Medical EM fields: a plausible correlate of consciousness?

[Moonbear]

[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.

 

[somasimple]

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.

 

[somasimple]

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.

 

[cotarded]

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

 

[somasimple]

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]