QUANTUM ENGINEERING #53: WHY IS MELANIN ALWAYS FOUND BETWEEN YOUR SENSES & THE ENVIRONMENT?

The auditory nerve transmits auditory information up a series of nuclei to the cortex, where perception occurs. These nuclei include 1) cochlear nucleus, 2) superior olivary nuclei, 3) lateral lemniscus, 4) inferior colliculus, and 5) medial geniculate nuclei.

Melanin pigment is normally present in the outermost layer of the eye's retina, the inner ear adjacent to capillaries in stria vascularis near hair cells and vestibular organs. In the skin, it is in the basal layers.  In the gut, it is found in the enterochromaffin cells.  Significant reduction in melanin pigment in mammals is associated with embryonic miswiring and disruption of visual and auditory functions. This has implications for human diseases like autism, which usually affects all sensory inputs to the thalamus.  In this way, it mimics what I wrote about Autism in this series in QE#45.    The consequences for the visual system include abnormal retina development and misrouting of optic pathways into the brain, impairing visual acuity, eye movement, and stereo vision. Lack of melanin pigment in the inner ear is associated with greater susceptibility to noise damage and poorer sound localization in space.

The auditory sense in mammals is unique in another way and may be critical to why melanin exists where it does.  Unlike other cells within the brain, hair cells within the Organ of Corti of the cochlea do not have axons. Neurons within the spinal ganglion have peripheral axons that synapse at the base of the hair cell soma. These axons make up the auditory nerve. Most (90%) of auditory nerve fibers receive their input from the inner hair cells. Thus, the inner hair cells facilitate a majority of auditory processing.  My bet is that this arrangement is how sound waves are converted to light waves that the auditory nerve can process.

The melanin sheets in the ear are proximal to the auditory nerves.  When melanin is hypoxic, it can break down into noradrenaline and dopamine, as line one below shows when you read the slide from right to left (catabolic pathway of melanin destruction).  The mammalian auditory brainstem, particularly the medial nucleus of the trapezoid body (MNTB) (Wynne and Robertson 1996), receives extensive adrenergic input.  This tells me that the sheet in the cochlea creates neurotransmitters by causing melanin degradation in the auditory pathways, as the slide below shows.

The mammalian auditory brain stem receives profuse adrenergic innervation, whose function is currently poorly understood by centralized science.  Noradrenaline increases high-frequency firing at the Calyx of Held synapse during development by inhibiting glutamate release.

The calyx of Held synapse plays an important role in the auditory system, relaying information about sound localization via fast and precise synaptic transmission, which is achieved by its specialized structure and giant size. During development, the calyx of Held undergoes anatomical, morphological, and physiological changes necessary for performing its functions. The large dimensions of the calyx of Held nerve terminal are well suited for direct electrophysiological recording of many presynaptic events that are difficult, if not impossible, to record at small conventional synapses. This unique accessibility has been used to investigate presynaptic ion channels, transmitter release, and short-term plasticity, providing invaluable information about basic presynaptic transmission mechanisms at a central synapse.

DECENTRALIZATION ANSWER: Why do all senses have melanin sheets between them and the environment?

Why does the spiral cochlea have this huge melanin sheet?  Melanin shows up in mammalian tissue because of the melanin concentration hormone.  Melanin-concentrating hormone (MCH) was originally isolated from salmon pituitaries (think of Huberman fish gaff on melanopsin now). It induces the aggregation of melanin granules in melanophores, resulting in pale skin color. MCH sequence is conserved in ALL MAMMALS analyzed to date, including mice, rats, rabbits, and humans. In mammals, the neurons that synthesize and release MCH are present mainly in the hypothalamus and nearby areas.  Is the cochlea near the hypothalamus?  No.  But the melanin stimulatory hormone is very prominent in the brainstem, and the cochlear is very close to that.  Lack of melanin pigment in the inner ear is associated with greater susceptibility to noise damage and poorer sound localization in space.

