Can cochlear functions (hearing, quantity and quality) be controlled from Pons by Medial Oloviocochlar complex?

(NB working draft)
(Below dysfunction can be partly hereditary? My mother and grandmother had a difficulty expressing themselves clearly, but probably because of their special and severe suffering, it may be what I call dysfunctional ”Olivoal Cochlea (Middle Pons) – Cochlea (Outer and Inner Hair Cells) Loop” – more work needed to investigate this)

Is it possible? Can cochlear functions (hearing, quantity and quality) be controlled from Pons by Medial Oloviocochlar complex?

Summarizing: If so then Medial Oloviocochlar (MOC) complex in Pons get feedback from cochlea activities (functional or different degree of dysfunctionality) and from that control actions of cochlea probably partly via outer hair cells and its influence on inner hair cells activities (functional or different degree of dysfunctionality. If then, e.g. head trauma influence MOC then sound distortion may relate to this. In my case I have 70 years of manageable noise damage associated tinnitus suddenly become a not manageable hard permanent alarm at the same frequency as the  ”old, more common tinnitus”

On other (adding?) explanation for my dysfunction may be ”sclerosing processes”, while during short sleeping periods (1-2 h) the symptoms increase perhaps due to tissue hardening ”Peripheral pons lesion location is a good discriminator of MS from vascular lesions.” https://pubmed.ncbi.nlm.nih.gov/32757905/

I have 2017 had sclerosing Basaliom  Glas typ III 2017 and 2018 Prostate cancer Gleason 9 (now well treated in Helsingfors) except since 5 year MRI documented spinal dysfunction (spondylosis and foraminal spinal stenos C3-C7, L4-L5 and S1)

Working text/draft below
Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells
https://journals.physiology.org/doi/full/10.1152/jn.00468.2021

 

 

 

 

 

 

NB  above conclusion: Medial olivocochlear efferent nerves have innervation with cochlear supporting gap junctions and eventually hair cell electromotility, thereby controlling hearing sensitivity and hearing portection against noise trauma outer trauma

“It is critical for hearing that the descending cochlear efferent system provides a negative feedback to hair cells to regulate hearing sensitivity and protect hearing from noise. The medial olivocochlear (MOC) efferent nerves project to outer hair cells (OHCs) to regulate OHC electromotility, which is an active cochlear amplifier and can increase hearing sensitivity. Here, we report that the MOC efferent nerves also could innervate supporting cells (SCs) in the vicinity of OHCs to regulate hearing sensitivity. MOC nerve fibers are cholinergic, and acetylcholine (ACh) is a primary neurotransmitter. Immunofluorescent staining showed that MOC nerve endings, presynaptic vesicular acetylcholine transporters (VAChTs), and postsynaptic ACh receptors were visible at SCs and in the SC area. Application of ACh in SCs could evoke a typical inward current and reduce gap junctions (GJs) between them, which consequently enhanced the direct effect of ACh on OHCs to shift but not eliminate OHC electromotility. This indirect, GJ-mediated inhibition had a long-lasting influence. In vivo experiments further demonstrated that deficiency of this GJ-mediated efferent pathway decreased the regulation of active cochlear amplification and compromised the protection against noise. In particular, distortion product otoacoustic emission (DPOAE) showed a delayed reduction after noise exposure. Our findings reveal a new pathway for the MOC efferent system via innervating SCs to control active cochlear amplification and hearing sensitivity. These data also suggest that this SC GJ-mediated efferent pathway may play a critical role in long-term efferent inhibition and is required for protection of hearing from noise trauma.

NEW & NOTEWORTHY The cochlear efferent system provides a negative feedback to control hair cell activity and hearing sensitivity and plays a critical role in noise protection. We reveal a new efferent control pathway in which medial olivocochlear efferent fibers have innervations with cochlear supporting cells to control their gap junctions, therefore regulating outer hair cell electromotility and hearing sensitivity. This supporting cell gap junction-mediated efferent control pathway is required for the protection of hearing from noise.“

https://en.wikipedia.org/wiki/Olivocochlear_system that has efferent control of and afferent feedback from the Cochlea, above all of external hair cells that ”control” the inner ones, where I have been damaged since 70 years – see audiogram (a hypothesis diagnosis  proposal for my ”5 year permanent difficult to stand ”alarm left side of my head”, except 2-3 minutes during the MRI scan (while right side heard the typical MRI sound (not very nice to hear) – very hopeful)”

The olivocochlear system is a component of the auditory system involved with the descending control of the cochlea. Its nerve fibres, the olivocochlear bundle (OCB), form part of the vestibulocochlear nerve (VIIIth cranial nerve, also known as the auditory-vestibular nerve), and project from the superior olivary complex in the brainstem (pons) to the cochlea. https://en.wikipedia.org/wiki/Olivocochlear_system

The MOCS’ response to sound is mediated through the MOC acoustic reflex pathway (see inset), which had been previously investigated using anterograde and retrograde labelling techniques (Aschoff et al., 1988; Robertson and Winter, 1988). Acoustic stimulation of the inner hair cells sends a neural signal to the posteroventral cochlear nucleus (PVCN), and the axons of the neurons from the PVCN cross the brainstem to innervate the contralateral MOC neurons. In most mammals, the MOC neurons predominantly project to the contralateral side (forming the ipsilateral reflex), with the remainder projecting to the ipsilateral side (forming the contralateral reflex).

