Nerve Cells Warn Brain of Damage to the Inner Ear

http://neurosciencenews.com/inner-ear-neuron-damage-3033/

"Some nerve cells in the inner ear can signal tissue damage in a way similar to pain-sensing nerve cells in the body, according to new research from Johns Hopkins. If the finding, discovered in rats, is confirmed in humans, it may lead to new insights into hyperacusis, an increased sensitivity to loud noises that can lead to severe and long-lasting ear pain."

 

yeah megaman

 

I posted about this in the retigabine thread some days ago because in this research they used retigabine:

Abstract
In the mammalian cochlea, acoustic information is carried to the brain by the predominant (95%) large-diameter, myelinated type I afferents, each of which is postsynaptic to a single inner hair cell. The remaining thin, unmyelinated type II afferents extend hundreds of microns along the cochlear duct to contact many outer hair cells. Despite this extensive arbor, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive to sound. Intriguingly, type II afferents remain intact in damaged regions of the cochlea. Here, we show that type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage. Selective activation of P2Y receptors increased type II afferent excitability by the closure of KCNQ-type potassium channels, a potential mechanism for the painful hypersensitivity (that we term “noxacusis” to distinguish from hyperacusis without pain) that can accompany hearing loss. Exposure to the KCNQ channel activator retigabine suppressed the type II fiber’s response to hair cell damage. Type II afferents may be the cochlea’s nociceptors, prompting avoidance of further damage to the irreparable inner ear.


Link:
http://www.pnas.org/content/early/2015/11/05/1515228112

 

It really does seem retigabine should be taken early in he T onset. Many recent papers seem to suggest so.

 

So why the shit did my Hyperacusis increase by about 50% during my Trobalt trial???!!!

Sigh! Zimichael

 

Preslys got his T in May 2014 and started to take Trobalt I think around July or August this year....and ended up with a complete cure. How long is early on to T onset?

 

I wondered the same thing.

 

Yes Presley got rid of t. with trobalt 1.5 year after onset. Many others did not have that result of trobalt using, even 6 months or less after onset.
So conclusion is that type (mechanism) of individual's t is most important for trobalt results, more than moment of using it.

Did u also get H after using trobalt as Zimichael did? :S

 

No, I've never tried Trobalt. I was referring to Zimichael's experience.

 

I don't think anyone knows this. For steroids it is a matter of hours. For AM-101, 3 months. Different target organs, different responses.

But it is not too crazy to believe it is better to act as earliest as possible, as per any other treatable medical condition.

For trobalt I guess it would be too late if the potassium channels are destroyed/no longer there. Malfunctioning nerve cells may or may not take a long time to die off, until then Trobalt might be of value.