Now that I have returned from my week long "vacation", I have decided to give writing my usual scientific minded posts another try, with a different approach.
For this post, I want to examine the role of serotonin and its role in the modulation of tinnitus. Serotonin is one of the big three neurotransmitters (the other two being dopamine and norepinephrine) that are considered the "happy" neurotransmitters due to their heavy involvement in the regulation of mood, arousal, pleasure, reward reinforcement, and heavy receptor presence in the limbic system.
The limbic system is primarily located in the frontal lobe of the brain and contains crucial and well studied areas such as:
hippocampus (a brain area that exists in both temporal lobes, is crucial in the formation of long term memory and emotional learning/conditioning)
amygdala (the brain's "fear center" that triggers extreme emotional responses and initiates the fight or flight response. In people with panic, phobic, anxiety, and depression disorders, it tends to hyperactive. In the case of depression, it hyperactivity continues after the depression subsides)
and Nucleus Accumbens (NAc) (a dopamine and serotonin receptor presence heavy area associated with mood, learning, and reward/pleasure)
So, how does all of this relate to tinnitus? Well, the jury is still out frankly, as the brain is very complicated. The point of this post is to purpose the question of whether or not serotonin's presence in a chronic tinnitus (6 months or longer) is good or bad, and alludes to the use of serotonin promoting treatments like SSRIs as the alleged "cure" for the noise.
While limbic areas have long been thought to be involved in tinnitus, it was Josef Rauschecker's 2010 study (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904345/) which brought it more into the spot light, as it purposed a so-called "gate-keeper" in the brain that, in a healthy person, blocks an annoying or unwanted noise by tuning it out of consciousness.
According to this model, (in a healthy person) the raphe nuclei (the serotonin producing cells in the Recticular Formation in the brain stem) normally project serotonin into the forebrain where it triggers the activation of GABA receptors in the Thalamic Recticular Nucleus (TRN), which inhibit the tinnitus signal, blocking it from reaching the auditory cortex, and thus consciousness. According to this model, tinnitus arises due to a reduction or loss of serotonin and dopamine neurons in places like the ventralmedial prefrontal cortex (vmPFC). I won't go into too much more detail, but the basic gist of Ruaschecker's model is that in healthy people, areas of the limbic system and thalamus talk to each other to coordinate whether a sound, such as a tinnitus signal, should be allowed to reach conscious level. The loss of dopamine and serotonin neurons in places like the NAc, vmPFC, or dysfunction of raphe forebrain projection cause the TRN to become under stimulated, allowing the tinnitus signal to become conscious.
To Ruaschecker, the solution seems simple, if the TRN fails to do its job because of a loss in serotonin neurons, then drugs that boost extracellular levels should therefore get the TRN working again and block the signal. Problem solved, right? Sadly, Ruaschecker is, in my opinion, mistaken. His paper (link provided) admits that there are limited and mixed findings on the use of SSRIs as effective tinnitus treatments (to be clear, when I say "treatment", this means reducing the intensity of the noise and not our perception of it). In general, from reading the many personal accounts of tinnitus users and SSRIs, I see to find that (in some) it can worsen or even induce tinnitus. At best, it improves mood, treats depression, and decreased negative reactivity to the noise. Addtionally, a meta-analysis study of numerous neuroimaging studies found that previously observed structural brain changes were inconsistent between studies (due either to methodological differences or differences in participant samples), and that Rauschecker's model was unsubstantiated.
Most damming however is a study from last year by Tang et al. (2017) (https://www.sciencedaily.com/releases/2017/08/170822123836.htm), which analysed brain slices in rats with tinnitus, and (basically) suggested that serotonin actually may worsen the hyperactive firing of the Dorsal Cochlear Nucleus (DCN), an area most commonly implicated as the potential source of tinnitus signal generation, evident by its unique but maladaptive synchronized and hyperactive firing pattern.
So, is serotonin your friend or foe if you suffer from tinnitus? It really depends on the individual sufferer I suppose. Not everyone will have tinnitus worsened by SSRIs or increased serotonin levels, while others might. The takeaway from Ruaschecker's study is that the limbic system has a defined role in why some people develop tinnitus over others. He even suggests that fleeting tinnitus (coming and going tinnitus) may be the result of fluctuating levels of serotonin in the individual, thus their TRN is still partially working some of the time.
