Low Amounts of GABA in the Auditory Cortex of Tinnitus Sufferers?

Discussion in 'Support' started by JasonP, Sep 25, 2016.

    1. JasonP
      No Mood

      JasonP Member

      Tinnitus Since:
      I was just watching a video on how a Dr. thinks that people with tinnitus have low amounts of GABA in the auditory cortex. Starts at 10:32

      Tinnitus Q & A 02/2016 Pt 1/ 4

      This is interesting because with some people benzo have reduction in T but others over long periods of time have increased T or they get T from coming off. I heard that long term benzo use can do some things that might cause this: downregulation GABA receptors and lead to excitability in the glutamate system, not only that but it supposedly upregulates the NMDA receptors which are activated by glutamate. Therefore, it makes sense that withdrawal after long term use could increase tinnitus by these things.

      It's also important to note also that Benzo use does NOT increase GABA, it only activates the GABAa receptor allowing chloride ions to enter the postynaptic neuron thereby having an inhibitory effect.

      According to my logic, (and I certainly could be wrong) I would think then, upregulating GABA receptors and downregulating NMDA receptors could help. But to be honest, I haven't looked into that part yet. Can you guys on here help me study this?

      According to Wikipedia:

      Tolerance results in a desensitization of GABA receptors and an increased sensitization of the excitatory neurotransmitter system, glutamate such as NMDAglutamate receptors. These changes occur as a result of the body trying to overcome the drug's effects. Other changes that occur are the reduction of the number of GABA receptors (downregulation) as well as possibly long-term changes in gene transcription coding of brain cells. The differing speed at which tolerance occurs to the therapeutic effects of benzodiazepines can be explained by the speed of changes in the range of neurotransmitter systems and subsystems that are altered by chronic benzodiazepine use. The various neurotransmitter systems and subsystems may reverse tolerance at different speeds, thus explaining the prolonged nature of some withdrawal symptoms. As a result of a physical dependence that develops due to tolerance, a characteristic benzodiazepine withdrawal syndrome often occurs after removal of the drug or a reduction in dosage.[19] Changes in the expression of neuropeptides such as corticotropin-releasing hormone and neuropeptide Y may play a role in benzodiazepine dependence.[20]Individuals taking daily benzodiazepine drugs have a reduced sensitivity to further additional doses of benzodiazepines.[21] Tolerance to benzodiazepines can be demonstrated by injecting diazepam into long-term users. In normal subjects, increases in growth hormone occurs, whereas, in benzodiazepine-tolerant individuals, this effect is blunted.[22]


      Kindling due to substance withdrawal refers to the neurological condition which results from repeated withdrawal episodes from sedativehypnotic drugs such as alcohol or benzodiazepines. Each withdrawal leads to more severe withdrawal symptoms than the previous withdrawal syndrome. Individuals who have had more withdrawal episodes are at an increased risk of very severe withdrawal symptoms, up to and including seizures, and death. Withdrawal from GABAergic-acting sedative–hypnotic drugs causes acute GABA-underactivity as well as glutamate overactivity which can lead to sensitization and hyper-excitability of the central nervous system, excito-neurotoxicity, and increasingly profound neuroadaptions.


      Animal studies have found that glutamergic changes as a result of benzodiazepine use are responsible for a delayed withdrawal syndrome, which in mice peaks 3 days after cessation of benzodiazepines. This was demonstrated by the ability to avoid the withdrawal syndrome by the administration of AMPA antagonists. It is believed that different glutamate subreceptors, e.g., NMDA and AMPA, are responsible for different stages/time points of the withdrawal syndrome. NMDA receptors are upregulated in the brain as a result of benzodiazepine tolerance. AMPA receptors are also involved in benzodiazepine tolerance and withdrawal.[5][23][23] A decrease in benzodiazepine binding sites in the brain may also occur as part of benzodiazepine tolerance.[24]

      Any suggestions, comments, or disagreements with this? I would love to hear them because I am trying to figure some of this stuff out.
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