EM fields: a plausible correlate of consciousness?

In summary, the conversation discusses a theory paper that proposes the role of electromagnetic fields in the brain as a potential explanation for consciousness. The conversation includes personal skepticism, but also an interest in the compelling arguments presented in the paper. The author shares their own speculation on how this theory could potentially explain certain aspects of memory. There is some disagreement and a call for further consideration and exploration of the theory.
  • #36
Well,

The problem with Damasio is that he is not totally clear and says that parts are mandadory and form as you said a NCC. He said with medical examples that cortices aren't necessary for consciousness neither language.
He proceeds by elimination and it seems probable that the core-consciousness which enables the extended one we are speaking is enabled by thalamus, hypo-thalamus, cingulates, brainstem. The pre-frontal is mandatory for the extended (as many other sites).
 
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  • #37
Moonbear said:
Several problems with this interpretation. First, "no obvious behavioral abnormalities," does not mean "NO behavioral abnormalities." It means the mice appear to locomote normally, are capable of breeding, and nothing really stands out as unusual. There was no reference to any rigorous behavioral testing in the Guldanagel et al., 2001 paper. It's basically a way of saying, "we think the mice are healthy enough to not require any special care."
Second, and more importantly, they provide NO evidence that gap junctions are disrupted or non-functional following this deletion. The Guldenagel paper refers to Connexin-36 being primarily found in retina (that was the focus of their study). Another study using hippocampal slices from the Cx36 KO mice found only subtle effects, and indicate that other gap junctions are likely preserved.
From: Maier N, Guldenagel M, Sohl G, Siegmund H, Willecke K, Draguhn A. 2002 Reduction of high-frequency network oscillations (ripples) and pathological network discharges in hippocampal slices from connexin 36-deficient mice. J Physiol. 541(Pt 2):521-8.
Just eliminating one protein found in one type of gap junction does not mean all gap junctions were disrupted, or that there wasn't a compensatory increase in another related protein that maintained function. All this says is that Connexin 36 isn't sufficient on its own to disrupt all neural synchronization.

[Johnjoe]
But connexion 36 is the major gap junction protein in the mouse brain. Subsequent have confirmed that the KO mice completely lacked ANY functional gap junctions in the brain. See for instance,

De Zeeuw, C. I. et al (2003) Deformation of Network Connectivity in the Inferior Olive of Connexin 36-Deficient Mice Is Compensated by Morphological and Electrophysiological Changes at the Single Neuron Level. The Journal of Neuroscience, June 1, 2003, 23(11):4700-4711

One of the tests the authors performed was to inject Lucifer yellow into olivary neurons. With functional gap junctions [of any kind!] in the wild-type mouse the dye spreads to adjacent neurons but “ in all Cx36-deficient mice, the injections resulted in labeling of single neurons only (n = 16), whereas those in the wild types always provided clusters of multiple neurons (n = 18, with an average of 8 ± 3.8).”
The authors go on to perform electrophysiology measurements that lead them to conclude that “no functional gap junctions exist in the homozygous mutants.”.
Similar studies have been performed by several other authors and the conclusion is firm that the KO mice lack functional gap junctions in those parts of the brain that have been investigated.
That the mice still demonstrate rhythmic oscillations in the brain is very interesting. The above study found evidence that the mice compensate for loss of gap junctions by making their neuronal membranes more electrically sensitive. This would make them more sensitive to EM fields (although that hasn’t yet been demonstrated) so it may be that EM fields are maintaining synchronicity in these mice.


johnjoe
 
  • #38
Moonbear said:
The most troubling part of this whole CEMI field theory to me is that I don't see how a signal that would be distorted by passing through the very substrate that produces it could have any useful function as a means of transmitting information. Wouldn't the field produced by a neuron in say the prefrontal cortex be completely degraded before it could reach the thalamus or hippocampus? The concept might work in a tiny mouse brain, but in something as large as a human brain, it just makes little sense that such a weak field could do much to synchronize function over large areas of the brain, as is proposed.
[johnjoe]
this objection is based on a misconception that the EM signals have to be free of distortion to convey information. Distortion is irrelevant so long as the information in a signal is not degraded. If the EM field and one point can predict the neural activity at another point then useful information is transmitted. so although the EM field may be largely deformed by its passage through the brain it can still funtion to transmit information rapidly through the entire volume of the brain.

Moonbear said:
Yet another contradiction to this idea that these EM fields, detectable by local EEG recordings, are involved in consciousness is that in anesthetized rats (I'm sure we can all agree that depending on the plane of anesthesia, an anesthetized animal at least has reduced consciousness) treated with amphetamine, EEG recordings in the frontal cortex show arousal. This EEG indicator of arousal in these anesthetized rats can be blocked with noradrenergic beta-receptor antagonists.
Berridge CW, Morris MF. 2000 Amphetamine-induced activation of forebrain EEG is prevented by noradrenergic beta-receptor blockade in the halothane-anesthetized rat. Psychopharmacology 148(3):307-13.

