Okay, watching the videos some, I observed that the resting point for a post synaptic cell is -70mv. Once the voltage increases to a certain point, it fires off an action potential. Is it possible that if there is a lot of excessive firing of a neuron, the post synaptic cell is getting too much positive ions and firing off too many action potentials? For example, Sodium is positive (Na+), Calcium ions are positive (Ca+), Potassium ions are positive (K+). However, Chloride ions are negative (Cl-) GABAa receptors in which Benzo's work on seem to send negative chloride ions (Cl-) to the post synaptic cell keeping it less likely to fire an action potential.
Therefore if openings of Sodium channels through glutamate and other amino acids, it seems that it would make the cell more depolarized and excitatory. Is it possible that in tinnitus certain post synaptic cells are being activated too much?
Is this why benzodiazipines lessen T for some people as well as anti convulsants?
Also, as far as the Potassium Channel Openers which seem to work on a lot of people's tinnitus like Trobalt, correct me if I am wrong, but in the case of positive potassium ions, when the channel is opened, they LEAVE the cell which would make the cell more negative. It seems to me that if certain cells or neurons in the brain could have more time at the resting potential of -70mv it would cause less excitement and less tinnitus.
Does this make sense to anyone or I am just "out there"?
Basically, this all has to do with neurotransmitter receptors, amino acids, ions, and voltage potentials. I am basically writing this for those that kind of know a little bit about this stuff. I don't expect most to know what I am talking about but wanted to get this out there.
I am posting the website, not my fault if the image comes up in this message (Source www.ric.edu):
http://www.ric.edu/faculty/jmontvilo/335graphics/action_potential/polarizations.JPG
Please correct anything that is incorrect.
Therefore if openings of Sodium channels through glutamate and other amino acids, it seems that it would make the cell more depolarized and excitatory. Is it possible that in tinnitus certain post synaptic cells are being activated too much?
Is this why benzodiazipines lessen T for some people as well as anti convulsants?
Also, as far as the Potassium Channel Openers which seem to work on a lot of people's tinnitus like Trobalt, correct me if I am wrong, but in the case of positive potassium ions, when the channel is opened, they LEAVE the cell which would make the cell more negative. It seems to me that if certain cells or neurons in the brain could have more time at the resting potential of -70mv it would cause less excitement and less tinnitus.
Does this make sense to anyone or I am just "out there"?
Basically, this all has to do with neurotransmitter receptors, amino acids, ions, and voltage potentials. I am basically writing this for those that kind of know a little bit about this stuff. I don't expect most to know what I am talking about but wanted to get this out there.
I am posting the website, not my fault if the image comes up in this message (Source www.ric.edu):
http://www.ric.edu/faculty/jmontvilo/335graphics/action_potential/polarizations.JPG
Please correct anything that is incorrect.