I think a relative lack of melanin in different areas of the cochlea is the cause of misophonia.  Misophonia is a disorder in which certain sounds trigger emotional or physiological responses that some might perceive as unreasonable given the circumstances. Those with misophonia might describe it as when a sound “drives you crazy.” Their reactions can range from anger and annoyance to panic and the need to flee.  If your centralized health professional doesn’t know about misophonia, they may take all that information and try to fit it with something they do know about. Here are some diagnoses you might hear before a health professional finally acknowledges your misophonia:

Melanocytes are distributed in the stria vascularis and spiral ligament regions, and recent evidence illustrates the distribution of melanin in the human cochlea with the lower relative amount of melanin observed in the basilar turns compared to apical turns.  Sensorineural hearing loss caused by presbycusis (old age heteroplasmy), maternal-fetal rubella infection, aminoglycosides, and noise exposure disproportionally impacts the basal turn with variable losses of spiral ganglion and hair cells reflected in a down-sloping audiogram.  Melanin is sparse in those regions.  The location of melanin and its known function as a free radical scavenger may explain some patterns of sensorineural hearing loss and highlight that melanin has special abilities in the sensory pathways of mammals.

Might it have to do with the binary code of biology and the fidelity of sound that I raised in the Kruse for Dummies lecture?  I believe it does.  Look at how many areas sound inputs are sent.  If we are built to semiconductor sound waves, this implies we need a big equalizer in our ear, right?

Since this synapse is massive in all mammals, it has been studied.  What do we know?  Researchers have studied multiple mammal species, and to the extent that a comparison is possible, the time course for development embryologically matches earlier experiments performed in rats, cats, mice, or gerbils, suggesting that the development of this synapse is highly conserved across all mammalian species. There is another surprise.  The essential steps to build hearing occur largely before the onset of hearing, supporting the view that sensory activity does not play a major role in forming this synapse.  So, the sound stimulus is unnecessary to morphology.  This is a clue that morphology likely links back to the binary code in morphogenesis.

Do you know what the Calyx of the Head is in humans?  It is the big equalizer mentioned above.

Function. The calyx of Held is a part of the auditory system, connecting the globular bushy cells (GBCs) of the anteroventral cochlear nucleus to the principal neurons of the medial nucleus of the trapezoid body (MNTB).

Most of the MCH-positive fibers in mammals have been detected throughout the brainstem, and the cochlea is very close to it in mammals. Interestingly, there was a profuse MCH innervation of brainstem areas involved in controlling REM sleep.

The calyx is a giant glutamatergic terminal formed by the main axon of globular bushy cells (Fig. 2, GBC). These cells have their cell body in the cochlear nucleus contralateral to the MNTB and receive large axosomatic terminals from the auditory nerve (endbulbs of Held).

The calyx of Held is probably the largest synaptic terminal in the brain, forming a unique one-to-one connection in the auditory ventral brainstem. During early development, calyces have many collaterals whose function is unknown.

During embryonic and postnatal development, the calyx of Held undergoes a significant transformation in order to possess morphological and functional properties necessary for performing its major role in relaying acoustic information from the environment to our brain.

SUMMARY

With Nature, not everything is as it appears. Only some people take the time to comprehend this and why it is the case.  My future tribe members must acquire this trait.  With blue light, RF, and microwaved brains inculcated with prescription drugs designed to ruin your endogenous photoreceptor system, it is no wonder people cannot think reasonably.  The centralized paradigm has built a world like this to control and dominate crony capitalism to rule the world.  The more this crowd sees with their radiated brains, the less they know for sure.  It is being done by design. Nature is full of magical things, waiting patiently for our senses to grow sharper. Those senses grow sharper when melanin between the environment and the sense organ is expanded by UV light exposure. This is why the architects of destruction want to bury the sun from you.  The manner in which you perceive the world is a reflection of how you use light in your inner world.  This is the wisdom buried deep in the melanin renovation Rx and one few of you see today.

