Stress impairs the normal matching of neuronal activity to increased blood flow in the amygdala

This 2014 rodent study showed one aspect of how stress changed the amygdala. Stress didn’t allow normal matching of neuronal activity to increased blood flow:

“Chronic stress — which is a contributing factor for many diseases — impairs neurovascular coupling in the amygdala..

Neurovascular coupling (is) the process that matches neuronal activity with increased local blood flow.”

http://www.pnas.org/content/111/20/7462.full “Stress-induced glucocorticoid signaling remodels neurovascular coupling through impairment of cerebrovascular inwardly rectifying K+ channel function”

Thalamus gating and control of the limbic system and cerebrum is a form of memory

This 2014 German rodent study showed how the thalamus actively controlled and gated information to and from the cerebrum.

The researchers elaborated in news coverage on how thalamic control and gating represented a form of memory:

“Q. When asked if, given that

  1. Sensory signals en route to the cortex undergo profound signal transformations in the thalamus,
  2. A key thalamic transformation is sensory adaptation in which neural output adjusts to statistics and dynamics of past stimuli, and
  3. The thalamus, hypothalamus and hippocampus being part of the limbic system, might memory reconsolidation play a role in the cortico-thalamic pathway?

A. “It’s conceivable that the cortico-thalamic pathway is subject to long term plasticity,” Groh conjectures. “In fact, on a synaptic level, these inputs can change their strength and retain adjusted strengths for long periods. This process represents another – albeit much slower – form of adaptation which some interpret as memory.”

Q. Conversely, might the thalamic-cortical pathway affect memory?

A. “If particular sensory-evoked activity patterns would cause long-term changes in the cortico-thalamic pathway, and thereby change the way incoming signals are processed before reaching the cortex,” he opines, “then this would indeed reflect a form of information storage.”

In other words, there are ways in addition to our usual ideas about memory that the limbic system remembers.

Other items in news coverage included:

“Rodents, cats, primates and humans show a common architecture of two feedback pathways from cortex to thalamus in the auditory, visual and somatosensory (but not olfactory) systems.

In this study we looked at processing of touch information, and we’d like to know how homologous pathways affect visual or auditory processing. It’s fascinating that despite fundamental differences between visual, auditory and somatosensory signals, basic layouts of thalamocortical systems for each modality are quite similar.”

Other areas of research that might benefit from their study include any medical research involving the thalamocortical system that might involve inappropriate gating of sensory signals.

For a given stimulus, output neural response will not be static, but will depend on recent stimulus and response history.”

http://www.pnas.org/content/111/18/6798.full “Cortical control of adaptation and sensory relay mode in the thalamus”

Active areas of the brain when making decisions in stressful conditions

This 2013 human study was of decision making under stressful conditions.

Acute stress (ice water immersion) evoked habitual behavior rather than deliberative behavior. In my view, the subjects’ behaviors when under stress were driven more by their limbic system and lower brain areas than their cerebrum.

This finding wasn’t a big surprise. However, the researchers went on to state:

“Subjects with more executive resources to spare find themselves less susceptible to the behavioral changes brought about by stress response.”

I interpreted this statement to mean that when stressed, the more-capable subjects didn’t act out as much as the less-capable subjects acted out their respective feelings, instincts and impulses.

I felt that to understand this statement called for more investigation into the individual histories of the subjects:

  • What happened in their lives that enabled each person to acquire “more executive resources” or not?
  • What happened in their lives that made each person more or less sensitive to stress?
  • How are these two avenues of investigation related?

http://www.pnas.org/content/110/52/20941.full “Working-memory capacity protects model-based learning from stress”

How oxytocin and vasopressin were repurposed through evolution to serve social functions

This 2013 primate summary study showed how nonsocial behaviors, neurology and neurochemicals were repurposed through evolution to serve social functions.

