Hangout nr. 2, Medical Neuroscience on-demand
Google Hangout nr.2. For all sessions (3 running at the time) on the new Coursera platform. The Hangout was on August, at 2 pm Eastern Time. Below you find a link to the video of the Hangout on YouTube and a short overview of the subjects addressed with the time slot that part of the discussion starts
Addiction relative to foods
First of all a question on material from the last week of the Course by Steve. Steve is a Medical Neuroscience learner from the United Kingdom.(starting at 03:55). Is there information on the Nucleus Accumbens and the Ventral Tegmental Area in relation to food addiction?
Prof. White answers that the dopamine system is mediating addiction of all sorts. Particularly dopamine affects the nucleus accumbans and the ventral tegmental area. As a result addictions to certain food types can shape the activity of that mesolimbic dopaminergic pathway and gain access to the brain’s intrinsic reward circuitry. It seems like the potency of addiction to certain food substances is less than that to drugs for most people. We need more research on the subject of these addictions and the possible interventions.
Pain and Temperature Pathways in relation to trauma
The next question is by Deborah, a therapist and clinician.(starting at 07:30). Deborah wants to hear more about the pain and temperature pathways and the collaterals in relation to trauma and emotional difficulties.
In response to Deborahs questions Prof. White explains that pain pathways enter the dorsal horn of the spinal cord. For the facial region the spinal trigeminal nucleus. Currently, we find that there is a remarkable amount of integration of incoming afferent signal at the level of the first gray matter station. As a result, incoming pain signals can interact with other somatic sensory channels. Very likely there is sensory integration at each subsequent gray matter relay.
For instance, touch can have a very different valance for someone experiencing pain. Possibly we can find new and innovative ideas to influence pain perception. That is a bottom-up approach. There is also top-down modulation of pain.
Pain should be distinguished from nociception. Nociception is the transduction of the stimuli that are provoking pain. While pain itself is something that the brain creates. That central circuitry at the level of the brain could also be addressed in pain management. Prof. White is very positive about future possibilities for pain management.
Most primitive part of the brain
Next, Nick reads a question from a learner who’s name is Jose that has microphone problems (starts at 12:05). What is the most primitive part of the brain? Is it the brainstem?
Prof. White agrees with Jose. The brainstem is the most conserved part of the human brain. There are other parts that are probably just as primitive. For example the medial part of the cerebellum (spinal cerebellum) and the inferior lateral division (vestibulocerebellum). We have an enormously expanded neocerebellum. Humans and all primates have a well-developed part of the cerebellum connected to facial expression and emotion.
Cognitive difference between humans and all other lifeforms
(Starting at 17:00) Nick reads a question by Matthew Jacob Smith: What are the neuroscientific differences between humans and other intelligent organisms? Is there evidence for introspection and consciousness in other animals?
Responding to Matthew prof. White explains that the most noteworthy difference between the human brain and other brains is the massive development of the cerebral cortex. Brains of great apes like gorillas, chimpanzees and orangutans are very similar to human brains. Although smaller relative to body size. Especially the prefrontal cortex is less pronounced in great apes.
First of all evolutionary anthropologists give a lot of attention to an area called Broadmans area 10 (front part of the prefrontal cortex). This area is particularly well developed in humans compared to great apes. In addition to this area other parts of the brain, deep in the insular cortex, are relatively more developed in humans. Especially the anterior part of the insular cortex superior to the brainstem is more developed. These parts of the brain are involved in social cognition.
In conclusion prof. White thinks that non-human animals have some kind of introspection and have a conscious experience of some sort. Non-human animals and humans share some of the fundamental capacities because we share some of the fundamental circuitry.
For example, dogs have some form of the conscious experience. Presumably without so much capacity for introspection and in particular with a more limited capacity for future projection. Planning for the future is a function associated with the prefrontal cortex.
Food for thought added to the article by Ellen Vos: Why elephants never forget by Alex Gendler.
Autism spectrum disorders and mirror neurons
Artem, from Armenia, asks (starting at 22:30): What are the current ideas on the relation between autism spectrum disorders and impairment of the mirror neuron system?
