hippocampal–PFC [prefrontal cortex] functional connectivity.

These results show how dopaminergic activation induces long-term hypofunction of NMDARs, which can contribute to disordered functional connectivity, a characteristic that is a hallmark of psychiatric disorders such as schizophrenia.”

One of the experiments applied theta-frequency (5 Hz) waves to the rats’ hippocampi and dampened the electrical activity of the NMDAR type of glutamate receptor.

However, this effect of theta waves was dependent on the activation of D2 dopamine receptors. The study’s findings should inform researchers who treat brain waves as base causes of behavior in studies such as What’s an appropriate control group for a schizophrenia study?

This study’s findings may also inform researchers of studies such as the What causes disconnection between the limbic system and the cerebrum? of a neurochemical basis for “the disruption of hippocampal–PFC functional connectivity.”

http://www.pnas.org/content/112/35/11096.full “Disruption of hippocampal–prefrontal cortex activity by dopamine D2R-dependent LTD of NMDAR transmission”

We first recognize familiar faces with our limbic system

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

This 2015 Belgian human study found:

“Medial temporal lobe structures (perirhinal cortex, amygdala, hippocampus) and anterior inferior temporal cortex responded abruptly when sufficient information for familiar face recognition was accumulated.

Activation in ventral occipitotemporal face-preferential regions increased with visual information, independently of long-term face familiarity.

[The researchers] isolated the discriminative neural responses to unfamiliar and familiar faces by slowly increasing visual information (i.e., high-spatial frequencies) to progressively reveal faces of unfamiliar or personally familiar individuals.”

A limitation of the study was, however:

“Behavioral data were acquired from only 11 subjects because of a technical error.”

http://www.pnas.org/content/112/35/E4835.full “Neural microgenesis of personally familiar face recognition”

A missed opportunity to study image-evoked emotional memories

gettingwell4 0-1 star Wasted resources, Hippocampus, Limbic system, Memory

This 2015 Ohio human study found that the:

“Hippocampus integrates distinct experiences, thereby providing a scaffold for encoding and retrieval of autobiographical memories.”

The researchers ignored the hippocampus’ role in emotional memories, although studies such as Emotional memories and out-of-body–induced hippocampal amnesia have shown emotional involvement to be desirable in order to properly study the hippocampus with human subjects.

The researchers missed quite a few good opportunities to advance science. Consider these opportunities:

  • All subjects were instructed during fMRI scans (here’s a video of one subject) to:

    “Try to remember the event depicted in each picture and relive the experience in their mind while viewing the photo for eight seconds.”

    The photos were taken during each subject’s day-to-day life by a smartphone hung around their neck. Following these instructions created an ideal situation for engaging the subjects’ emotions when they successfully remembered and relived. Although the experiment probably engaged the subjects’ emotions;

  • None of the subjects were asked anything that would lead the researchers to discover WHY the subjects remembered! The researchers had a perfect setup to make even a bare-bones inquiry, or to ask the subjects to immediately rate the emotional impact of each remembered event/relived experience, or to have them identify what emotions were evoked. But the researchers didn’t use any emotional measures to help understand how and why events were remembered or not.
  • Wouldn’t it also have potentially helped the subjects to become somewhat aware of how they processed memories, of how they felt with each remembered event/relived experience? They probably wouldn’t have remembered personally unimportant events, or forgotten personally significant ones.

  • “One subject recalled all of the items presented” and another had “very few unrecalled items.”

    Why? Weren’t the researcher interested in what was potentially the same between these two and different from the other subjects?

The researchers instead focused on rodent studies with statements such as:

“Validating the relevance of decades of rodent studies for human memory.”

They lost track of the reason rodent studies exist: to help humans.

In order for the research to help humans, move forward on the evolutionary scale, not backward! A rat or mouse can’t define and describe the emotional impact of an image of their life that evokes a memory.

http://www.pnas.org/content/112/35/11078.full “Human hippocampus represents space and time during retrieval of real-world memories”

Reflections on my four-year anniversary of spine surgery

gettingwell4 5+ stars Premium, Beliefs, Brain development, Cerebrum, Epigenetics, Limbic system, Lower brain, Memory, Primal Therapy, Stress , , , , ,

At age 55, I found out that I’d suffered for maybe 45 to 50 years from a childhood injury, and I didn’t know anything about it. It still seems unbelievable to me that I was physically ill for decades before I received a diagnosis.

