Neuron Synapse by QED Induced Radiation

Chemical signaling by binding of presynaptic neurotransmitter molecules to postsynaptic receptors is superseded by EM signaling using the spectra of the molecules excited by QED induced radiation
Neuron Synapse by QED Induced Radiation
Neuron Synapse by QED Induced Radiation
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Action Potential
Chemical Signaling
Quantum Mechanics


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May 18, 2011 - PRLog -- Background

Classical biology assumes exocytosis ejects neurotransmitter (NT) molecules into the cleft between presynaptic and postsynaptic cells. The NTs are submicron vesicles containing small molecules or neuropeptides. Vesicles of small molecules have diameters from 40 to 60 nm while those of neuropeptides are 90 to 250 nm. In neuron signaling, the NTs may therefore be considered biological nanoparticles (NPs).

But the neuronal cleft is only 20 to 50 nm wide, and therefore the larger NPs cannot enter without dissolving into constituent NT molecules before leaving the presynaptic cell. Of importance, the neuron signal can only be completed if the NT molecules chemically bind to the correct receptor on the postsynaptic cell. In this regard, a description of classical biology of neuron synapse is given in

Problems with Chemical Signaling

Chemical signaling by binding of NT molecules to postsynaptic receptors is consistent with the shape theory of olfaction where the odorant molecule in the manner of a “lock and key” fits into precisely matched receptors. But the probability of this occurring even in olfaction is unlikely. In humans, the odorant molecule must bind with a receptor over a few square centimeters of surface area in the nose. Even far less likely is chemical signaling in mating moths where scent molecule from a female must bind to the receptor of a male at distances of hundreds of meters. For a discussion of QED radiation as a solution to  human and moth olfaction see this Homepage and

In neuron signaling, the submicron cleft improves the probability of chemical binding  over that by odorants in the nose and scents in mating moths, but it can be safely concluded that it is still unlikely NT molecules bind to postsynaptic receptors. Given that neurons do signal quite efficiently suggests a mechanism other than the “lock and key” is at play.

Proposed QED Signaling Mechanism

Signaling by chemical binding of NT molecules with receptors is proposed superseded by signaling from a burst of QED induced emission corresponding to the unique EM spectra of the NT molecules. QED stands for quantum electrodynamcis and EM for electromagnetic. Chemical binding is not required. By this theory, the EM spectra induced by QED are emitted at the instant of exocytosis as the NPs begin to dissolve in the surface of the presynaptic cell. The thumbnail depicts NPs on the presynaptic surface beginning to dissolve into NT molecules in the rapid expansion that accompanies exocytosis.  QED radiation is depicted coming from both the NPs and NT molecules. Only a fraction of the NT molecules in the NPs are shown entering the cleft.  

What this means is the notion may be entertained that both exocytosis and endocytosis may occur in a prompt Exo/Endo cycle. During endocytosis, the NPs are in contact with the presynaptic cell, but in exocytosis are momentarily isolated from the presynaptic cell. Moreover, the NT molecules essentially remain in the presynaptic cell. Even if some NT molecules enter the cleft, they are promptly returned to the presynaptic cell by endocytosis. The QED radiation emitted as a burst terminates itself, thereby avoiding long standing problems with terminating chemical signaling, i.e., how to unbind NT molecules from postsynaptic receptors, the need for enzymes to chemically render the NT molecules remaining in the cleft nonfunctional, and the removal of NT molecules from the cleft before the next action potential.

QED Radiation

During endocytosis, the NPs including the NT molecules acquire the thermal kT energy of the postsynaptic cell. Here k is Boltzmann’s constant and T is absolute temperature. But during the expansion accompanying exocytosis, the NPs become momentarily isolated, and therefore have thermal kT energy not allowed by quantum mechanics (QM). Since QM also requires the heat capacity of the NPs to vanish, the kT energy cannot be conserved by an increase in temperature. Instead, conservation proceeds by the creation of QED photons inside the NPs. The QED photons  have Planck energies beyond the UV that  excite the NT molecules to emit a burst of QED radiation  given by their EM spectra, thereby providing a unique signal for recognition by the postsynaptic receptors.

In this way, the burst of QED induced radiation triggered by action potentials may be repeated successively with essentially the same NPs. Since NPs are transported along the axon at speeds < 400 mm / day, depletion may occur in chemical signaling, but is not a problem in signaling by QED induced radiation. Details are given for a diverse range of applications of QED radiation at , 2009-2011, and specifically, the Paper at "Neuron Signaling by QED," 2011.

Summary and Conclusions

1. Chemical signaling by the “lock and key” binding of NT molecules from the presynaptic cell to the postsynaptic cell is proposed superseded by a signal corresponding to the QED induced EM emission spectra of the NT molecules in a Exo/Endo cycle while keeping the NT molecules essentially within the presynaptic cell.

2. Advantages of the proposed EM spectra emission in the Exo/Endo cycle over chemical binding by the “lock and key” mechanism are:

(a) Avoiding the unlikely probability of a NT molecule finding and binding to the correct receptor by the “lock and key” mechanism,

(b) Dissociation of NT molecules bound to receptors in chemical signaling is not necessary,

(c) The need for enzymes in the cleft to chemically render the NT molecules nonfunctional,

(d) Eliminating the removal of NT molecules from the cleft prior to the next neuron signal,


(e) Allowing repetitive action potentials with limited axonal transport of NPs.

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About QED Induced EM Radiation: Classically, absorbed EM energy is conserved by an increase in temperature. But at the nanoscale, temperature increases are forbidden by quantum mechanics. QED radiation explains how absorbed EM energy is conserved at the nanoscale by the emission of nonthermal EM radiation.
Source:Thomas Prevenslik
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Tags:Neuron, Action Potential, Synapse, Neurotransmitter, Chemical Signaling, Exocytosis, Endocytosis, Quantum Mechanics
Industry:Science, Medical, Research
Location:Youngwood - Pennsylvania - United States
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Page Updated Last on: May 18, 2011

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