[johnjoe]
I'm not clear on the significance of these findings. amphetamines are thought to induce arousal noradrenergic beta-receptorin the brain and this arousal can be detected by EEG. the paper showed that blocking the noradrenergic beta-receptors prevented the EEG arousal signal in anaesthetised rats. Is the point that you get EEG signals of arousal in a (presumably unconscious) anaesthetised animal? But the EEG signals are generated by neuronal firing that similarly would be an neural 'indicator' of arousal. Does that indicate that neurons aren't necessary for consciousness? The conclusion must surely be that either neuronal activity and/or EM fields are necessary but not sufficient for reportable consciousness. anaeasthetics must block some downstream processes (eg. motor and/or memory) that prevents reportable consciosuness.

johnjoe
 
  • #39
Johnjoe,

Supposing that I take your theory.

1/ shape of brain and orientation of pyramidal cells (they are quite ever oriented to the cortex surface).
2/ the resulting EM field will be then ever a sum/subtraction linked of firing cells.
3/ the resulting field couldn't be a legit representation of the original neural activation.
4/ we are encountering the same limitations with other modalities (RMI, PET, EEG...)

IMHO, it is like I get all characters that make a Bible and try to reconstruct it.
The unified/integrated field is just like making this huge trial.
 
  • #40
somasimple said:
Well,
The problem with Damasio is that he is not totally clear and says that parts are mandadory and form as you said a NCC.
Actually, I never use the term NCC.
He said with medical examples that cortices aren't necessary for consciousness neither language.
He proceeds by elimination and it seems probable that the core-consciousness which enables the extended one we are speaking is enabled by thalamus, hypo-thalamus, cingulates, brainstem. The pre-frontal is mandatory for the extended (as many other sites).
This makes sense to me in principle. When things are subtracted by disease or trauma you get a more diminished consciousness. The notion of cross referencing between patients to see what parts appear to be necessary for what level or kind of consciousness seems sound.
 
  • #41
Hi,

Damasio says, too, that core-consciousness is an old thing because its first goal is an enhancing of the homeostatis process. Homeostasis is governed by old brainstem structures.

Many patients who lost consciousness (seizures/kinetic automatism) lost egally the ability to shows the primary emotions. Primary emotions are located also in these old structures and many animals share the same ones.

Thus, it seems probable that core-consciousness is an enhancement of the reward system used to maintain homeostasis.
 
  • #42
somasimple said:
Hi,
Damasio says, too, that core-consciousness is an old thing because its first goal is an enhancing of the homeostatis process. Homeostasis is governed by old brainstem structures.
This, I can't say anything about. Never looked into it.
Many patients who lost consciousness (seizures/kinetic automatism) lost egally the ability to shows the primary emotions. Primary emotions are located also in these old structures and many animals share the same ones.
I get the impression from "kinetic automatism" that he's talking about what are called complex-partial seizures. Partial seizures are either classified as simple, which means there is no impairment of consciousness whatever, or complex, which means there is a greater or lesser defect of consciousness.
As far as they know, so long as seizure activity remains in one single hemisphere, regardless of how many lobes the activity spreads to, the seizure will remain simple: consciousness will not be impaired. The impairment of consciousness in a complex partial seems only to arise from the spreading of simple partial seizure activity across into the other hemisphere.
The defect of consciousness that results is extremely peculiar and manifests quite differently from patient to patient. It is also quite distinct from the complete loss of consciousness that you get in absense seizures ("Petite Mal"), tonic-clonic seizures ("Grand Mal") and atonic seizures ("Drop Seizures") . These latter render the person completely unconscious by interfering with the thalamus.
In the complex-partial seizure you get all kinds of levels of this "defect" of consciousness, and always amnesia for the incident after it occurs. The "average" CP renders the person about as responsive to the environment as a sleepwalker: they're still vaguely responsive to some sensory imput, but seem more focused on some compelling illusory world, or just plain stupified. This state is usually accompanied by "automatisms": repeated movements and gestures.
As for not being able to show primary emotions, I'm not sure that is generally true. It is only true that whatever emotions they show aren't going to be appropriate to the stimulus. One woman posted on an Epilepsy website saying her husband told her that during her seizures she pulled him close and whispered gibberish with a high emotional valence to him "It sounded like you were trying to tell me something really important". Another person at that site was told by relatives his seizures were screaming sessions. Also: a caution that is repeated over and over again to the loved ones of people with complex partials is to never try to move them around during a seizure, because the reaction is almost always one of hostility, and even violence:
In "The Making Of A Psychiatrist", by David Viscount, he tells of an "uncooperative" man who was brought into a psych ward where he was an intern, by police. This man was surly, and had fought them when they brought him in. He looked directly at anyone who addressed him and responded with an answer that was not gibberish, but which had nothing to do with what they'd asked. No one could figure this out. They put him in a room and left him there. Later the author happened to walk by and see the guy was having a tonic-clonic seizure. Suddenly he realized the initial behaviour was a complex-partial which had later generalized to the tonic-clonic.
People having CP's are certainly not unconscious, a term which applies to someone in a coma, but they aren't what you could properly call conscious either. That's why they've settled on speaking about this as a "defect of consciousness". And while sometimes they have a flat affect and seem stupified, I don't think this represents an inability to feel emotion. Some people with CP's get plenty emotional despite the defect of consciousness.
 
