I'm not much of an expert either. I know a very basic level of neuroscience and how to read and interpret research articles, so my knowledge pool is limited.I admit my ignorance on brain chemistry, but this is not the first time I'm reading that the NMDA receptors and glutamate might be at the center of this sh*t show called tinnitus.
Maybe a stupid question, but could the NMDA receptors or the glutamate be somehow inhibited, disabled, redirected or killed alltogether?
Glutamate is the most common excitatory neurotransmitter in the brain. It is found everywhere and is a vital part of conducting neural activity. NMDA receptors are known to cause what is known as excitotoxiity, which is when too much glutamate is released and can cause cell damage and death. NMDA receptors are known to do this, and glutamate is implicated in the hyperactive burst firing in the brainstem (the dorsal cochlear nucleus).
The trick, from what I have read, with NMDA antagonization is this: They play a crucial role in not just facilitation of neural firing, but in learning and memory. NMDA antagonists such as ketamine work effectively at suppressing those receptors from firing. However, because we have no current selective antagonist drug, by suppressing them we also suppress their role in learning and memory.
There is also the problem of very few NMDA antagonisst being available. Magnesium is said to antagonize them, as is dextromethmorphan (DXM) a common ingredient in some cough syrups. More powerful ones like ketamine are controlled substances that can be dangerous for unsupervised use. Yet an analysis of tinnitus treatments paper by Susan Shore seemed to indicate that it may be the future of treatment. Even Rauschecker's "gate keeper" paper proposed that they could stop or even reverse tinnitus.
Still, the limitations mentioned above are an issue.