As explained to me by two surgeons, the cause of my spondylolisthesis between L5 and S1 was a sudden injury sometime between ages 5 and 10. Here’s a further explanation:

“In children, spondylolisthesis usually occurs between the fifth bone in the lower back (lumbar vertebra) and the first bone in the sacrum (pelvis) area. It is often due to a birth defect in that area of the spine or sudden injury (acute trauma).

Other causes of spondylolisthesis include bone diseases, traumatic fractures, and stress fractures (commonly seen in gymnasts). Certain sport activities, such as gymnastics, weight lifting, and football, put a great deal of stress on the bones in the lower back. They also require that the athlete constantly overstretch (hyperextend) the spine.”

I played a lot of baseball when I was a kid growing up in Miami. I didn’t suffer from a birth defect or bone disease, play football before I was a teenager, do gymnastics, or lift weights.

I don’t remember a specific “sudden injury (acute trauma)” per the above explanation. Maybe I incurred the acute trauma that started my spondylolisthesis sliding into bases playing baseball. Maybe I incurred it playing in the other rough-and-tumble activities that I did as a boy.

Please stop at the first hint of any pain that you feel while reading the rest of this post. I don’t want to cause you pain.

I re-experienced while in Primal Therapy a day when I was seven or eight years old. A most exhilarating day, one that filled me with light and joy.

What brought on my elevated mood? It was the day I finally ran faster than my father did, and he couldn’t catch me to give me a beating as I ran out of the house.

My father never beat me on the sidewalk, the street, or the front yard anyway. That would make the abuse public.

My father’s job was assistant principal/dean of boys at West Miami Junior High School. He whipped boys with a thick belt or paddled them daily as part of his job requirements.

My father kept a wooden paddle with holes in it at home. For me.

I don’t remember that my three siblings ever received a paddling or belting, although they were spanked. I’ve remembered while in Primal Therapy that my younger sister and brother were spanked for crying.

I re-experienced the dread of waiting (in an exact place with visual details), waiting for my father to come home to administer a spanking or belting or paddling to me for some “transgression” my mother observed. She had dozens of rules of conduct for her children.

I re-experienced my early childhood feelings that my father’s punishments depended more on my mother’s mood than on what I did.

I re-experienced my early childhood feelings that I didn’t deserve the beatings. I didn’t deserve any beatings, not one!

My father continued, though, until I was around age 11 or so. I’m sure that the beatings were a factor in how I felt at age 12:

Suicidal. Needing to escape from my life.

When I was a child, I needed my parents’ love.

I re-experienced many times while in Primal Therapy the overwhelming hopelessness, helplessness, worthlessness, and betrayal when the people I needed to love me were cruel to me instead.

My parents knew what they did was wrong. Neither one of them ever told me that, though.

My father never apologized for beating me so much before he died 19 years ago. Even before he retired, 17 years before he died, the Miami-Dade County public school system stopped him and the rest of their employees from spanking, whipping, beating, and paddling children.

What could he even tell me to take away those experiences?

  • That he beat me as a child because he himself was beaten as a child?
  • That he couldn’t help it?
  • That how he and my mother frequently went out of their way to help me along in life after my childhood somehow made up for the beatings?

I’m certain that my father was beaten as a child. I bring this up not as a defense for what he did, but as part of my history, too.

It wasn’t enough for my father’s mother to beat me while she was babysitting my siblings and me at our parents’ house. I re-experienced crying as a five-year old when I was required to go cut off palm fronds from the tree in front of our house for her to use as a switch, and bring them to her.

It was a mark of my grandmother’s cruelty that she threatened to beat me with a broom handle when I tried to not participate in my own torment. I re-experienced exact places of my legs where she switched me with the palm fronds, giving me even more when I cried during the punishment.

These wounds left scars that haven’t gone away.

Run your hand down your spine until you reach the top of your sacrum. That’s the area on which I had surgery four years ago, where I now have a titanium cage, replacement disc, and two rods to keep the area stable.

I received a lot of beatings pretty close to that area. Maybe my boyhood activities didn’t cause the “sudden injury (acute trauma).”

I write frankly about my parents because that’s my history: the realities of who they were.

And the realities of who I needed them to be.

I express it because getting well has to address reality.

From Dr. Arthur Janov’s book, Primal Healing, page 133:

“Another cognitive technique is to help the patient understand and forgive his parents. ‘After all, your parents did the best they could. They had a pretty tough childhood too.’ ‘Oh yes, I understand. They did have it tough and I do forgive’ comes forth from the left side. Still, of course, the right side is crying out its needs and its pain, and will go on with its silent scream for the rest of our lives.

There is no way around need.

‘Forgiveness’ is an idea that has no place in therapy.

