Mo's Neurophilosophy blog

[Diane]

I can't figure out why I never started a Wind Rose thread for Mo's blog, Neurophilosophy, before today - I certainly love to point out his blogposts. Well, it's never too late..

This post is a very nice one, pointing out 6 dogmas about the nervous system that have been destroyed by new waves of science.

The dogmas that are gone are:

1: The adult human brain is not plastic. ...the brain is capable of reorganizing itself extensively, particularly in response to experience and injury. Learning is now thought to occur as a direct result of the modification of synaptic connections in the brain; reorganization of the brain's wiring is widely believed to take place following injury, and to underly phenomena such as phantom limb syndrome in amputees.

2: The adult human brain cannot regenerate. ... it is now well established that the adult human brain contains small populations of neural stem cells, which are capable of dividing to generate new neurons throughout adulthood. The function of these new cells is still unclear, and researchers have so far had little success in coaxing them to divide in vivo. Nevertheless, once they do so, stem cells can potentially be used to develop treatments for neurological conditions such as stroke, epilepsy and Alzheimer's, Parkinson's, and Huntington's diseases.

3: Neurons are the functional elements of the nervous system. In the 19th century, the discovery of the neuron was quickly followed by the realization that the nervous system contains another cell type: the glial cell. Glial cells were quickly relegated to a secondary role in which they provide neurons with structural and nutritional support. In recent years, however, this view has begun to change. Glial cells are now known to regulate communication between neurons and to control blood flow through the capillaries in the brain. They can also communicate with neurons, with each other, and with blood vessels, and a study published in April of this year shows that glial cells can generate action potentials. Rather than being mere support cells, glia may yet be shown to be the main players in brain function.

I would like to point out that glial cells arise from neural crest, which comes off the ectoderm layer just before what's left of it turns into skin.

4: Neurotransmitters are released from the nerve terminal. According to the conventional view, neurons receive inputs from other nerve cells on their dendrites, integrate these signals in the cell body, and generate an action potential which is propagated along the axon. When the action potential reaches the nerve terminal, it triggers the release of neurotransmitters, which diffuse across the synaptic cleft and elicit a response in the postsynaptic membrane. However, several studies published published last year show that neurotransmitters can also be released from axons in the white matter of the corpus callosum.

Wow.

5: Neurons are binary switches. In other words, a nerve cell is either on or off: at any given time, it is either generating an action potential, or it is not. The action potential was regarded as an "all or nothing" response. That is, a minimum amount of stimulation is required before a neuron will produce a nervous impulse, and a sub-threshold stimulus (one that is smaller than the minimum stimulus amplitude) will not produce a response. It has long been known that cells of the invertebrate nervous system produce graded potentials, whereby the amount of transmitter released is proportional to the intensity of the stimulus. We now have evidence that mammalian neurons can generate graded potentials as well - they are not simple on/off switches, and the action potential is not all or nothing.

Wow.

6: Neurons communicate with each other by propagating action potentials. Neurons evolved to communicate with each other, and they do so by generating nervous impulses which are propagated along the nerve fibres. But because this electrical activity cannot cross the synapse, it is converted to a chemical signal which transmits the signal from one cell to the next. Although all neurons communicate in this way, we now know that some cells in the nervous system can convey signals by the propagation of a secondary messenger cascade. These biochemical signalling cascades can travel along the nerve fibre, and can elicit the release of neurotransmitters from the nerve terminal, in the absence of electrical activity.

Wow.

[Gary]

Diane,
Great post. I can't help but wonder if quote 3 referring to the glial cells and ectoderm / skin connection might be a major player in explaining the mechanism of how simple contact can stimulate ideomotion.

[Diane]

I can't help but wonder if quote 3 referring to the glial cells and ectoderm / skin connection might be a major player in explaining the mechanism of how simple contact can stimulate ideomotion.

Yes yes yes. I think so.

[EricM]

Quote:
I can't help but wonder if quote 3 referring to the glial cells and ectoderm / skin connection might be a major player in explaining the mechanism of how simple contact can stimulate ideomotion.

Yes yes yes. I think so.

You've lost me on this one. Simple Contact doesn't stimulate ideomotion, rather it permits it's expression. I fail to see what the function of glial cells has to do with it, regardless of how remarkable glial cells might be. Am I missing something?

[Diane]

Simple Contact doesn't stimulate ideomotion

Well, skin contact does..