Oxytocin and vasopressin retained their:

  • water regulation,
  • reproduction, and
  • anxiety relief

functionalities while they also evolved to become instrumental in:

  • pair-bonding,
  • parental care,
  • selective aggression,
  • social prominence,
  • generosity, and
  • trust.

http://www.pnas.org/content/110/Supplement_2/10387.full “Neuroethology of primate social behavior”

A mother’s care affects the infant’s hippocampus structure and function through epigenetic regulation of genes

This 2012 McGill University rodent study found:

“Variations in maternal care in the rat affect hippocampal morphology and function as well as performance on hippocampal-dependent tests of learning and memory in the offspring.

Thus, in the rat, as in humans, social influences operate during early life to influence the structure and function of brain regions critical for cognitive capacity.

Variations in maternal care can influence hippocampal function and cognitive performance through the epigenetic regulation of genes.”

http://www.pnas.org/content/109/Supplement_2/17200.full “Variations in postnatal maternal care and the epigenetic regulation of metabotropic glutamate receptor 1 expression and hippocampal function in the rat”

The effects of early-life stress are permanent alterations in the child’s brain circuitry and function

The sobering application of this 2013 rodent study’s finding was that if the limbic systems of human children weren’t already permanently damaged before they entered an orphanage, the orphanage experience would probably do that to them:

“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.”

http://www.pnas.org/content/110/45/18274.full “Early-life stress has persistent effects on amygdala function and development in mice and humans”

One way that mothers cause fear and emotional trauma in their infants

This 2014 rodent study showed that infants learned to fear specific items in the environment that their mothers feared. The imprinting memory happened at a stage in the infants’ lives when they hadn’t yet developed the physiology to respond to the environment with fear on their own.

The learning cue was the mothers’ fear response – in this case, her distress odor, even when the mother was not present – coupled with the infants’ stress. The fear memory was stored in the infants’ amygdalae:

“These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning.

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.”

There’s no scientific reason why this and related studies shouldn’t inform researchers who ignore the earliest stages of human life when studying limbic system disorders in humans.

For an example of researchers choosing to NOT be informed, look at Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects.

http://www.pnas.org/content/111/33/12222.full “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear”

Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects

This 2013 Wisconsin human study’s goal was to assess effects of childhood trauma using both functional MRI scans and self-reported answers to a questionnaire. The families of the study’s subjects (64 18-year-olds) participated with researchers before some of the teenagers were born.

How could the teenagers give answers that described events that may have taken place early in their lives, before their cerebrums were developed, around age 4? Even if the subjects were old enough to remember, would they give accurate answers to statements such as:

“My parents were too drunk or high to take care of the family.

Somebody in my family hit me so hard that it left me with bruises or marks.”

knowing that affirmative answers would prompt a visit to their family from a government employee?

Although some data may have been available, data from the teenagers’ prenatal, birth term, infancy, and early childhood wasn’t part of the study design. Intentional dismissal of early influencing factors ignored applicable research!

No

Was the study’s limited window due to the political incorrectness of placing importance in the development environment provided by the subjects’ mothers? The evidence was there for those willing to see.


One clue of ignored early traumatic events was provided by the lead researcher’s quote in news coverage:

“These kids seem to be afraid everywhere,” he says. “It’s like they’ve lost the ability to put a contextual limit on when they’re going to be afraid and when they’re not.”

This finding of “fear without context” possibly described the later-life effects of traumas that were encountered in utero and during infancy. A pregnant woman’s terror and fear can register on the fetus’ lower brain and the amygdala from the third trimester onward.

Storing a memory’s context is one of the functions that the hippocampus performs. Because the hippocampus develops later than the amygdala, though, it would be unable to provide a context for any earlier feelings and sensations such as fear and terror.

The researchers attempted to place the finding of unfocused fear into later stages of child development without doing the necessary research. They tried to force this finding into the subjects’ later development years by citing rat fear-extinction and other marginally related studies.

But citing these studies didn’t make them applicable to the current study. Cause and effect wasn’t demonstrated by noting various “is associated with” findings.


Was this science? Was it part of furthering an agenda like protecting publicly funded jobs?

Was this study published to make a contribution to science? Were the peer reviewers even interested in advancing science?