  • #43
Hi,

Here is a link for some usefuls paper by Damasio
http://www.medicine.uiowa.edu/adolphs/documents.html
 
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  • #44
Hypnagogue, thanks for the post on NCC's. It seems to me there must be a fairly localized portion of the brain which is responsible for consciousness, some boundry must exist within the body between neurons that support consciuosness and those that don't. One can use extreme examples as a way of proving this, obviously we can remove neurons in the limbs, and even quadrapalegics have no significant impact to consciousness. I would suspect there are neurons even in the brain which are used to interpret visual, audible, and other sensory signals which shouldn't have any significant impact on consciousness along with neurons that control various involuntary parts of the body such as the heart, breathing, etc...

I'm not suggesting there's a single group of neurons that are solely responsible, the group could even change from moment to moment, conscious experience dancing around within the brain as it were. But I have to believe that everyone recognizes there is a boundry and the only issue is where that boundry is. Saying it is the entire brain and cutting it off at the spinal cord may not correspond to reality.
 
  • #45
Brain. 2003 Jul;126(Pt 7):1524-36. Epub 2003 Jun 4.
Neuroanatomical correlates of brainstem coma.

Parvizi J, Damasio AR.

Department of Neurology, Division of Cognitive Neuroscience, University of Iowa College of Medicine, Iowa City, IA 52242, USA. parvizi.josef@mayo.edu

The brainstem tegmentum, including the reticular formation, contains distinct nuclei, each of which has a set of chemical, physiological and anatomical features. Damage to the brainstem tegmentum is known to cause coma, the most radical disturbance of consciousness. However, it has remained unclear which nuclei within the tegmentum are crucial for the maintenance of consciousness in humans. Accordingly, we initiated a retrospective study of MRIs obtained from 47 patients with brainstem stroke. The lesion boundaries were charted on patient MRIs and transferred onto a corresponding series of 4.7 T MRIs obtained from a control brainstem specimen that later was cut on a freezing microtome and analysed histologically. In addition, medical charts and available post-mortem materials were used to obtain relevant clinical and anatomical data to verify the MRI readings in each case. We found that in the 38 patients who did not have coma, brainstem damage either was located outside the tegmentum (n = 29) or produced a very small and unilateral compromise of the tegmentum (n = 9). In contrast, in patients who had coma (n = 9), the lesions in the tegmentum were mostly bilateral (n = 7) and were located either in the pons alone (n = 4) or in the upper pons and the midbrain (n = 5). The maximum overlap territory of the lesions coincided with the location of the rostral raphe complex, locus coeruleus, laterodorsal tegmental nucleus, nucleus pontis oralis, parabrachial nucleus and the white matter in between these nuclei. We also found that four coma subjects developed hyperthermia and died in the absence of any infections. In these cases, the maximum lesion overlap was centred in the core of pontine tegmentum. Our findings suggest that lesions confined to the upper pons can cause coma in humans even in the absence of damage to the midbrain. The findings also point to the brainstem nuclei whose lesions are likely to be associated with loss of consciousness and fatal hyperthermia in humans.

PMID: 12805123 [PubMed - indexed for MEDLINE]
 
  • #46
Hi Job. I like your question, and thought it would be a good kick off point to some discussion around the central feature of the cemi field theory.
One thing that seems to go against this theory is the fact that some people who have undergone brain surgery while conscious report feeling normal even though the brain is exposed.
There are two ways to reduce or eliminate the impact of stray em fields and I believe both are needed for the cemi field theory and both are actually discussed in the papers.
1. Neurons must be reasonably well isolated from stray noise.
2. Neurons must be capable of filtering the noise from the fundamental signal.

This issue is discussed in the second paper under the heading "Pockett's difficulty 2". McFadden recognizes the large amount of information present in the brain's em field and suggests "only a tiny component of the information" corresponds to consciousness, so the excess information must be discarded. Em receiving devices such as radios, tv's, cell phones or other electronic devices are actually designed to accomplish these two features. One primary goal of an antenna for instance, is to provide for reception of a limited band of frequencies. The circuitry then filters out everything but the signal being tuned for.

Shouldn't neurons also accomplish the same two features? I believe so, and in fact this may lead to a more rigorous prediction for the theory. A focus on the mechanisms involved and a computational analysis on neurons' abilities to interact with specific fields may be just what is needed to help prove or disprove this theory. The field signal of interest is said to be integrated and distributed (ID) throughout the brain, but it comes along with much excess noise. If it exists, this ID information should in principal be measurable. It should also be calculable, such as is being done with the Blue Brain project, assuming they are modeling the em field in addition to the rest of the neocortical columns.
 