We are not here to pardon parents; we are here to address the needs of patients, and what the lack of fulfillment did to them.

I regret to say that much of current therapy and particularly cognitive therapy is about a moral position; well hidden, couched in psychological jargon, but, at bottom, moralizing. The therapist becomes the arbiter of correct behavior.

After all, the therapist is trying to change the patient’s behavior toward some preconceived goal. That goal has a sequestered moral position.”

Words are neither the problem nor the solution

gettingwell4 4-5 stars Advanced knowledge, Cerebrum, Limbic system, Lower brain, Primal Therapy , , , , , ,

“Words are neither the problem nor the solution. They are the last evolutionary step in processing the feeling or sensation. They are the companions of feelings.

We cannot make progress on the third-line cognitive level alone. We can become aware of why we act the way we do but nothing changes biologically; it is like being aware of a virus and expecting the awareness alone to kill it. Our biology has been left out of the therapeutic equation.”

Janov’s Reflections on the Human Condition: On the Difference Between Abreaction and Feeling (Part 6/9).

Another factor in producing new brain neurons in the adult hippocampus

gettingwell4 4-5 stars Advanced knowledge, Glutamate, Hippocampus, Limbic system, Neurochemicals

This 2015 New York rodent study provided further details on the production of new neurons in the adult hippocampus. The researchers found that a protein that regulated a glutamate receptor also:

“Significantly influences hippocampal neurogenesis and that both the proliferation and survival of newborn neurons are impaired in the absence.”

The study showed:

“The effect of Norbin [the protein] on neurogenesis is likely caused by a nonautonomous niche effect.

These results show that Norbin is a regulator of adult hippocampal neurogenesis and that its deletion causes depressive-like behaviors.”

http://www.pnas.org/content/112/31/9745.full “Norbin ablation results in defective adult hippocampal neurogenesis and depressive-like behavior in mice”

Emotionless brain research that didn’t deal with human reality

gettingwell4 0-1 star Wasted resources, Amygdala, Anterior cingulate cortex, Brainstem, Cerebrum, Hippocampus, Limbic system, Lower brain, Thalamus

Are tasks you do at work and home never influenced by emotional content or contexts?

Does your ability to focus on a task always have nothing to do with your emotional state?

The researchers who designed this 2015 Boston human study acted as if both of your answers to these questions were “Yes” by stripping out any emotional content from their experiments. As a result, this study which purported to:

“Have the potential to provide additional insights into how inhibitory control may break down in a wide variety of individuals with neurological or psychiatric difficulties”

couldn’t achieve anything near its goal.

This study included fMRI scans of subjects’ entire brains. Limbic system areas were in 3 of the 5 modules, and lower brain areas were in one.

Functional MRI signals depend on changes in blood flow that follow changes in brain activity. Given this study’s goal, did it make sense for researchers to design experiments that didn’t actively engage scanned areas of subjects’ brains?

It wasn’t all that difficult to include emotional content that could potentially contribute to the purported goal. This 1996 review described studies that developed varieties of emotional content with the same test type (Stroop) used. Presumably these approaches had made progress since 1996 incorporating emotional content in Stroop tests given to normal people, who were subjects in this study.

http://www.pnas.org/content/112/32/10020.full “Flexible brain network reconfiguration supporting inhibitory control”

How brain neurons remain stable when constantly stimulated

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

This 2015 UK rodent study provided details of how neurons in the hippocampus respond to stimuli. The researchers found that hippocampal neurons:

“Remain electrically stable when confronted with chronic increases in neuronal activity.”

Changes in electrical potential changed the initial segment of the neuron’s axon.

Synapses formed along the segment, and stayed in place while this highly-plastic segment moved along the axon. The location mismatch:

“Allows the GABAergic [producing gamma-Aminobutyric acid, an inhibitory neurochemical] synapses to strongly oppose action potential generation, and thus downregulate pyramidal cell excitability.”

The researchers also used the two antioxidants endogenous to humans, superoxide dismutase and glutathione, to supplement the culture medium.

http://www.pnas.org/content/112/31/9757.full “Activity-dependent mismatch between axo-axonic synapses and the axon initial segment controls neuronal output”

Are a child’s genes the causes for their anxiety?

gettingwell4 0-1 star Wasted resources, Amygdala, Brain development, Brainstem, Cerebrum, Epigenetics, Limbic system, Lower brain, Stress , , ,

This 2015 Wisconsin macaque study was another attempt to justify the school’s continuing captivity of thousands of monkeys. The researchers performed a study that – if its experimental design was truly informative for helping humans – could have been done with humans.