And what about the 64 18-year-old subjects? If the lead researcher’s statement was accurate, did these teenagers receive help that addressed what they really needed?

http://www.pnas.org/content/110/47/19119.full “Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence”


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How mothers-to-be program lifelong low testosterone into their unborn male children

This 2014 rodent study was one of many on how pregnant mothers-to-be epigenetically program their developing children. The enduring changes made to the male fetuses in the womb led to lifelong low testosterone, which produces a variety of ill health effects:

“Leydig cells do not develop until puberty but the team showed that their function is impaired if their stem cell forefathers are exposed to reduced levels of testosterone in the womb.

There is increasing evidence that a mother’s diet, lifestyle and exposure to drugs and chemicals can have a significant impact on testosterone levels in the womb.”

http://www.pnas.org/content/111/18/E1924.full “Fetal programming of adult Leydig cell function by androgenic effects on stem/progenitor cells”

When recognition memory is independent of hippocampal function

This 2014 human study provided additional details on the specialized brain circuits we have for recognizing faces.

Damage to the hippocampus didn’t impair recognition of new faces, “..but only at a short retention interval. Recognition memory for words, buildings, famous faces, and inverted faces was impaired.”

http://www.pnas.org/content/111/27/9935.full “When recognition memory is independent of hippocampal function”

Conserved epigenetic sensitivity to early life experience in the hippocampus

This 2012 human study was done by McGill University, whose researchers in Canada are at the forefront of epigenetic studies. The subject was epigenetic DNA methylation in the hippocampus of people who experienced abuse as children and who also committed suicide.

Comparisons were made with rats that were stressed in early life to identify genomic regions that are epigenetically changeable in response to a range of early life experiences.

http://www.pnas.org/content/109/Supplement_2/17266.full “Conserved epigenetic sensitivity to early life experience in the rat and human hippocampus”

Left–right dissociation of hippocampal memory processes in mice

This 2014 rodent study provided more details on the CA3 segment of the hippocampus:

“Silencing of either the left or right CA3 was sufficient to impair short-term memory…

Only left CA3 silencing impaired performance on an associative spatial long-term memory task, whereas right CA3 silencing had no effect.”

http://www.pnas.org/content/111/42/15238.full “Left–right dissociation of hippocampal memory processes in mice”

Hippocampal mechanisms involved in the enhancement of fear extinction caused by exposure to novelty

This 2014 Brazilian rodent study provided more information on the workings of the hippocampus. The researchers measured the effects of re-experiencing a fear within a specific context:

“Within a restricted time window, a brief exposure to a novel environment enhances the extinction of contextual fear.

The enhancement of extinction by the exposure to novelty depends on hippocampal gene expression..on hippocampal but not amygdalar processes.”

http://www.pnas.org/content/111/12/4572.full “Hippocampal molecular mechanisms involved in the enhancement of fear extinction caused by exposure to novelty”

Rebooting the brain with anesthesia: Implications for Primal Therapy and evolution

Here are some paragraphs from a 2013 summary article of 105 studies entitled Evolution of consciousness: Phylogeny, ontogeny, and emergence from general anesthesia:

“The emergence of consciousness (from anesthesia) (as judged by the return of a response to command) was correlated primarily with activity of the brainstem (locus coeruleus), hypothalamus, thalamus, and anterior cingulate (medial prefrontal area). Surprisingly, there was limited neocortical involvement that correlated with this primitive form of consciousness.

In the sleep study, midline arousal structures of the thalamus and brainstem also recovered function well before cortical connectivity resumed. Thus, the core of human consciousness appears to be associated primarily with phylogenetically ancient structures mediating arousal and activated by primitive emotions, in conjunction with limited connectivity patterns in frontal–parietal networks.

The emergence from general anesthesia may be of particular interest to evolutionary biology, as it is observed clinically to progress:

  1. from primitive homeostatic functions (such as breathing)
  2. to evidence of arousal (such as responsiveness to pain or eye opening)
  3. to consciousness of the environment (as evidenced by the ability to follow a command)
  4. to higher cognitive function.