I fail to see what the function of glial cells has to do with it

Nothing- just that glial cells are neural crest/ecodermally derived/signalers in their own right. And it seems skin is too. One more little tidbit that supports ectodermal signalling capacity ahead of any claims for fascia et al.

[EricM]

glial cells are neural crest/ecodermally derived/signalers in their own right. And it seems skin is too. One more little tidbit that supports ectodermal signalling capacity ahead of any claims for fascia et al.

Agreed.

[Diane]

Mo has a new post - link to a new book by the same name, Welcome to Your Brain. Great video embedded in the post about an hour long, featuring the authors. A woman in the audience asks, "What is a headache?" The answer involves a definition of pain, which is stated by one of the authors, "the brain responding to skin and skull."

I think I might send for that book.

[Diane]

GREAT post this morning from Mo at Neurophilosophy about Wilder Penfield and his work, an in depth description of Penfield's development of the S1M1 cortical map we all know and love, i.e., sensory and motor homunculi).

Wilder Penfield, Neural Cartographer.

Lots of links at the bottom to old posts. Good paragraph or two about glia and brain scars.

[Diane]

Check out one of Mo's latest posts, Memories are made of molecular motors.

Even at the level of a synapse in the hippocampus, some little contractile element is necessary to open and close gates. Some bits of excerpts and stray thoughts beg to be included under a PT hypothesis of some kind some day.

LTP primarily involves changes in the postsynaptic membrane.

LTP = long term potentiation, a type of learning that involves reduction in the threshold to a stimulus. In the case of pain, not so good. We don't want our brains "learning" to more easily produce pain. Which is why anesthetists/anesthesiologists exist I reckon.

This leads to activation of the enzyme CaMKII, which then triggers, among other things, the insertion of new AMPA receptors into the membrane of the postsynaptic cell. AMPA receptor insertion causes morphological changes in the neuron - it increases the surface area of the membrane, and consequently to an enlargement of dendritic spines, the mushroom-shaped protruberances at which much of the inter-neuronal signalling in the brain takes place, leading to strengthening of the synapse.

My bold. As if neurons were not ectomorphic enough already...

More recently, it has been shown that membrane-bound structures called recycling endosomes, which are located at the base of the dendritic spines, contain reservoirs of inactive AMPA receptors which are rapidly delivered to the cell membrane in response to neuronal activity. The receptors are inserted into the membrane by a process called exocytosis; a part of the endosome membrane, which has AMPA receptors embedded in it, buds off and fuses with the cell membrane. (Hence the increase in the surface area of the cell membrane, which can be measured by an increase in membrane capacitance, or the capacity of the membrane to store electrical charge).

Sounds like the fact neurons are these long skinny things makes it more convenient for the inner cell bits to get their stuff to the surface - there is a lot of surface relative to cell volume, in fact, neurons are the only cells that look like that.

Myosin is closely associated with another protein called actin, which forms microfilaments throughout the interior of neurons, including in the dendritic spines. Myosin is the prototypical molecular motor - it generates force by converting chemical energy into mechanical energy, and produces the cellular movements in processes such as muscle, by using that force to slide along actin microfilaments. Myosin Vb is enriched in the hippocampus, a region in the medial temporal lobe known to be critical for memory, and is therefore a prime candidate for a role in receptor trafficking.

So, looking at general culture, it looks to me (very superficially) that some have more myosin in their brains, perhaps, while others have more out in their periphery.

There is quite a long part about endosomes, then this:

myosin Vb is highly sensitive to the small calcium currents which flow into the cell through the activated NMDA receptor. Calcium induces a conformational change in the structure of myosin Vb, during which the molecule increases in length. This enables it to bind to a small "adaptor" protein called Rab11-FIP2, whose other end is bound to the endosomes. Subsequently, myosin Vb binds to actin microfilaments, and trafficks the endosome into the body of the dendritic spine.

Calcium has to do with glia. Glia have to do with most synapses. Post synaptic membranes have to do with large numbers of proteins of all sorts, the study of which an entire new science, system proteomics, (Seth Grant, Singer Institute) had to be invented.

[Diane]

Mo does Moseley.

[Karen L]

Copyright 2008 Elsevier Ltd. All rights reserved.
Current Biology, Volume 18, Issue 22, R1047-R1048, 25 November 2008
doi:10.1016/j.cub.2008.09.031
Correspondence


Visual distortion of a limb modulates the pain and swelling evoked by movement

G. Lorimer Moseley1,2,,Timothy J. Parsons1andCharles Spence3
1 Department of Physiology, Anatomy & Genetics, University of Oxford, UK
2 Prince of Wales Medical Research Institute, Sydney, Australia
3 Crossmodal Research Laboratory, Department of Experimental Psychology, University of Oxford, UK



Summary

The feeling that our body is ours, and is constantly there, is a fundamental aspect of self-awareness [[1]]. Although it is often taken for granted, our physical self-awareness, or body image, is disrupted in many clinical conditions [[2]] (see also [[3]] for a list of such conditions). One common disturbance of body image, in which one limb feels bigger than it really is, can also be induced in healthy volunteers by using local anaesthesia or cutaneous stimulation [[4]]. Here we report that, in patients with chronic hand pain, magnifying their view of their own limb during movement significantly increases the pain and swelling evoked by movement. By contrast, minifying their view of the limb significantly decreases the pain and swelling evoked by movement. These results show a top-down effect of body image on body tissues, thus demonstrating that the link between body image and the tissues is bi-directional.


1: Proc Natl Acad Sci U S A. 2008 Sep 2;105(35):13169-73. Epub 2008 Aug 25. Links
Psychologically induced cooling of a specific body part caused by the illusory ownership of an artificial counterpart.

Moseley GL, Olthof N, Venema A, Don S, Wijers M, Gallace A, Spence C.
Department of Physiology, Anatomy and Genetics, Oxford University, Oxford OX1 3QX, United Kingdom. lorimer.moseley@medsci.ox.ac.uk
The sense of body ownership represents a fundamental aspect of our self-awareness, but is disrupted in many neurological, psychiatric, and psychological conditions that are also characterized by disruption of skin temperature regulation, sometimes in a single limb. We hypothesized that skin temperature in a specific limb could be disrupted by psychologically disrupting the sense of ownership of that limb. In six separate experiments, and by using an established protocol to induce the rubber hand illusion, we demonstrate that skin temperature of the real hand decreases when we take ownership of an artificial counterpart. The decrease in skin temperature is limb-specific: it does not occur in the unstimulated hand, nor in the ipsilateral foot. The effect is not evoked by tactile or visual input per se, nor by simultaneous tactile and visual input per se, nor by a shift in attention toward the experimental side or limb. In fact, taking ownership of an artificial hand slows tactile processing of information from the real hand, which is also observed in patients who demonstrate body disownership after stroke. These findings of psychologically induced limb-specific disruption of temperature regulation provide the first evidence that: taking ownership of an artificial body part has consequences for the real body part; that the awareness of our physical self and the physiological regulation of self are closely linked in a top-down manner; and that cognitive processes that disrupt the sense of body ownership may in turn disrupt temperature regulation in numerous states characterized by both.

Latest L. Moseley papers.

[Diane]

Today's post from Mo is called Tactile-emotion synesthesia, and describes a paper Ramachandran and co-author David Brang have recently published, by the same name. Thank you for that informative post, Mo.

Abstract
We discuss experiments on two individuals in whom specific textures (e.g., denim, wax, sandpaper, silk, etc.) evoked equally distinct emotions (e.g., depression, embarrassment, relief, and contentment, respectively). The test/retest consistency after 8 months was 100%. A video camera recorded subjects' facial expressions and skin conductance responses (SCR) were monitored as they palpated different textures. Evaluators' ratings significantly correlated with the valence of synesthetes' subjective reports, and SCR was significantly enhanced for negative synesthetic emotions. We suggest this effect arises from increased cross-activation between somatosensory cortex and insula for 'basic' emotions and fronto-limbic hyperactivation for more subtle emotions. It may represent an enhancement of pre-existing evolutionarily primitive interactions between touch and emotions.
Keywords: Synesthesia; Emotion; Multisensory; Synaesthesia; Tactile

My own visual cortex seems primed to have the word "insula" jump out at it.

[Diane]

Mo writes about Lorimer in Scientific American.

Here's his own blogpost about it, Disowning Pain with Binoculars.

Thanks for being interested in pain perception, Mo.

[Diane]

Check out How we perceive others influences our sense of touch. (I.e., our sense of being touched.)

Thank you Mo.

Here's another along the same theme but from a different angle.

[Diane]

Mo has a recent blogpost about the evolution of the nervous system. Jon recently posted a few links to another blog, on the topic, but I cannot find his post. Jon, what thread was it?

Anyway, here's Mo's post. Evolutionary origins of the nervous system.

[Jon Newman]

It's here.

[Diane]

Thank you Jon. Analogue axon. AK's Ramblings. Check.