  • #47
HI,

1. Neurons must be reasonably well isolated from stray noise.
2. Neurons must be capable of filtering the noise from the fundamental signal.

Shouldn't neurons also accomplish the same two features? I believe so

  1. Some neurons are inhibitors.
  2. Some neurons are facilitators.
Is there a way that an EM field created by these different classes may be different?
How a distant neuron will regognize the difference?
 
  • #48
ELF or extremely low electromagnetic fields are related to human brain functions and in fact as the existence of Schuman resonance has demonstrated that there is an implied relation between human brainwave and ELF .
 
  • #49
reena,

We are all agreeing with this opinion. That is not the subject of the thread.
 
  • #50
The brainstem tegmentum, including the reticular formation, contains distinct nuclei, each of which has a set of chemical, physiological and anatomical features.

Hi Somasimple. Thanks for the info regarding 'seat of consciousness' or NCC's. Not sure what to call them, but unless there's a better word, I'll use NCC's.

You asked:
Is there a way that an EM field created by these different classes may be different?
From an engineering standpoint, if the cemi field theory is to have any significant predictive power, I have to believe it must predict there is a fundamental difference between neurons which provide a substrate for consciousness and those that don't. The theory must predict that the cemi field interacts in some mechanistic way with specific neurons in some specific portions of the brain and not others. If all neurons (ie: even nerves) interacted with the cemi field then our legs and fingers would be conscious too, provided they were close enough to interact. Locating a seat of consciousness and suggesting those neurons interacted directly with the cemi field seems to be a prediction of the theory. Although it is not listed as one of the eight, it seems to be implied.

These neurons that form a substrate for consciousness must also be 'tuned' to a specific field since the field has so much additional garbage in it.

Conclusion: there is a portion of neurons that interact with a portion of the em field. The portion of neurons might be called NCC's and the portion of the field is referred to as the cemi field. What sets the cemi field apart from other em noise is that it contains the information needed for a unified conscious experience. The cemi field must also be distinct from the noise such as perhaps by operating at a different frequency. (Does anyone see a problem with this conclusion given the theory provided?)

That conclusion results in a prediction. Prediction: If we locate the NCC's, then we should similarly find something unique about them which interacts with the cemi field. We should be able to model those neurons using typical finite element or control volume analysis techniques and find they have properties which are particularly receptive to em fields to the point of being able to interact with them. That analysis should also indicate a frequency or some other unique property of the field which sets it apart from the noise. Similarly, we should be able to do this type of analysis on other neurons and find they have significantly less ability to interact with em fields and the cemi field in particular. Another finding might be that NCC's are well protected from stray em fields.

I think this prediction may go counter to what is proposed by McFadden though. Thoughts? Johnjoe, are you still there? :)
 
  • #51
Hi reena. You obviously have a good background for discussing this concept. Please have a gander at the paper under discussion. To summarize very briefly, the cemi field theory suggests that em fields, analogous to TV fields/transmissions, are used by the brain to bind or unify information. These fields are external to the neurons. It has been suggested by many that the em fields within neurons that are passed between gap junctions are insufficient to provide for unity. Such signals are discrete, local, and not integrated.
 
  • #52
Hi again,

If all neurons (ie: even nerves) interacted with the cemi field then our legs and fingers would be conscious too, provided they were close enough to interact.

But nerves are neurons!? and are connected to brain by neurons.
Some medical trials say that body stimuli are mandatory to process/create consciousness. So body is an indiscutable part of it (because body is just a way for brain to apprehend world)

See Damasio's books; Looking for Spinoza and the Descartes' Error.
 
  • #53
Some medical trials say that body stimuli are mandatory to process/create consciousness.
Interesting. Are you saying a "brain in a vat" would result in the brain not being conscious? Are stimuli provided by external means (ie: an electric impulse) not equal to actual stimuli? I can only remember a single bit of research that suggested they were, but that's not my field. I believe the whole point of the 'brain in a vat' thought experiment was to suggest there are no special signals, that any equivalent signal would produce identical reactions and would feel the same to the person. Hence, no loss or change in consciousness despite the brain being disconnected from a human and inside a vat.
 
  • #54
Hi,

I wasn't thinking so directly to the "brain in a vat" story. It is perhaps possible to reproduce all incoming "electrical" stimuli with patience and time?

But it will not work if you limit brain, to an electrical "computer" (it is not).
But brain is the first endocrine system of body and hormones/peptides produced are modifying directly the manufacturer. :wink:

Consciousness needs a "body state" to create a "reference Self". Brain works with differences comparing a state to a newer one and updating continuously the reference material.

Some medical states as psychosis and phantom limbs problems, for an example show that an impairment/perturbation of incoming stimuli create a distortion and "painful solutions".

It is why I persist to think that a cemi field is an integrated "reflection" of brain activity but it can't directly rely the subtle changes in the brain endocrine system.
Do not forget that a neuron is able to synthetize around... 20,000 peptides.
 