There is a link between tinnitus and depression. Those who have tinnitus are twice as likely to develop depression, while those with depression are more vulnerable to tinnitus. Imaging studies show that those afflicted with major depressive disorder and various anxiety disorders and PTSD have a smaller left hippocampus. In the case of PTSD (in a twin study), the twin without PTSD also had a smaller hippocampus as their twin with PTSD did. A smaller left hippocampus has also been shown in tinnitus sufferers. Serotonin, a neurotransmitter commonly associated with happiness and positive mood, is a powerful tool in fighting depression, but could potentially worsen or cause tinnitus in the process.
So what's the answer? I personally would say focus on promoting non-serotonin neurotransmitters, such as dopamine and norepinephrine, instead of boosting serotonin. You can gain a positive mood without it, though serotonin also plays a role in the regulation of sleep, pain, and appetite, so it cannot be discarded.
Finally, if you're new to tinnitus and are reading the studies I have posted and are worried about terms like "grey matter reduction", well, you should and shouldn't be. Tinnitus is complex and affects everyone differently. Even observed hyperactive brain regions differ between some sufferers.
Is this condition permanent? Is your brain damaged? I honestly cannot say. Some on this forum report their tinnitus going away entirely or dramatically reducing years after it arises. It may get better for you, it may get worse. As the meta-analysis study I linked to showed, there is too much variance in observed evidence to definitively say if one change happens in a tinnitus brain or not, though there are consistent trends.
In my personal opinion, tinnitus and whether it is severe or mild depends entirely on affect (your emotional response) rather than the sound's intensity. For example, my tinnitus on an average day is a 3 or 4/10. Pretty quiet compared to the 8's and 9's many on here report. However, due to my family history of depression and anxiety issues, tinnitus (even as quiet as it is) is still detrimental to me, as I view it as nothing short of a threat to my sanity and quality of life.
Don't be like me, don't catastrophize it. It's awful, we can all agree on that. If you're new, it may still go away and not be permanent. If you suspect it is permanent (because a trained medical professional told you they think so), then while you're in the acute phase (up to 3 months) is probably the most effective period in which you can influence or effect your tinnitus, as many of the neuroplastic changes associated with chronic tinnitus (6 months or longer) have not happened yet.
Stay informed, but stay happy or at least active.
-Glow
For this post, I want to examine the role of serotonin and its role in the modulation of tinnitus. Serotonin is one of the big three neurotransmitters (the other two being dopamine and norepinephrine) that are considered the "happy" neurotransmitters due to their heavy involvement in the regulation of mood, arousal, pleasure, reward reinforcement, and heavy receptor presence in the limbic system.
The limbic system is primarily located in the frontal lobe of the brain and contains crucial and well studied areas such as:
hippocampus (a brain area that exists in both temporal lobes, is crucial in the formation of long term memory and emotional learning/conditioning)
amygdala (the brain's "fear center" that triggers extreme emotional responses and initiates the fight or flight response. In people with panic, phobic, anxiety, and depression disorders, it tends to hyperactive. In the case of depression, it hyperactivity continues after the depression subsides)
and Nucleus Accumbens (NAc) (a dopamine and serotonin receptor presence heavy area associated with mood, learning, and reward/pleasure)
So, how does all of this relate to tinnitus? Well, the jury is still out frankly, as the brain is very complicated. The point of this post is to purpose the question of whether or not serotonin's presence in a chronic tinnitus (6 months or longer) is good or bad, and alludes to the use of serotonin promoting treatments like SSRIs as the alleged "cure" for the noise.
While limbic areas have long been thought to be involved in tinnitus, it was Josef Rauschecker's 2010 study (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904345/) which brought it more into the spot light, as it purposed a so-called "gate-keeper" in the brain that, in a healthy person, blocks an annoying or unwanted noise by tuning it out of consciousness.
According to this model, (in a healthy person) the raphe nuclei (the serotonin producing cells in the Recticular Formation in the brain stem) normally project serotonin into the forebrain where it triggers the activation of GABA receptors in the Thalamic Recticular Nucleus (TRN), which inhibit the tinnitus signal, blocking it from reaching the auditory cortex, and thus consciousness. According to this model, tinnitus arises due to a reduction or loss of serotonin and dopamine neurons in places like the ventralmedial prefrontal cortex (vmPFC). I won't go into too much more detail, but the basic gist of Ruaschecker's model is that in healthy people, areas of the limbic system and thalamus talk to each other to coordinate whether a sound, such as a tinnitus signal, should be allowed to reach conscious level. The loss of dopamine and serotonin neurons in places like the NAc, vmPFC, or dysfunction of raphe forebrain projection cause the TRN to become under stimulated, allowing the tinnitus signal to become conscious.