Prof. White answers: In the first place, autism is a very complex spectrum of disorders. Consequently, there are likely multiple manifestations that individuals experience as a manifestation of this disorder complex.
There was a lot of early excitement about a dysfunctional or disordered mirror system. There is still reason to think that there is a relation between the mirror neuron system and autism spectrum disorder. But it is a controversial hypothesis and there is a lot of debate on this theory.
Prof. Whites view is that there may be differences in the architecture of associational connections within the brain that produces some of the phenomena that we associate with autism spectrum disorders.
There is quite a large diversity of functional connectivity patterns seen in with relatively high functioning of autism spectrum disorder. How do those differences arise in the lifespan? We do not know. Some think that the young autistic brain is over-connected and that the older autistic brain is over-connected. But those are just gross simplifications.
Prof. White thinks that there could very well be a difference in the capacity for synaptic potentiation and synaptic depression. That might ultimately lead to differences in growth and pruning of connections., consequently leading to differences in brain architectures particularly across the associational network. Prof. White illustrates his view with examples of differences in the experience between neurotypical people and individuals with severe autism.
Conclusion and further discussion on Autism spectrum disorder and the immune system
In conclusion, there is certainly a lot of new information that is coming forward. The mirror neuron hypothesis remains a hypothesis. We need to understand more how important that possibility is within that broader spectrum of divers cortical wirings.
Artem agrees on Prof. White view and also draws our attention to association with tumor suppressor genes, which is also controversial. Mutation in these tumor suppressor genes leads to a symptom in the autism disorder spectrum. Prof. White states that one of the interesting discoveries in neuroscience is how immune molecules seem to have an interaction with developing circuits in the brain. Neuroscientists need to investigate this relation further.
Other aspects of autism spectrum disorder also deserve attention. People with severe autism experience far more detail in the world as neurotypical individuals. That suggests that something about the associational networks where information is brought together might just be different. Are autism spectrum disorders really a pathology? Or is it simply a difference? (See this wonderful: The world needs all kinds of minds by Temple Grandin (a scientist diagnosed with a disorder in the autistic spectrum, a resource provided by Ellen Vos).
Advice from a neurological perspective
(Starting at 33:00) Oner complements prof. White and he is interested in personal advice from prof. White on living your life from a neurological perspective.
Prof. White says that there are principles of plasticity that we are starting to use in practice. Above all, there is repetition, for example in musical performance, the 10.000-hour rule. But there is more to consider besides repetition. You should reduce the variance from trial to trial. The same thing applies to the mental domain as well. As we repeat we are reinforcing plasticity. Ongoing repetition creates the opportunity to refine and to reinforce the appropriate circuits.
Also, Sleep (The benefits of a good night’s sleep – Shai Marcu, a resource added by Ellen Vos) is very important from a neuroscience perspective. It facilitates learning. The right balance between performance, practice, rest and sleep is very important. We do not understand that fully yet.
Acquisition of new skills after acquired brain injury
Raphael, a medical student from Brazil. Rafael has a question (starting at 37:42) about an individual with hydrocephalus as a baby. The hydrocephalus was acquired after birth. The person is 22 years old now. He never developed good skills, for example, speech. But exposed to stimulation he developed new skills. How is this possible to develop new skills with so much damage?
First of all prof. White warns you must never underestimate the power of neuroplasticity. Especially the very young brain has great plasticity. The earlier insults happen the more redistribution of function can occur. Had the hydrocephalus formed later in life the outcome might have been worse. There are limits to the resilience of the brain. But there is always hope to improve the qualities of life.
Compensation for sensory weakness
Then (starting at 41:39) we meet a wonderful member of our learning community in the hangout: Gouri. She is 11 years old (she is using her father’s Gmail account. That is why her name does not appear). Ever since she was nine she was very interested in learning about neuroscience. Gouri has a prescription of minus five for contacts to improve her eyesight. She wants to know how the lateral geniculate nucleus deals with near- and farsightedness.
Prof. White is especially pleased to meet a passionate learner of Medical Neuroscience of such a young age. To appear in the Hangout is very brave and courageous. Prof. White thanks Gouri for her participation.