The strength of the reflex is weakest for pure tones, and becomes stronger as the bandwidth of the sound is increased (Berlin et al., 1993), hence the maximum MOCS response is observed for broadband noise (Guinan et al., 2003). Researchers have measured the effects of stimulating the MOCS with sound. In cats, Liberman (1989) showed that contralateral sound (resulting in MOCS stimulation) reduced the N1 potential, a suppression which was eliminated upon transection of the olivocochlear bundle (OCB). In humans, the largest amount of evidence for the action of efferents has come from the suppression of otoacoustic emissions (OAEs) following acoustic stimulation.

 

 

 

Fig: The basic MOC acoustic reflex. The auditory nerve responds to sound, sending a signal to the cochlear nucleus. Afferent nerve fibres cross the midline from the cochlear nucleus to the cell bodies of the MOCS (located near the MSOC), whose efferent fibres project back to the cochlea (red). In most mammals, the majority of the reflex is ipsilateral (shown as a thicker line), effectuated by the crossed MOCS.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311680/
“Our ability to effectively perceive and interact with the environment integrates the activity of efferent pathways that can modulate the signals transmitted by the afferent sensory systems. In the auditory system, the efferent pathways form a neural network comprised of several feedback loops with numerous subcortical nuclei, including the thalamus, inferior colliculus, superior olivary complex, and cochlear nucleus (Malmierca and Ryugo, 2011). The auditory efferent pathways extend from auditory cortex to the peripheral sensory organ via the olivocochlear (OC) system (Figure 1). The OC system, originally described by Rasmussen (1946), is formed by two neuronal groups: (i) the medial olivocochlear neurons (MOC) and (ii) the lateral olivocochlear neurons (LOC) (Warr and Guinan, 1979).”

“ … Consequently, it has been difficult to associate deficits of olivocochlear neurons with pathogenesis, although there is some evidence of abnormal olivocochlear activity in listeners with tinnitus, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6496333/

https://pubmed.ncbi.nlm.nih.gov/2013642/
“Olivocochlear neurons have somata in the superior olivary complex and provide an efferent innervation to the cochlea. One subgroup of olivocochlear neurons, medial olivocochlear neurons, sends fibers to innervate the cochlear outer hair cells.

BvS-> After 60 years of ”normal” noise damage inner hair cells (manageable) change after an head trauma accident damage (head first into concrete pillars) into an impossible permanent ”alarm” (see more above) 

Svenska
(Nedan dysfunktion kan vara delvis ärftlig? Min mor och mormor hade en svårighet att formulera sig tydligt, men sannolikt av deras speciella och svåra lidande kan det vara det jag kallar för dysfunktionell ”Olivoalcochlea (Middle Pons) – Cochlea (yttre och inre hårcelller) loopen”, Mer arbete behövs för att undersöka detta.)

Är det möjligt? Kan cochleafunktionerna (hörsel, kvantitet och kvalitet) styras från Pons med hjälp av Medial Oloviocochlar complex?

Sammanfattning: Om så är fallet får Medial Oloviocochlar (MOC) komplexet i Pons feedback från cochleaaktiviteter (funktionella eller olika grader av dysfunktionalitet) och från det kontrollåtgärder av cochlean troligen delvis via yttre hårceller och dess påverkan på inre hårcellers aktiviteter (funktionell eller olika grad av dysfunktionalitet. Om då t.ex. huvudtrauma påverkar MOC så kan ljudförvrängning relatera till detta. I mitt fall har jag 70 år av hanterbara bullerskador i samband med tinnitus som plötsligt blivit ett ohanterligt hårt permanentlarm på samma frekvens som den ”gamla, vanligare tinnitus”

En annan (tilläggande?) förklaring till min dysfunktion kan vara ”skleroserande processer”, eftersom symtomen under mina korta sömnperioder (1-2 timmar) ökar, kanske på grund av ”vävnadshårdning”: ”Perifer ponslesions plats är en bra särskiljare av MS från vaskulära lesioner.” https://pubmed.ncbi.nlm.nih.gov/32757905/

Jag har 2017 haft skleroserande Basaliom Glas typ III 2017 och 2018 Prostatacancer Gleason 9 (nu väl behandlad i Helsingfors) förutom sedan 5 års MRT dokumenterad spinal dysfunktion (spondylos och foraminal spinal stenos C3-C7, L4-L5 och S1)