To Ruaschecker, the solution seems simple, if the TRN fails to do its job because of a loss in serotonin neurons, then drugs that boost extracellular levels should therefore get the TRN working again and block the signal. Problem solved, right? Sadly, Ruaschecker is, in my opinion, mistaken. His paper (link provided) admits that there are limited and mixed findings on the use of SSRIs as effective tinnitus treatments (to be clear, when I say "treatment", this means reducing the intensity of the noise and not our perception of it). In general, from reading the many personal accounts of tinnitus users and SSRIs, I see to find that (in some) it can worsen or even induce tinnitus. At best, it improves mood, treats depression, and decreased negative reactivity to the noise. Addtionally, a meta-analysis study of numerous neuroimaging studies found that previously observed structural brain changes were inconsistent between studies (due either to methodological differences or differences in participant samples), and that Rauschecker's model was unsubstantiated.
Most damming however is a study from last year by Tang et al. (2017) (https://www.sciencedaily.com/releases/2017/08/170822123836.htm), which analysed brain slices in rats with tinnitus, and (basically) suggested that serotonin actually may worsen the hyperactive firing of the Dorsal Cochlear Nucleus (DCN), an area most commonly implicated as the potential source of tinnitus signal generation, evident by its unique but maladaptive synchronized and hyperactive firing pattern.
So, is serotonin your friend or foe if you suffer from tinnitus? It really depends on the individual sufferer I suppose. Not everyone will have tinnitus worsened by SSRIs or increased serotonin levels, while others might. The takeaway from Ruaschecker's study is that the limbic system has a defined role in why some people develop tinnitus over others. He even suggests that fleeting tinnitus (coming and going tinnitus) may be the result of fluctuating levels of serotonin in the individual, thus their TRN is still partially working some of the time.
There is a link between tinnitus and depression. Those who have tinnitus are twice as likely to develop depression, while those with depression are more vulnerable to tinnitus. Imaging studies show that those afflicted with major depressive disorder and various anxiety disorders and PTSD have a smaller left hippocampus. In the case of PTSD (in a twin study), the twin without PTSD also had a smaller hippocampus as their twin with PTSD did. A smaller left hippocampus has also been shown in tinnitus sufferers. Serotonin, a neurotransmitter commonly associated with happiness and positive mood, is a powerful tool in fighting depression, but could potentially worsen or cause tinnitus in the process.
So what's the answer? I personally would say focus on promoting non-serotonin neurotransmitters, such as dopamine and norepinephrine, instead of boosting serotonin. You can gain a positive mood without it, though serotonin also plays a role in the regulation of sleep, pain, and appetite, so it cannot be discarded.
Finally, if you're new to tinnitus and are reading the studies I have posted and are worried about terms like "grey matter reduction", well, you should and shouldn't be. Tinnitus is complex and affects everyone differently. Even observed hyperactive brain regions differ between some sufferers.
Is this condition permanent? Is your brain damaged? I honestly cannot say. Some on this forum report their tinnitus going away entirely or dramatically reducing years after it arises. It may get better for you, it may get worse. As the meta-analysis study I linked to showed, there is too much variance in observed evidence to definitively say if one change happens in a tinnitus brain or not, though there are consistent trends.
In my personal opinion, tinnitus and whether it is severe or mild depends entirely on affect (your emotional response) rather than the sound's intensity. For example, my tinnitus on an average day is a 3 or 4/10. Pretty quiet compared to the 8's and 9's many on here report. However, due to my family history of depression and anxiety issues, tinnitus (even as quiet as it is) is still detrimental to me, as I view it as nothing short of a threat to my sanity and quality of life.
Don't be like me, don't catastrophize it. It's awful, we can all agree on that. If you're new, it may still go away and not be permanent. If you suspect it is permanent (because a trained medical professional told you they think so), then while you're in the acute phase (up to 3 months) is probably the most effective period in which you can influence or effect your tinnitus, as many of the neuroplastic changes associated with chronic tinnitus (6 months or longer) have not happened yet.
Stay informed, but stay happy or at least active.
-Glow
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