Anesthetes again

The writing of the summary about SSE-2016 conference forced to think again the model for anesthetes in light of the vision about cell membrane as sel-loading battery relying on TGD based model for Pollack's exclusion zones (EZ) in terms of h_eff/h=n phases.

First however a philosophical remark.

1. According to the behavioristic definition of consciousness, the ability to respond to sensory input and perform motor actions are essential aspects of consciousness. To my opinion these abilities correspond to only particular type of consciousness and consciousness might be possible even without neural activities (OBEs and NDEs). In any case, the inability to generate nerve pulse patterns would be an essential aspect for what we call loss of consciousness. This happens if there is hyperpolarization of neuronal membrane.
   
   
2. Hyperpolarization means reduced rate of spontaneous nerve pulse generation. This would be achieved if microtubules gain additional negatively charge so that the radial component of microtubule electric field increases. Hence the interaction of anesthetes with the microtubuli should generate this negative charge. One possibility is that Pollack effect generates in the presence of anesthete negatively charged exclusion zone (EZs). The TGD based model assumes that the protons are transferred to the magnetic flux tubes as dark protons and perhaps end up to the exterior of cell membrane and transform to ordinary protons. This would induce hyperpolarization. The neutral anesthete atoms or molecules in turn could be transferred to the microtubules along flux tubes.
   
   

Consider next a model for the cell membrane.

1. In TGD Universe cell membranes could be generalized Josephson junctions. The energy of generalized Josephson photons (dark with energies in bio-photon range) would be the difference of cyclotron energies for flux tubes at the two sides of the membrane plus the ordinary Josephson energy. Generalized Josephson photons would take care of communications of sensory data to MB.
   

   Unless the cyclotron energies at the two sides of the membrane are same, the new contribution would dominate in the communications to MB for large values of h_eff since cyclotron energy is proportional to h_eff, and neuronal contribution would represent frequency modulation allowing to code nerve pulse patterns to kind of "whale's song". For smaller value of h_eff ordinary Josephson energy would dominate.
   

   There is a temptation to assume that the value of h_eff serves as a kind of intelligence quotient of cell. Frequency scale and energy scale for the analog of EEG would serve for the same purpose. For instance, pyramidal neurons responsible for EEG would represent the intellectual elite of brain and ordinary cells could have much smaller value of h_eff being say by factor 2^-10 smaller than for pyramidal cells so that generalized Josephson energy would be of the same order of magnitude as ordinary Josephsone energy and in IR range.
   
   

2. Generalized Josephson photons with biophoton energies would also generate Pollack's EZs by ionizing one proton from hydrogen bonded pair of water molecules. The reduction of the membrane potential below the threshold for nerve pulse generation could reduce the energy of Josephson photons below threshold for generating Pollack's EZs and neuronal membrane would cease to be self-loading battery: this would replace ionic Josephson currents with ohmic currents through cell membrane and generate nerve pulse.
   

   The objection is that for low values of h_eff generalized Josephson energy reduces to ordinary one in IR range and for high values to cyclotron energy in visible-UV range. It is known that IR photons generate EZs in the experiments of Pollack. The process could occur in two steps involving cyclotron radiation - perhaps from MB - kicking of hydrogen bonded water molecules to a state, where proton is almost ionized so that the IR radiation would take care of the ionization. The mechanism generating EZs cannot be different for ordinary cells and neurons. Either the notion of generalized Josephson junction must be given up or in the case of neurons glial cells accompanying also axons generate the IR radiation giving rise to EZs inside axons.
   
   

3. It is also attractive to see at least ordinary cell membrane as a self-loading battery. The generation of Pollack's EZs with negative charge and dark proton charge at magnetic flux tubes of the associated MB could make cell a self-loading battery ".
   

   Generalized Josephson photons from cell membrane or cyclotron photons could generate EZs by kicking protons to dark protons at flux tubes of MB of the cell. The energy must be in some critical range in order that this can happen. For too small energies the process stops. Besides ionic charge distributions EZs and the delocalized dark proton charges and the flux tubes extending beyond cell interior would be responsible for the resting potential.
   

   EZs are not expected to be completely stable. The h_eff→ h phase transition would bring dark protons back as ordinary protons and destroy EZs and reduce the magnitude of membrane potential. There could be a competition between the generation and destruction of EZs by h_eff→ h phase transition.
   
   

4. This picture is enough to explain the effect of anesthetes. Anesthetes at microtubules would generate a negative charge assignable to additional EZs thus increasing the magnitude of the membrane potential. This would imply stable hyperpolarization preventing the generation of nerve pulses.
   
   

What about generation of nerve pulses in this framework? I have suggested a TGD based model for nerve pulse relying on the idea about cell membrane as array of Josephson junctions consisting of membrane proteins (channel and pump proteins) but the model leaves open what exactly generates the nerve pulse. The expectation has however been that microtubules play a key role in the generation of nerve pulse. A charge wave with positive charge propagating along microtubule could induce the reduction of the membrane potential and lead to a generation of nerve pulse as a secondary wave.