  • #55
Wow. The development of this thread has been an immensely pleasant suprise. Thanks to everyone, especially johnjoe - to who I am most grateful for sparing us the time -, q_goest, and somasimple, for putting such effort into what has become a great discourse. I've been humbled into silence thus far, since others have consistently provided a more eloquent and perspicious presentation of whatever questions, confusions, or observations I might have been able to offer. This has been a thoroughly thought-provoking experience, and has impelled me into quite a bit of illuminating research and questioning as well.
But anyway, nobody wants a bunch of praise and gratitude from someone who has nothing to say for themselves. So here's my input:
Somasimple said:
"But it will not work if you limit brain, to an electrical "computer" (it is not). ...
It is why I persist to think that a cemi field is an integrated "reflection" of brain activity but it can't directly rely the subtle changes in the brain endocrine system."
This all seems irrelevant to the cemi field theory, which, though it has claimed that the field has access to all of the information repersented by neural firing, doesn't need complete access to all the biology or chemistry that influences our neural processes. It seems to me that since we've already both accepted that the field is primarily effected ('e' intended) by large, synchronous groups of neurons, and that only a small part of the fields' content even comprises our consciousness, it seems cavilling to try and dismiss the idea on the basis of neglecting to factor a certain type of neural input.
From an evolutionary standpoint, this new system evolved in addition to the old, so it is seems only valid that it integrates less information than the system below it (unnecessary to reproduce the entire existing system - not even productive) to distill meaningful data to be returned to that system.
Somasimple:
"But nerves are neurons!? and are connected to brain by neurons.
Some medical trials say that body stimuli are mandatory to process/create consciousness. So body is an indiscutable part of it (because body is just a way for brain to apprehend world)"
As far as the first sentence, it seems you've forgotten this paper acknowledges a dichotomy between conscious and unconscious neural processing.
In addition, I'm willing to bet that those medical trials didn't induce unconsciousness, but simply disrupted normal functioning. Even someone lost in a fugue is still conscious, though functioning may be disrupted (I'm asserting sentience, which is generally assumed to be a conscious thing). Assuming knocking someone out through sensory deprivation were possible, a loss of sensory input may compromise lower systems in the brain that preceded the conscious, higher level systems evolutionarily, causing a loss of consciousness (as the conscious systems grew taking the others' nominal functioning for granted). A program for which internet access isn't essential, but assumed, can cease to function without an internet connection, because of the assumption, not due to an inherent requirement. This is relevant, because it implies the possibility of using pharmacological intervention to artifically compensate for the lack of afferent arousal and revive consciousness in a discarnate brain.
somasimple:
"Do not forget that a neuron is able to synthetize around... 20,000 peptides."
Man, the complexity of our brains is just unfathomable .
q_goest:
"If all neurons (ie: even nerves) interacted with the cemi field then our legs and fingers would be conscious too, provided they were close enough to interact."
Not conscious, but contributing information to the conscious field. One of the advantages of this theory was it's elegant resolution of the binding problem... we can't simutaneously entertain the idea of delocalized consciousness.
q_goest:
"here are two ways to reduce or eliminate the impact of stray em fields and I believe both are needed for the cemi field theory and both are actually discussed in the papers.
1. Neurons must be reasonably well isolated from stray noise.
2. Neurons must be capable of filtering the noise from the fundamental signal."
It seems to me that these concerns about noise, or a distored signal, are misplaced. Assuming evolution, the whole thing developed with the distortion/noise concurrent. Perhaps I am forgetting that the position of neurons in your brain is far from set in genetic stone. Dismissing genetic evolution, there's the evolution of your conscious system as you develop from a- nebulously conscious -newborn. Your consciousness cohering and becoming "capable of communicating self-generated inrreducibly complex concepts like 'self'," could repersent the slow acquisition of neural configuration that considers the distortion of signal, interference, etc.
lates,
cotarded.
 
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  • #56
motor neurons: decisive for consciousness?

Again and again, motor neurons are mentioned in this paper and in this thread as what divides the consciousness-relevant bits of the em field from the rest. I propose something that at least to me seems far more reasonable.
After all, what makes consciousness so enigmatic is how private and personal the experience is; I can't reconcile that with a dependency on outward expression (here come the studies that show subvocalisation for our internal speech).

Memory. What is a flash of sentience in the dark? Our consciousness could be what it feels like to be an evolving feedback loop inside short-term memory, with input supplied by the outside world. So maybe there is field consciousness, and all the other sorts described in the paper, but what makes us self-reflective is the fact that we CAN reflect off of ourselves: our stored snapshots in memory. So I opine that the part of our EM field that can affect the memory encoding process is the part that is conscious.

Feedback?

-cotarded.
 
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  • #57
cotarded said:
Memory. What is a flash of sentience in the dark? Our consciousness could be what it feels like to be an evolving feedback loop inside short-term memory, with input supplied by the outside world. So maybe there is field consciousness, and all the other sorts described in the paper, but what makes us self-reflective is the fact that we CAN reflect off of ourselves: our stored snapshots in memory. So I opine that the part of our EM field that can affect the memory encoding process is the part that is conscious.
If you read any of Bernard Baars' work, his model of consciousness largely implicates working memory and attention as two of the main cognitive functions associated with consciousness. (Any in-depth further discussion on this is probably better left for another thread.)