Regarding ontogeny of H. sapiens, peripheral sensory receptors are thought to be present from 20 wk of gestation in utero. The developmental anlage of the thalamus is present from around day 22 or 23 postconception, and thalamocortical connections are thought to be formed by 26 wk of gestation. Around the same time of gestation (25–29 wk), electrical activity from the cerebral hemispheres shifts from an isolated to a more continuous pattern, with sleep–wake distinctions appreciable from 30 wk of gestation.

Both the structural and functional prerequisites for consciousness are in place by the third trimester, with implications for the experience of pain during in utero or neonatal surgery.


I recently came out of anesthesia after being anesthetized for three hours during rotator cuff surgery. I felt pain, and went into a primal reliving of a painful memory.

I interpret the event as a reliving of my birth experience because of the following:

  • The beginning point was complete anesthetization as it was at my birth. My mother was completely anesthetized, so I, weighing less than one twentieth of her, was also completely anesthetized.
  • I felt a great urge and impulse to “get out” as it was at my birth. The attending nurse told me the next day that she called over another person to help her restrain me in the post-op chair.
  • I had a great need for oxygen and started breathing rapidly as it could have been at my birth. The nurse told me the next day that she was already giving me oxygen, and per the monitors, I didn’t need more oxygen.
  • I had to frequently “spit up” as it could have been at my birth. There was nothing in my current situation to cause me to expectorate.
  • My lower brain and limbic system were in control, as I thrashed, cried and moaned. I probably used primarily the same brain areas as what were the developed parts of my brain at birth.

The attending nurse told me the next day when I called her that she followed the established protocol, which was to get me out of the experience. She intentionally distracted me away from my pain. I was instructed to sit still, to think of some place pleasant, and to calm down.

I heard her as though she was at the other end of a tunnel at first, and then started to comply as I regained cognitive awareness.


I understand how such a powerful event could present a danger to a patient. It didn’t occur to me until the next day to tell the nurse of relevant history, that I’ve had relivings while in therapy, and wasn’t in the same danger that her regular patients may have been.

Even if I had said something, however:

  • Neither the anesthesiologist nor the attending nurse had a method of understanding how an evolutionary-determined sequential process – such as rebooting a person’s brain after prolonged anesthesia – may have therapeutic benefits.
  • They had no training to recognize aspects of neurobiologic therapeutic value in what was going on inside of me during this event, as a therapist in Dr. Arthur Janov’s Primal Therapy has.
  • The default response per medical protocol would be to shut down a patient’s expressions of their feelings.

As a result, my experience of this event was pretty much the opposite of what happens in Primal Therapy. Although I didn’t feel harmed, my reliving wasn’t therapeutic, as previous re-experiencings had been. The reliving’s progression through my levels of consciousness was purposely interrupted, and approached from a non-therapeutic direction.

Unlike my experience of coming out of anesthesia, Dr. Arthur Janov’s Primal Therapy isn’t something the patient is thrown into and potentially overwhelmed by their feelings. It’s a gradual process where the patient is in control.

This summary study showed that existing science is already in alignment with the background of Primal Therapy, that the core of human consciousness is in the limbic system and lower brain structures. My anesthesia experience showed that medical professionals are familiar with at least the outward signs of a primal reliving.

The challenge seems to be how to use this complementary knowledge for people’s benefit. What can be done with therapeutic re-experiencing so that people aren’t burdened with the continuing adverse effects of traumas?

How can scientists and medical professionals get the eyes to see what’s in front of them?

Weakening memories by mispredicting their contexts

This 2014 human study showed that:

“Item memories are weakened when they are mispredicted by their context..weakening of the synapses that support the item’s representation in memory.

Note that our use of the term “pruning” is not meant to imply that traces are being deleted completely from memory.

Connecting the dots, two studies showed that our memories are formed within specific contexts and that our memories have contexts with specific places and times.

http://www.pnas.org/content/111/24/8997.full “Pruning of memories by context-based prediction error”