A problem I saw in the news coverage was that the finding of:

“35 percent of variation in anxiety-like tendencies is explained by family history”

was attributed to genetics, with headlines such as “Anxious Brains Are Inherited, Study Finds.” The lead researcher encouraged this misinterpretation with statements such as:

“Over-activity of these three brain regions are inherited brain alterations that are directly linked to the later life risk to develop anxiety and depression.”

However, the researchers produced this finding by running numbers on family trees, not by studying genetic samples to assess the contributions of genetic and epigenetic factors!

The study’s “family history” correlation was different than finding an inherited genetic causation that wasn’t influenced by the subjects’ caged environments!

The study found:

“Metabolism within a tripartite prefrontal-limbic-midbrain circuit mediates some of the inborn risk for developing anxiety and depression.

The brain circuit that was genetically correlated with individual differences in early-life anxiety involved three survival-related brain regions. These regions were located in the brain stem, the most primitive part of the brain; the amygdala, the limbic brain fear center; and the prefrontal cortex, which is responsible for higher-level reasoning and is fully developed only in humans and their primate cousins.”

The 592 subjects were the human-equivalent ages of 3 to 12 years old. Primate brainstems and limbic systems are fully-developed BEFORE these ages.

The researchers skipped over potential evidence for the important contributions of epigenetic factors to “the later life risk to develop anxiety and depression” that change the studied brain areas during womb-life, infancy, and early childhood. Studies such as:

show:

  1. A developing fetus adapts to being constantly stressed by an anxious mother.
  2. When these adaptations persist after birth, they may present as physiological and behavioral maladaptations of the infant and young child to a non-stressful environment.
  3. Later in life, these enduring changes may be among the causes of symptoms such as the anxious overreactions the current study found.

http://www.pnas.org/content/112/29/9118.full “Intergenerational neural mediators of early-life anxious temperament”

Perpetuating the meme that rodent PTSD experiments necessarily apply to humans

gettingwell4 0-1 star Wasted resources, Cerebrum, Limbic system, Lower brain, Memory, Neurochemicals, Stress

This 2015 Texas A&M rodent study found:

“Propranolol administration dampened the stress-induced impairment in extinction observed when extinction training is delivered shortly after fear conditioning.”

The researchers were way off base in extrapolating this study to humans:

“Propranolol may be a helpful adjunct to behavioral therapy for PTSD, particularly in patients who have recently experienced trauma.”

Would National Institutes of Health Grant R01MH065961 money have been available without perpetuating the meme that rodent PTSD experiments necessarily apply to humans? Or are a priori findings necessary in order to get research funded?

In rodent studies such as this one, the origins of both the disease and the “cure” are all exerted externally. But humans aren’t lab rats. We can perform effective therapy that doesn’t involve some outside action being done to us.

Studies such as Fear extinction is the learned inhibition of retrieval of previously acquired responses make clear that extinction is equivalent to suppression. “Behavioral therapy for PTSD” that suppresses symptoms can’t be a “cure” for humans since the original causes for the symptoms aren’t treated.

Even if this study’s recommendation to administer a drug applied to humans, neither drugs nor “behavioral therapy for PTSD” address the underlying causes.

http://www.pnas.org/content/112/28/E3729.full “Noradrenergic blockade stabilizes prefrontal activity and enables fear extinction under stress”

Interruptions to the circadian cycle negatively affect memory consolidation

gettingwell4 2-3 stars Required further work, Anterior cingulate cortex, Cerebrum, Hippocampus, Limbic system, Memory, Stress

This 2015 German rodent study found:

“The control of sleep and memory consolidation may share common molecular mechanisms.”

Somewhat counter to the “Enhanced memory consolidation” in the study’s title, the researchers also found:

“Elevated IGF2 [insulin-related growth factor 2] signaling in the long term, however, has a negative impact on cognitive processing.”

The IGF2 finding was in genetically altered mice that had their circadian rhythm permanently disturbed, however. The study didn’t clearly determine the contribution of other factors that could have contributed to the cognitive decline.

The study traced fear memories induced by stress through the cerebrum to the anterior cingulate cortex and hippocampus parts of the limbic system.

Researchers have no problems studying emotional memories in these brain areas with rodents. In human memory experiments, however, emotional content is consistently excluded, as if none of our memories had anything to do with our feelings.

http://www.pnas.org/content/112/27/E3582.full “Enhanced memory consolidation in mice lacking the circadian modulators Sharp1 and -2 caused by elevated Igf2 signaling in the cortex”