Next prof. White reacts to the question. Inputs from the retina go to the lateral geniculate nucleus. Optics of the eye influence the inputs. If glasses or contacts do not correct the optics of the eye to produce a sharp image. Therefore blurred signals might reach the lateral geniculate nucleus . Those signals have less information than the signals from a sharp image formed on the retina.
The visual cortex is very sensitive to the quality of the information. The brain will tune itself for the quality of information and will have limited capacity to process the full range of information that is available when inputs are restored. That is why glasses or contacts need to correct the imperfect optical image in the critical period. Gouri is wearing contacts and she is already past the critical periods The basic circuits needed for sensory perception are formed.
Interact in “Let’s discuss” and “Clinical Case Studies “
At 46:32 prof. White invites me, a mentor from the course Medical Neuroscience living in the Netherlands, to take the floor.
I get the opportunity to tell that I’m very fond of the creative atmosphere in the current sessions. The only improvement I can suggest is to respond to each other in the threads “Let’s discuss: ..” and “Clinical Case Studies: ..”
As a result of the lack of interaction, those threads are strings of opinions without feedback from other learners. Much as creating a load of bricks without building a wall from them. Seems the learning result could be improved by interaction in these threads.
Help in psychological trauma
(Starting at 48:00) Madhu, who works with a girl that are rescued from human trafficking, victims or psychological trauma. Some of these girls are young like 14 years old. They are deeply traumatized. Do you see hope in the long run with help like movement therapy? What is your view on these traumas?
First of all prof. White thanks Madhu for the wonderful work that she does. Secondly prof. White addresses the issue. In post-traumatic stress the amygdala and the influence of the amygdala on neural networks throughout the brain are important. That can have a profound impact on memory, cognition and all sort of behaviors.
One strategy is to gain access to that part of the brain end try to recalibrate its output. It is very, very difficult. Caregivers use strategies to try to extinguish triggering of experiences, memories etc. Thus trying to promote a long-term depression and long-term potentiation that would favor more normal types of association.
Prof. White loves a multi-nodal approach. To use art. To use other kinds of social relations. In conclusion, there are lots of approaches like the pharmacological approach. But prof. White thinks we have to go beyond that approach and try to normalize the function of this part of the brain.
Compliments to prof. White coming from Nigeria
In addition to all participants with questions (Starting at 52:52) Saddek, in a residency program neurology in Nigeria, takes the floor. Saddek compliments prof. White and the course and states that having this material at a basic level of neuroscience is a great help. Prof. White appreciates the compliments and thanks Saddak for participating in the Hangout.
Long-term potentiation in real life
Finally, the last question is from Elgin from Brazil (starting at 54:44). She loves the course and thinks it is a great opportunity that should not be missed. She has a question on week 4. It is a question on plasticity: Application of a tetanus stimulus can have a lifelong effect. Elgin wants to know: Can we provoke such stimuli purposefully and how we can do this?
Prof. White says that tetanus itself is artificial. In an experiment we create tetanus stimuli to measure long-term potentiation. However, there is a more natural equivalent to that tetanus stimulus in our own nervous system. This is connected to the discussion on Oner’s question (Advice from a neurological perspective, above). Principles of repetition and specificity. Specificity requires a focus on a particular act. Thus you have to rehearse in a highly specific way, in order to get a life-long change in synaptic connectivity. Repeating the same act over and over again with minimal variation may favor potentiation
On the level of a spike, we have the following information. We know that presynaptic input firing a postsynaptic neuron in a relatively short interval will strengthen potentiation. If we add repetition and continue to drive the same circuit in the same way with that very short interval of presynaptic before postsynaptic stimulation. Then we can strengthen that network. In conclusion, to apply these things to real life is to minimize the variation in our repetition and execute the repetition rigorously.
Concluding on: Long-term potentiation in real life and Help in psychological trauma .
Previously we discussed with Madhu (Help in psychological trauma) the role of emotion. Emotion increases the intensity of signaling. As a result, we possibly can use emotion in a constructive way. Not to elicit traumatic emotion but much as trying to think back to our childhood and recall the earliest memories. Alterations in the brain that stem from childhood persist in the adult brain. We can change childhood memories when we remember them but they still remain. Prof. White foresees more insight in this field in the future.