In a sense, focusing on motor systems makes sense, since presumably any mental content that is within consciousness can be poised to guide flexible kinds of motor behavior, even if it does not wind up doing so (e.g. as in Ned Block's conception of access consciousness). So a reasonable constraint on any theory of consciousness is that the phenomena in the brain proposed to be correlated/synonymous/whatever with consciousness have the requisite kind of power to affect the brain's motor outputs. Though of course, that will not be the only useful constraint.
 
  • #58
I feel a bit let down by the 8 predictions provided by the theory. I'm not convinced the predictions, if proven, would thus prove the theory. I'd be glad to hear arguments to the contrary.

However, I think there's a very solid prediction the theory could make. The theory suggests that motor neurons are the ones interacting with the cemi field, but it is acknowledged this field is analogous to a single TV station signal among hundreds of signals which are simply garbage (per McFadden). From the second paper under "Pockett's difficulty 2"
Pockett's second difficulty points out that 'there actually is no one-to-one correspondence between electromagnetic patterns measurable at the scalp or the surface of the brain and the conscious sensations experienced by the "owner" of the brain' (p. 53). However, I would argue that this is only a problem for em field theories that propose an identity between the brain's total em field and conscious experience. Indeed, the issue highlights a difficulty with any identity theory between the brain's em field and consciousness. Since every action potential generates a perturbation in the surrounding em field, the information flow through the brain's em field must be of a similar order of magnitude as the spike rate of cortical neurons, about 10^12 bits per second. But this is far greater than the approximately 40 bits per second that are estimated to be involved in conscious thinking (Norretranders, 1998). Clearly only a tiny component of the information held in the brain's em field can correspond to consciousness so any identity theory must find some means of discarding the excess information. In the cemi field theory this is explained by the requirement for the field information to be downloaded to motor neurons. In my paper, I showed that induced transmembrane voltages are in the range of several microvolts up to about one millivolt. Neurons will thereby only be sensitive to em field effects when they are within a millivolt or less of the firing threshold. Since transmembrane voltages vary across approximately 130 mV, very crudely, we would expect less than one hundredth of neurons to be receptive to information held in the surrounding extracellular field. The corollary of this is that most of the information in the brain's em field will not be downloaded into neurons. Therefore, in the cemi field theory, only a tiny portion of the informational content in EEG or MEG signals would be expected to correlate with consciousness. A one-to-one correspondence between perturbations of the brain's em field and consciousness is not therefore expected in the cemi field theory. Although the failure to make a clearly verifiable prediction of a correlation between the gross structure of the brain's em field and consciousness may be considered to be a weakness of the cemi field theory, the theory does make many alternative predictions as described in my earlier paper, and I describe a direct test in the final section of this paper.
In the final section of the paper, a very unique prediction is provided (Discussion section) but the prediction requires the manufacture of an artificially aware computer. I'd agree this would be a much more solid, even indisputable test of the theory. Unfortunately for us, it is so far off into the future we probably won't see such a test in our lifetimes.

Instead, I would suggest one could make a prediction about the theory which is testable today using current technology.

The theory MUST predict that the portion of the em field in the brain, the cemi field, is somehow different from the rest. If it didn't then the motor neurons would also pick up all the other garbage in the em field and not be able to distinguish, just as a TV signal that had another signal of the same frequency on top of it could not receive the TV signal. Your TV would give you lots of static and garbage because both signals were using the same frequency. The same applies to the cemi field, it has to be different enough (not necessarily frequency, though I'm unsure of this) that the motor neurons can separate it out from the garbage.

Similarly, the cemi field theory must predict that the motor neurons are different than other neurons with respect to certain em fields. One can for example, analyze an antenna and/or a radio and determine what signal frequency it is able to interact with. Conversely, the motor neurons (if they really are picking up this cemi field) must be able to interact with whatever is unique about the cemi field. One should be able to analyze a motor neuron and a neuron in your finger for example, and show that these neurons are capable of interacting with different em fields. This is normally done in engineering using sophisticated finite element or "control volume" concepts. Such tools should be capable of indicating what em fields a neuron is susceptible to and prove one way or another if the cemi field theory is correct or not.

Cotard said: Not conscious, but contributing information to the conscious field.
Yes, exactly. Sensory neurons, per the cemi field theory, must relay information which contributes to the cemi field, but not be sensitive to it (they are not motor neurons in the brain). The only way I can see that being possible is for the sensors (ie: nerves in your hand) to transmit a signal to your brain, and some other neurons in the brain must then convert that information to the cemi field. One has to ask the question, "What neurons create the cemi field?" I don't see that in the paper, but in principal, I believe the answer is that sensory neurons transmit information to the brain which is then converted by other neurons into em vibrations which can be interpreted by the motor neurons or something like that.