The implication of this blog is that hearing, tinnitus, and acoustic changes can all be changed by solar exposure on the skin.  If this is true, is there evidence that heavily melanated human skin leads to less acoustic disease?

There is. There is a ton of data I provided you below.

Many studies have shown that blacks have a 40%–70% lower prevalence of hearing loss than whites.

In a previous cross-sectional study, Lin et al. (below in cites) demonstrated an association between certain Fitzpatrick skin phototypes and lower odds of hearing loss among Hispanics, which they suggested might be due to differences in melanocytes between darker-skinned and lighter-skinned individuals. Melanocytes are known to be present in the inner ear, and results from evolutionary studies have suggested that darker-colored individuals tend to have more internal (nonskin) melanin. Furthermore, human studies have demonstrated a positive association between the number of melanocytes in the skin and inner ear.

Melanocytes have antioxidant functions that might protect against reactive oxygen species associated with the death of inner ear hair cells in noise-induced hearing loss. Furthermore, cochlear melanocytes serve as intermediate cells in the stria vascularis and are important in generating the endocochlear potential.  All this tells me that getting a tan is a great way of maintaining your acoustic system and lowering your risk for both acoustic diseases like tinnitus and misophonia, ocular diseases like retinopathy, and thalamic diseases like autism.  Get your skin in the game.  Decentralize your biology to get back what you've lost.

CITES

https://optimalklubs.com/kruse-for-dummies-general/

J Kil, GH Kageyama, MN Semple, LM Kitzes, Development of ventral cochlear nucleus projections to the superior olivary complex in gerbil. J Comp Neurol 353, 317–340 (1995).

K Kandler, E Friauf, Pre- and postnatal development of efferent connections of the cochlear nucleus in the rat. J Comp Neurol 328, 161–184 (1993).

BK Hoffpauir, JL Grimes, PH Mathers, GA Spirou, Synaptogenesis of the calyx of Held: Rapid onset of function and one-to-one morphological innervation. J Neurosci 26, 5511–5523 (2006).

VC Wimmer, H Horstmann, A Groh, T Kuner, Donut-like topology of synaptic vesicles with a central cluster of mitochondria wrapped into membrane protrusions: A novel structure-function module of the adult calyx of Held. J Neurosci 26, 109–116 (2006).

DK Morest, The growth of synaptic endings in the mammalian brain: A study of the calyces of the trapezoid body. Zeitschrift Anat Entwicklungs 127, 201–220 (1968).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521893/

Lin FR, Maas P, Chien W, et al.. Association of skin color, race/ethnicity, and hearing loss among adults in the USA. J Assoc Res Otolaryngol. 2012;13(1):109–117.

Lin CS, Zak FG. Studies on melanocytes. VI. Melanocytes in the middle ear. Arch Otolaryngol. 1982;108(8):489–490.

Dubey S, Roulin A. Evolutionary and biomedical consequences of internal melanins. Pigment Cell Melanoma Res. 2014;27(3):327–338.

Wolff D. Melanin in the inner ear. Arch Otolaryngol Head Neck Surg. 1931;14(2):195–211.

LaFerriere KA, Arenberg IK, Hawkins JE Jr, et al.. Melanocytes of the vestibular labyrinth and their relationship to the microvasculature. Ann Otol Rhinol Laryngol. 1974;83(5):685–694.

Nofsinger JB, Liu Y, Simon JD. Aggregation of eumelanin mitigates photogeneration of reactive oxygen species. Free Radic Biol Med. 2002;32(8):720–730.

Meyskens FL Jr, Farmer P, Fruehauf JP. Redox regulation in human melanocytes and melanoma. Pigment Cell Res. 2001;14(3):148–154.

Henderson D, Bielefeld EC, Harris KC, et al.. The role of oxidative stress in noise-induced hearing loss. Ear Hear2006;27(1):1–19.

Takeuchi S, Ando M. Inwardly rectifying K+ currents in intermediate cells in the cochlea of gerbils: a possible contribution to the endocochlear potential. Neurosci Lett. 1998;247(2-3):175–178.