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Olfaction by Contact Induced EM Spectra
The inability of vibration theories of olfaction to correlate odor with the EM spectra of odorants only proves the brain encoded odors individually allowing totally different odors to be correlated with almost identical EM spectra
In 1954, Wright proposed that osmic (smell activated) vibrations of the odorant are excited by EM signals in the FIR between 50 and 500 /cm. EM stands for electromagnetic and FIR for far infrared. But Wright in 1957 showed the vibration theory cannot account for the powerful odors of H2S, NH3, and HCN that are absent FIR frequencies. In 1991, Buck and Axel proposed odor correlates with the shape theory where the odorant interacts in binding pockets of various shapes formed in the G protein – coupled receptors (GPCRs). But how the odorants enter the binding pocket to activate the GPCRs was not disclosed. Nevertheless, Buck and Axel’s shape theory was widely accepted, and remains the mainstream theory today. However, Turin in 1996 questioned the correlation of odor with shape. Turin claimed Buck and Axel actually measured molecular vibrations in the binding pocket using phonon assisted inelastic electron tunneling. Turin’s theory also relies on binding pockets, but is more complicated than Buck and Axel’s in that the odorant must also have vibration levels that match those of the GPCR. Turin’s theory also does not identify how electron tunneling is activated.
Today, the status of olfaction is based on the premise that the brain during evolution encoded odor by an overall theory based on the signals received from odorant vibration or shape, the failures of which only prove the correlations encoded by the brain were made separately on an individual basis independent of any odor theory. We like to think an overall theory exists between an odor and the odorant’s vibration or shape, but the brain obviously thought otherwise allowing totally different odors to be correlated in with almost identical vibration or shape signals. Without an overall odor theory, only the uniqueness of the odorant’s signal is important for the brain to encode odor with the odorant’s signal.
Contact Induced EM Spectra is proposed as the mechanism that activates the GPCRs to send the unique EM signal of the odorant to the brain for odor interpretation. What this means is the GPCR itself does not interpret odor based on the odorant’s EM spectra, but rather converts the odorant’s EM spectra to an electrical signal that is interpreted by the brains as an odor. See “Olfaction by Contact Induced EM Spectra" at http://www.nanoqed.org , 2011.
Correlation of Odor Unlike Wright’s correlation of odor with FIR vibration, the brain did not correlate odor by any theory applicable to all odors and odorants. Instead, during evolution the brain is assumed to have been conditioned to simply correlating individual odors with the unique EM signal from the GPCR.
Alternatively, the brain by Contact Induced EM Spectra simply encoded each and every odor based on the odorant’s EM spectra. Conditioned encoding of an odor with individual odorants may only proceed provided the odorant signal is unique, and therefore the brain relied solely on the FIR/NIR content of the odorant’s EM spectrum for odor correlation. But seemingly contrary correlations were found, i.e. pungent and fragrant odors correlated with unique, but almost identical FIR/NIR spectra. In retrospect, the GPCR was the spectroscope during evolution that allowed the brain to correlate the perceived odor with the EM signal of the odorant on a separate basis without an overall odor theory. Wright’s attempt to correlate odor with the theory that odor is correlated by the odorant’s FIR spectra failed because the brain simply did not encode odor that way, but rather by its own odor correlation based on the FIR spectra of the odorant.
GPCR Activation GPCR activation by Contact Induced EM Spectra occurs upon simple contact of the odorant with the GPCR. The difficulty of evolution creating GPCRs with precisely shaped binding pockets in Buck and Axel’s shape and Turin’s theories is therefore avoided, and even if pockets are formed, the odorant must find the GPCR with the correct pocket. Otherwise, GPCR activation of the cilia channel follows mainstream theory, i.e., the GPCR activation excites the G-olf protein to produce adenylyl cyclase that increases intracellular cAMP.
1. The Contact Induced EM Spectra mechanism is proposed to activate the GPCR, but odor does not correlate by any overall theory based on the FIR/NIR spectra. Instead, the brain is assumed to have been conditioned during evolution to encode each odor separately in its own way based on the unique FIR/NIR signal of the odorant. Because of this, totally different odors are correlated with odorants having virtually identical EM spectra.
2. Once the GPCR is activated, mainstream theory is followed, i.e., the G-olf protein initiates a cascade of Ca2+ ions within the cilia channel and the neuron fires once Cl- ions flow.
3. Experimental data on the frequency response of the GPCR under FIR/NIR radiation necessary to initiate the G-olf protein cascade is required to confirm the Contact Induced EM Spectra mechanism of olfaction.
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About QED Indcued 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.