1. The propagation of h_eff→ h phase transition followed by its reversal along axon interior could serve as a weak control signal inducing the nerve pulse propagation at quantum criticality. This phase transition could be assignable to microtubules. Battery would temporarily discharge during the nerve pulse. If glial cells generate the EZs making axons glial-cell loaded batteries then the return back to the normal state after nerve pulse would be possible by the presence glial cells.
   
   
2. During nerve pulse either the generation of EZs ceases and/or the existing EZs suffer an h_eff reducing phase transition so that flux tubes are shortened and the positive dark charge returns to EZs and cell membrane potential is reduced. The generation of nerve pulse is usually modelled using ohmic ionic currents, which suggests that quantum coherence is lost by a reduction of h_eff, which is predicted to be proportional to ion mass so that cyclotron energy spectrum is universal and in visible-UV range for bio-photons.
   
   
3. Nerve pulse could be a "secondary wave induced by a wave of positive charge propagating along microtubule. This wave of positive charge would rather naturally result from the reduction h_eff→ h and return back to h_eff. A pair of phase transitions dark-ordinary-dark would propagate along the microtubule. The unidirectionality of the propagation direction would be forced by the fact that it can begin only from axonal hillock. Axonal hillock contains a large number of voltage gated ion channels, which would serve as generalized Josephson junctions in TGD framework.
   
   
4. What one can one conclude about the development of total charge during the time development of membrane potential V(t)? Nerve pulse corresponds to certain segment of axon and lasts for few milliseconds. The cell membrane voltage goes from resting potential V(t=0)= V_rest to approximately V(t=T)= -V_rest and returns back. The total charge in cell interior defines the value of electric field E at the interior side of cell membrane and approximation interior as conductor, the value of Ein good approximation one has V= Ed= Q_celld/4π R² in spherical geometry and V= Ed= dQ_tot/dl d/2π R in cylindrical geometry of axon. Here Q_tot is the charge of the piece of axons at which nerve pulse is located. Total charge is sum of microtubular charge Q_mt serving as a control parameter and the total ionic charge Q_I changing due to the presence of ohmic ionic currents during the pulse (ionic currents are Josephson currents except during nerve pulse).
   

   To get some quantitative grasp, let us idealize the situation by assuming that during nerve pulse the negative microtubular charge Q_mt(0)<0 goes to Q_mt(T)=0 for V(T)= -V_rest (EZs disappear totally) and returns back to its original value as the phase transition returning the value of h_eff occurs.
   

   One has Q_tot(0)=Q_mt(0)+Q_I(0) before the nerve pulse. At V= -V_rest one has Q_tot (T)=-Q_tot(0), which gives -Q_tot(0) = Q_I(T). This gives Q_mt(0)= Q_I(T)-Q_I(0).
   

   What can one say about the magnitude of Q_mt? If this charge serves control purpose and if the system is kicked off from quantum criticality, the change of Q_mt need not be large so that no large modifications of the ordinary model of nerve pulses are needed. The negative microtubular charge is partially due to the GTPs along microtubular to which EZs are associated. The value of resting potential of order .06 eV at threshold for nerve pulse generation and estimates for linear ionic charge densities dQ_I(0)/dl and dQ_I(T)/dl and Q_mt(0)/dt would allow to test the model.
   The h_eff→ h phase transition outside quantum criticality would take place in millisecond time scale.
   

The distinctions between neurons and ordinary cells allow to invent objections against the proposed scenario.

1. Ordinary cell membrane should act as a self-loading battery with Josephson radiation generating Pollack's EZs. Axonal microtubules are missing but the cytoskeleton consisting also of microtubules is present. Inside the cell soma the microtubules meet the cell membrane transversally. There is also T-shaped antenna like structure involving microtubules whereas ordinary neurons have axonal microtubules. Also now a microtubular positive charge generated by h_eff→ h phase transition could induce the reduction of membrane potential.
   
   
2. Why the analog of nerve pulse does not take place also now? In the case of cancer cells membrane potential is reduced and can become even vanishing, and one might think that the lack of recovery is due to the absence of glial cells taking care that EZs are generated. For too low Josephson energies the self-loading would stop and due to the spontaneously occurring h_eff→ h phase transitions, the membrane potential would be gradually reduced.
   

   In the case of neurons the h_eff→ h phase transition would occur fast. The transition away from quantum criticality could cause this since long range quantum fluctuations would disappear. The value of membrane potential or the difference between neuronal and glial membrane potentials could serve as a critical parameter changing as the membrane potential is reduced. The quantum criticality of ordinary cell membrane would be analogous to self-organized quantum criticality. That of neuronal axon to quantum criticality induced by glial cells.
   
   

See the chapter Quantum model for nervepulse. See also the article Comments about the representations in SSE-2016 conference about consciousness, biology, and paranormal phenomena .

For a summary of earlier postings see Latest progress in TGD.

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