I'd also suggest another prediction but I'll hold off on that one for now.
 
  • #59
Ok, I think I just fell off the deep end and would like to know if there are any sharks in these waters. <grin> I'm looking at a picture of various types of neurons. If I use my imagination, the axon looks a lot like an antenna, and the nodes of Ranvier look like the neuron's way of tuning that antenna. The distance between these nodes might act to selectively transmit/receive specific em frequencies. And I'd think the general shape would have a distinct effect on em field interaction as well (though I suspect that shape is generally straight). This suggests that the length of an axon, and the distance between nodes (and possibly the general shape) will characterize the frequency of response to any em field that the neuron is exposed to. If there is something unique about specific neurons in the brain which might interact with a field, it might be these characteristics of the axon. Can anyone comment on the role of the nodes?
 
  • #60
Q_Goest said:
Ok, I think I just fell off the deep end and would like to know if there are any sharks in these waters. <grin> I'm looking at a picture of various types of neurons. If I use my imagination, the axon looks a lot like an antenna, and the nodes of Ranvier look like the neuron's way of tuning that antenna.
You're looking at a stylized drawing for the purpose of schematically illustrating the parts of a neuron. It's not what they really look like if you look at them under a microscope. Besides, similarity in shape does not translate into similarity in function.
 
  • #61
johnjoe said:
[Johnjoe]
But connexion 36 is the major gap junction protein in the mouse brain. Subsequent have confirmed that the KO mice completely lacked ANY functional gap junctions in the brain. See for instance,
De Zeeuw, C. I. et al (2003) Deformation of Network Connectivity in the Inferior Olive of Connexin 36-Deficient Mice Is Compensated by Morphological and Electrophysiological Changes at the Single Neuron Level. The Journal of Neuroscience, June 1, 2003, 23(11):4700-4711
One of the tests the authors performed was to inject Lucifer yellow into olivary neurons. With functional gap junctions [of any kind!] in the wild-type mouse the dye spreads to adjacent neurons but “ in all Cx36-deficient mice, the injections resulted in labeling of single neurons only (n = 16), whereas those in the wild types always provided clusters of multiple neurons (n = 18, with an average of 8 ± 3.8).”
The authors go on to perform electrophysiology measurements that lead them to conclude that “no functional gap junctions exist in the homozygous mutants.”.
Thanks. That article is far more convincing that functional gap junctions are absent than the previously cited ones.

That the mice still demonstrate rhythmic oscillations in the brain is very interesting. The above study found evidence that the mice compensate for loss of gap junctions by making their neuronal membranes more electrically sensitive. This would make them more sensitive to EM fields (although that hasn’t yet been demonstrated) so it may be that EM fields are maintaining synchronicity in these mice.
johnjoe

It seems you've misunderstood what they mean by rhythmicity here. The rhythmic oscillations are detected in single-cell recordings. In the field of circadian rhythms, that individual cells can maintain rhythmicity is well-established, especially in recent years, and the mechanism for this at a molecular level is worked out in great detail (although not complete by any means).

However, what is lacking in these Connexin-36 knock-out mice is the synchronization. In other words, while each cell has a rhythm, those rhythms are not synchronized across cells. This is demonstrated by:
Long MA, Deans MR, Paul DL, Connors BW. 2002 Rhythmicity without synchrony in the electrically uncoupled inferior olive. J Neurosci. 22: 10898-905.

If anything, this seems to demonstrate pretty strongly that gap junctions are required for synchrony (not rhythmicity), and in the absence of gap junctions AND synchrony, behavior (and consciousness) is not grossly affected in these mice (I still haven't come across anything reporting any real battery of behavioral tests in these KO mice to find out if there are any deficits that may be more subtle). That consciousness is not affected by loss of synchrony suggests this synchrony you refer to is not required for consciousness. And, if synchrony can be disrupted by loss of gap junctions, it would also indicate that these CEMI fields are not sufficient for synchrony.

I'm afraid I need to cut this post short though...I forgot my power cord at the office today and my laptop battery is running low. :redface:
 
  • #62
Hi All,
I took the time to find the thing that ran in my head since I read this piece =>
I showed that induced transmembrane voltages are in the range of several microvolts up to about one millivolt. Neurons will thereby only be sensitive to em field effects when they are within a millivolt or less of the firing threshold. Since transmembrane voltages vary across approximately 130 mV...
Transmembranes voltages during action potential are effectively around 130mV for myelinated axons/soma and "trunks" of pyramidal cells (a very good integrator). That is only true for communication pathways but false for dendritic trees and synaptic trees. The potential is heavily linked to the shape diameter of cell. It is yet a riddle for many "electrical" thinkers about neurons... but it finds its explanation with ions channels, geometry and... Gauss' law.
It is not known how there is an amplification of signals all along these trees since it violates the "orthodox" cable theory.
It remains true that in dendrite and small axons (like C fibres) action potential have only an amplitude of 2 mV and is not measurable on their endings. It means that some axons, with 130 mv APs, travel close to branches where small/non measurable signals are added forming a tree and finally an exploitable AP. The two are existing at the same time and must definitely conclude that noise immunity is enabled at a level that discard the above hypothese. It is well known that in these trees, strong electric stimulations have local effects but it is needed multiple stimuli for an axon firing. That is a protection against stochastic firing and ephactic contamination.
Of course, an EM field may enhance the functionning at this level but it is difficult to understand how a system who share at the same time a collecting of small signal below 1mV (in dendrites and terminals) with an AP of 130 mV which has no effect on the previous, may be perturbed by long distance fields, since close did not.
 
