Hypothalamus

Hypothalamic oxytocin and vasopressin have sex-specific effects on pair bonding, gregariousness, and aggression

gettingwell4 4-5 stars Advanced knowledge, Hypothalamus, Limbic system, Neurochemicals, Oxytocin, Stress, Vasopressin

This 2014 bird study showed the complementary effects of neurochemicals vasopressin and oxytocin in the hypothalamus.

Oxytocin neurons in the hypothalamus promote pair bonding and gregariousness in females.

Vasopressin neurons in the hypothalamus promote maternal care, social recognition, and gregariousness in both males and females, and aggression in males toward females.

Vasopressin and oxytocin released generally and in other parts of the brain have different effects. For example:

“Central administration of oxytocin also attenuates stress-induced effects on the brain and reverses stress-induced social avoidance.”

http://www.pnas.org/content/111/16/6069.full “Hypothalamic oxytocin and vasopressin neurons exert sex-specific effects on pair bonding, gregariousness, and aggression in finches”

Flooding the hypothalamus with neurochemicals affects reward-seeking, motivated, and depressive behavior

gettingwell4 4-5 stars Advanced knowledge, Hypothalamus, Limbic system, Lower brain, Neurochemicals

This 2014 rodent study showed the opposing effects of neurochemicals orexin (excitator) and dynorphin (inhibitor) in the hypothalamus.

The hypothalamus plays a role in behaviors such as addiction and impulsiveness. Food and cocaine self-administration were the main techniques used.

Flooding the hypothalamus with orexin produced reward-seeking and motivated behavior. That was greatly reduced when dynorphin levels were increased, and depressive behavior set in.

http://www.pnas.org/content/111/16/E1648.full “Hypocretin (orexin) facilitates reward by attenuating the antireward effects of its cotransmitter dynorphin in ventral tegmental area”

Sex hormone exposure to the developing female fetus causes infertility in adulthood

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This 2014 rodent study was of polycystic ovarian syndrome, which is the leading cause of human female infertility.

The researchers could reliably induce this disease in mice while they were still fetuses, but effects didn’t manifest until adulthood! The inducement method exposed the developing female fetuses to androgens such that their testosterone concentration was significantly increased.

Comparing this study with How mothers-to-be program lifelong low testosterone into their unborn male children, we can see that in early development:

  • too much testosterone for a female fetus and
  • too little testosterone for a male fetus

both have lifelong ill effects.

http://www.pnas.org/content/112/2/596.full “Enhancement of a robust arcuate GABAergic input to gonadotropin-releasing hormone neurons in a model of polycystic ovarian syndrome”

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

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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”

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

gettingwell4 4-5 stars Advanced knowledge, Anterior cingulate cortex, Brain development, Brainstem, Hypothalamus, Limbic system, Locus coeruleus, Lower brain, Memory, Primal Therapy, Thalamus , , ,

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?

Are 50 Shades of Grey behaviors learned in infancy?

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Ever wonder how someone could become attached to their early childhood abuser?

Ever wonder what underlying neurobiological conditions may account for the popularity of Fifty Shades of Grey?

This 2014 rodent study “Enduring good memories of infant trauma” linked below showed how trauma changed infants’ limbic system and lower brains. As adults, they derived a neurochemical benefit from re-experiencing the traumatic conditions:

“Trauma and pain experienced in infancy clearly led to higher rates of adult rat depression-like behavior..(but) the infant brain has limited ability to link trauma to fear areas in the brain, such as the amygdala.

These results are surprising because cues associated with trauma experienced as adults provoke fear and do not rescue depressive behavior.

It is possible that giving SSRI medications to children could be detrimental to mental health in adulthood,” Dr. Sullivan says. “We believe that our research offers the first evidence for the impact of serotonin pathways.

The infant trauma increases serotonin to produce brain programming of later life depression, and the infant trauma cue increases serotonin to alleviate the adult depressive like symptoms.”

As the study may apply to humans, let’s say that as an infant, someone was traumatized by a caregiver who, for example, bound them too tightly and left them alone for too long. What adult behaviors and other symptoms may develop as results? The person may:

  • Show depression-like symptoms that would strangely be alleviated by being bound tightly and left alone for an extended period.
  • Develop attachments to people who treated them poorly in a way that triggered them to re-experience their early childhood traumas.
  • Feel their mood lift when their infancy traumas were cued.
  • Be unable to explain and integrate with their cerebrum what was going on with their limbic system and lower brains.
  • Be caught in a circle of acting out their feelings and impulses, with unfulfilling results.

Isn’t it curious that this acting-out behavior – driven by unconscious memories of traumatic conditions – is a subject for popular entertainment? It may have resonated with personal experiences of the people who read the books and watched the movie.

What about people who want to be relieved of their symptomatic behavior? Is it a justifiable practice:

  • To pass affected people over to talk therapies that aren’t interested in directly treating the cause – a neurobiological condition that exists in the limbic system and lower brains – only the symptoms?
  • To drug affected people with the neurochemicals that their condition makes scarce – the symptoms – instead of addressing the source?

A principle of Dr. Arthur Janov’s Primal Therapy is that people are capable of treating their own originating neurobiological conditions. One of the therapeutic results is that the patient is relieved of being caught in endless circles of acting-out behavior.

That way we can have our own lives, and not be driven by what happened during early stages of our lives.

http://www.pnas.org/content/112/3/881.full “Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction”