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Brain interconectivity question?

  1. Aug 1, 2014 #1
    What would happen if you ran conductive nanowires all over the surface of the brain? For the sake of this argument we'll say that the wires are biocompatible. Would it be benificial or would it mess up the brain to have two different parts interconnected?
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  3. Aug 1, 2014 #2
    Why would you think it would beneficial? To just aimlessly start connecting different areas together without any plan or purpose? Are you thinking of that movie, Phenomenon, with John Travolta? Lol.:http://en.wikipedia.org/wiki/Phenomenon_(film [Broken])

    In any case, back to your particular example, I'm guessing that these nanowires would be conducting electricity at close to c, which is far faster than the cable velocities of organic neurons, which are much, much slower, and which have a complex patterned weave of differentiation. Different types of axons have different cable velocities. It depends on whether they are short range, long range, myelenated, etc. How the brain works is very much wrapped up the sophisticated timing of signals that run through these cables.

    Running conductive nanowires all over the surface of the brain as you suggest would likely do little more than cause the brain to seizure.
    Last edited by a moderator: May 6, 2017
  4. Aug 1, 2014 #3
    Ok what about down the spinal cord? Your right biology really isn't my thing I was just wondering about something I read in a book.
  5. Aug 1, 2014 #4


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    Most likely all you're going to do is cause brain damage. There's a reason that when electrodes are implanted into a brain they have to be very carefully placed.
  6. Aug 2, 2014 #5


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    I agree with what others have said. It would be similar to randomly connecting the components of a complicated electrical circuit. You could cause feedback or clutter (signals that aren't supposed to be there) assuming you did it in a way that conserved signals.

    Of course, there is a possibility that, given time, an organism could adapt to make use of the signals, particularly during more plastic phases of development... but you also run the risk that some circuits wouldn't develop correctly if they were recieving irrelevant signals.
  7. Aug 3, 2014 #6


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    How big would the effect be, given that the brain is already bathed in cerebral spinal fluid, which is a conductor? There can be "ephaptic" electrical connectivity between neurons, but a large part of interneuronal communication is chemical, not electrical.
  8. Aug 3, 2014 #7


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    I would imagne something similar to axo-axonic gap junction coupling; a passive flow from the higher potential to lower potential. Though there would be some kind of capacitive coupling involved since ions can't flow through the wire.
  9. Aug 4, 2014 #8


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    That's larger than what I would guess. What sort of phenomena or behaviour do axo-axonic gap junctions produce?
  10. Aug 4, 2014 #9
    Ephaptic coupling including electrical gap junctions are prevalent in the brain but are more of an anomaly than a selected design feature, as far as we can tell. There doesn't seem to be any conserved pattern of any type of ephaptic coupling across brain taxa that would suggest it has any specific role in sensory-motor information processing, at least.

    For example, we don't consider any form of ephaptic coupling in our mathematical models of neuronal population dynamics, and I don't know of any group that does, although there might be. We've found the effects to be negligible relative to axo-dendritic electrochemical synapses, which far outweigh any anomolous ephaptic contributions. Typically, a neuron population will simply "overpower" any anomalously formed gap junction by simply producing more electrochemical axo-dendritic synapses to make up for any communication issue it may effect.
  11. Aug 4, 2014 #10
    Christof Koch's group have been working on ephaptic coupling, and they would argue that it plays and important functional role in brian dynamics (e.g., http://www.nature.com/neuro/journal/v14/n2/abs/nn.2727.html). Note that this is not even gap junction coupling, it is the influence of extracellular fields on action potentials. Gap junction coupling is much stronger and can synchronise neural networks (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2744332/, http://www.jneurosci.org/content/21/15/5824.short).
  12. Aug 4, 2014 #11


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    That's interesting, but with respect to the question in the OP, my guess was that what he was suggesting could be carried out by simply pouring CSF (artificial CSF, say normal saline) on the brain, since CSF is conducting, and will infiltrate the entire extracellular space. But why would pouring CSF on the brain have any effect, given that the brain is bathed in CSF already?
  13. Aug 4, 2014 #12
    The first article is behind a paywall, but the entirety of the articles you posted deal with ephaptic/gap junction contributions to "synchrony" of oscillations in neural tissue.

    My comment was:

    And there doesn't seem to be. While gap junctions may affect and potentiate local synchrony, more global synchronies, such as thalamocortical oscillations, are regulated by the ascending reticular activating system and neurotransmitter/hormones that act through axo-dendritic synapses.


    And, as I stated above, ephaptic contributions to neuronal synchrony do not have a mechanism for the plasticity needed to moderate sensory-motor information processing. In our models, synchrony is driven globally and locally by populations of excitatory and inhibitory neurons, whos behavior is normally chaotic. That chaos is important in keeping the brain in a "ready" state to respond to stimulus input, at which point the entire brain converges to a near limit-cycle attractor which reflects the response to that stimulus.

    All of this action is driven by axo-dendritic electrochemical synapses. While a axo-axonic gap junctions or any other ephaptic contribution to "synchrony" may exist, its effects are buried under the more relevant axo-densritic effects, which is why we don't include them in our models.
  14. Aug 4, 2014 #13
    I don't see the equivalence of pouring CSF on the brain and hooking up all regions of the cortex with conductive nano-wires. Doing the latter would simply cause the brain to "short out" and seizure. Doing the former (pouring CSF on the brain) would do as you implied, nothing, seeing as that the brain is already bathed in CSF. Whether CSF presents a deleterious issue of shorting neural communications is self-evident, obviously it doesn't or our brains wouldn't work.
  15. Aug 4, 2014 #14
    I'm not sure I get your point here. Of course synaptic and chemical mechanisms have an important effect on brain function, but that doesn't rule out a role for ephaptic coupling. Of course it can be difficult to demonstrate that something has a direct functional role for sensory and motor processing, but the fact that these studies have shown that ephaptic coupling has a clearly measurable influence on neural activity is reasonable evidence. Apart from at neuromuscular junctions and sensory organs, we don't have much direct evidence that chemical synapses play a specific role in sensory-motor processing, but we assume that they do because we can see how they affect the neural activity in parts of the brain that process the relevant information.
  16. Aug 4, 2014 #15
    I didn't rule out a role for ephaptic coupling, I agreed that it plays a minor role in population synchronization.

    That is simply an incorrect statement. The entire dogma of neuroscience is built on the premise that chemical synapses play a specific role in sensory-motor processing. This dogma goes back 100 years to the time when Ramón y Cajal first identified the chemical synapse. The evidence for this is overwhelming. Contrarily, there is essentially zero evidence that gap junctions or ephaptic coupling is related in any way to executing complex behavioral routines or any kind of sophisticated sensory processing.
  17. Aug 5, 2014 #16
    There is evidence that gap junctions execute behavioural routines http://jn.physiology.org/content/85/4/1543.short.

    Secondly, the "entire dogma of neuroscience" is based on observing how chemical synapses determine the activity patterns in neural circuits and correlating these activity patterns with behaviour. The evidence for the role of chemical synapses in behaviour is no more direct or concrete than that for ephaptic coupling or gap junctions, it is just more abundant because it has been studied for longer.
  18. Aug 5, 2014 #17
    Is that right? Rhythmic respiration does not qualify as a behaviorally sophisticated motor expression. Here are the authors conclusions to the paper you posted:

    Where in there is any mention of gap junctions mediating any form of hierarchically sequenced goal-directed behavior which is the hallmark of mammalian brain function? It's not there, because they are not involved. Did you even read this article?

    Sorry, but that statement is just patently absurd. Show me a study that links gap junction dynamics to a behavior of even modest complexity, and not a tonic or rhythmic process. You won't be able to find one. And the way the brain works has nothing to do with what "platform" of neuronal modeling has been studied for a shorter or longer amount of time.
  19. Aug 5, 2014 #18

    Show me a study which directly and causally links chemical synapses to hierarchically sequenced goal-directed behaviour.

    What are you even talking about? I haven't even mentioned modelling. We're discussing the evidence for chemical synapses and other mechanisms for controlling neural circuits and behaviour. Please don't put quotation marks around words that I didn't use.
  20. Aug 5, 2014 #19
    Well, it's essentially almost every paper written on neurobiology/neurophysiology, with perhaps the exception of the few papers you've seemed to be able to fish out on gap junctions.

    Here's a short list for your perusal...


    I could list 100 others, but what's the point? The point is that we have models that are based on decades of experimental research which indicate that populations of neurons form "nodes" which have an irregular communication which puts the brain in a basal, aperiodic chaotic state. These oscillations are primarily driven all over the cortex by the competing activity of excitatory glutameric populations and interneuron inhibitory GABA-ergic populations, not gap junctions. It is well established that the learning of complex behavioral routines and the memory of sensory events is accomplished through the "Hebbian" strengthening of existing electrochemical synapses and formation of new synapses.

    http://www.ncbi.nlm.nih.gov/pubmed?term=Skarda CA[Author]&cauthor=true&cauthor_uid=3006863


    Ultimately, sensori-motor processing in mammals boils down to a process whereby the oscillations in the cortex, driven by electrochemical synapses, play out a cinematographic sequence of frames, which are temporary burst states which confer a patterned output in primary motor cortex which feeds down through the cortico-spinal pyramidal tract to enact an associated motor behavior. You can get the details here:



    You'll notice that nowhere in any of these papers/models is there postulated or modelled a significant role for the participation of gap junctions or any other ephaptic influences.

    In light of that, I am very eager to hear your explanation of how gap junction interactions execute a complex behavioral routine or perform, say, a sensory discrimination. References are great, but I'd really like to hear your personal interpretation/explanation of how it works.
    Last edited: Aug 5, 2014
  21. Aug 5, 2014 #20
    DiracPool, none of the papers you referenced demonstrate what you say they do. They either study the timing of neural responses or the large scale EEG activity. Where is a specific (experimental) demonstration of chemical synapses executing a complex heirarchical goal directed task?

    At present, the best we can do is investigate the dynamics of neural circuits and their relationship to simlpe perceptual and behavioural tasks. Clearly chemical synapses are central to the behaviour of neural circuits, but there is increasing evidence of the importance of electrical and ephaptic coupling and astrocytes in circuit dynamics. Of course I wouldn't claim that electrical synapses generate behaviour alone (although the previous reference I posted shows that in some instances they can). However, I think it is disingenuous to ignore the experimental evidence for other forms of neuronal communication simply because you haven't included them in your model.
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