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  • #63
Hi guys,

I found unfortunately another failure in the hypothesis.

1/ EM field enhances neuron firing.
2/ neuron firing creates an EM field.

These assertions are components of a divergent system. It functions exactly as a microphone put close to loudspeakers. Good chances to create a Larsen effect.
 
  • #64
Hey somasimple, I am not sufficently knowledgeable about transmembrane voltages,etc to do anything but continue my reading to investigate that point.
But as far as this goes:
Hi guys,
I found unfortunately another failure in the hypothesis.
1/ EM field enhances neuron firing.
2/ neuron firing creates an EM field.
These assertions are components of a divergent system. It functions exactly as a microphone put close to loudspeakers. Good chances to create a Larsen effect.
Neuronal firing leads to more firing - so why aren't we in a constant state of seizure? Because there is negative inhibition in the system (there wouldn't need to be much to quell things - the receptive neurons need to be on the knife edge of firing to be so). And it could be the same with this.
Also, just like some neurons are inhibitory, certain bits of the EM field can have an inhibiting effect (perhaps by lack of relative amplitude at that point), or excite inhibitory networks of neurons. And again, we've accepted that only a small contingent of neurons would be responsive to the field - who's to say there's unmitigated feedforward from that region to whatever regions are generating the most field? I'm sure my arguments are swiss cheese, but I'm certain that "there'd be feedback" is far from a theory killer.
If I'm missing something and you can elucidate, please do so. I hope I don't come off as antagonistic.
lates,
cotarded
 
  • #65
Cotarded,

I like/love arguing and I do not want to be a theory killer, really.

Maybe I was to quick with my two points and they need a refinement.

1/ Theory says that EM field enhances neuron firing. (hypothese).
2/ neuron firing carries EM field (fact)
3/ AP, EM field and threshold are related to diameter. (fact)
4/ axons have higher diameter than dendrites (fact)
5/ axon transmits information (fact)
6/ dendrites collect/spread information (fact)

If the hypothese is true thus all the following facts are modified accordingly.
It may be normal thus to suppose that it enhances all the components of neuron.
It is of course possible to suppose that soma/axon are enhanced and dendrites inhibited.
You will fall in a divergent system too since you'll get an auto-damped looked loop. The system trends to shut off while EM field is created.

Below is a fine abstract that is saying exactly what you're saying.
Inhibition is coupled with gaps junctions producing a stable system that shows few divergent behaviours.

Neural Comput. 2005 Mar;17(3):633-70.
The combined effects of inhibitory and electrical synapses in synchrony.

Pfeuty B, Mato G, Golomb D, Hansel D.

Neurophysique et Physiologie du Systeme Moteur, Universite Rene Descartes, 75270 Paris Cedex 06, France. bpfeuty@biomedicale.univ-paris5.fr

Recent experimental results have shown that GABAergic interneurons in the central nervous system are frequently connected via electrical synapses. Hence, depending on the area or the subpopulation, interneurons interact via inhibitory synapses or electrical synapses alone or via both types of interactions. The theoretical work presented here addresses the significance of these different modes of interactions for the interneuron networks dynamics. We consider the simplest system in which this issue can be investigated in models or in experiments: a pair of neurons, interacting via electrical synapses, inhibitory synapses, or both, and activated by the injection of a noisy external current. Assuming that the couplings and the noise are weak, we derive an analytical expression relating the cross-correlation (CC) of the activity of the two neurons to the phase response function of the neurons. When electrical and inhibitory interactions are not too strong, they combine their effect in a linear manner. In this regime, the effect of electrical and inhibitory interactions when combined can be deduced knowing the effects of each of the interactions separately. As a consequence, depending on intrinsic neuronal properties, electrical and inhibitory synapses may cooperate, both promoting synchrony, or may compete, with one promoting synchrony while the other impedes it. In contrast, for sufficiently strong couplings, the two types of synapses combine in a nonlinear fashion. Remarkably, we find that in this regime, combining electrical synapses with inhibition amplifies synchrony, whereas electrical synapses alone would desynchronize the activity of the neurons. We apply our theory to predict how the shape of the CC of two neurons changes as a function of ionic channel conductances, focusing on the effect of persistent sodium conductance, of the firing rate of the neurons and the nature and the strength of their interactions. These predictions may be tested using dynamic clamp techniques.

PMID: 15802009 [PubMed - indexed for MEDLINE]
 
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