Interestingly I have never experienced bruxism from any prescribed substance or otherwise (and I've run the gambit). I did however suffer from in my sleep as a child and believe I have recently begun to once again. I think serotonin or norepinephrine may be playing a major role as I had untreated anxiety for a long while as a child and now as an adult I feel the occasional jaw pain after waking up after a few recently nightmarish weeks. In both periods of my life my dreams were incredibly vivid and I would wake up sweating at the peak of what I would guess was REM sleep.
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N&PD Moderators: Skorpio | thegreenhand
Is jaw clenching caused by serotonin?
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Solipsis
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If 5HT2A is such a huge culprit, how come bruxism or 'tightness in the face' are mostly associated with stimulants (MDMA is an empathogenic stimulant which action on 5HT2A / or the MDA metabolite / are to be considered a side effect in this story not shared by lesser psychedelic empathogen analogues), while the majority of psychedelics show rather mild bruxism effect afaik?
I think 5HT2AR is - either direct or indirect - one of several possible causators ... demonstrated by the bruxism compounds like 25I-NBOMe can cause, but that does not prove it is a major one.
And 5HT2AR does not seem like it can be seen separate from the sympathomimetic CNS (massive overstimulation from NBOMe OD leads to toxic weirdness all over, in extreme cases). So I think Crook has given us a lot of information (as have you all) on it being multifactorial and CNS stimulation top-down, where 5HT2A also ties in but not as a major player.
As for magnesium, I have no reason to believe it is depleted in particular but think - vaguely and correct me if wrongly worded - imbalance of magnesium vs calcium concentrations can cause problems with osmotic muscular or nerve potential and tonus as an effect... The aforementioned causes of bruxism may possibly exaggerate sensitivity to these electrolyte imbalances? I would personally recommend supplementing with both calcium and magnesium as I do not believe that you can actually control the levels by what you take as supplement.. you supplement your supply, thereby at least decreasing your sensitivities or vulnerability when it comes to electrolytes and muscle function.
Not to mention the possible loss of electrolytes in hot sweaty partying people, hydrating with water that is not isotonic? As far as any depletion would go, that could lead to imbalances if the body can't keep up properly.
Obviously that is an entirely different thing than thinking any sports drink will stop your teeth grinding during sleep..
I think 5HT2AR is - either direct or indirect - one of several possible causators ... demonstrated by the bruxism compounds like 25I-NBOMe can cause, but that does not prove it is a major one.
And 5HT2AR does not seem like it can be seen separate from the sympathomimetic CNS (massive overstimulation from NBOMe OD leads to toxic weirdness all over, in extreme cases). So I think Crook has given us a lot of information (as have you all) on it being multifactorial and CNS stimulation top-down, where 5HT2A also ties in but not as a major player.
As for magnesium, I have no reason to believe it is depleted in particular but think - vaguely and correct me if wrongly worded - imbalance of magnesium vs calcium concentrations can cause problems with osmotic muscular or nerve potential and tonus as an effect... The aforementioned causes of bruxism may possibly exaggerate sensitivity to these electrolyte imbalances? I would personally recommend supplementing with both calcium and magnesium as I do not believe that you can actually control the levels by what you take as supplement.. you supplement your supply, thereby at least decreasing your sensitivities or vulnerability when it comes to electrolytes and muscle function.
Not to mention the possible loss of electrolytes in hot sweaty partying people, hydrating with water that is not isotonic? As far as any depletion would go, that could lead to imbalances if the body can't keep up properly.
Obviously that is an entirely different thing than thinking any sports drink will stop your teeth grinding during sleep..
Last edited:
serotonin2A
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.
If you delve quite deeply into the electrophysiology literature then there are some answers to the issue you raised. 5-HT2A activation facilitates the ability of other excitatory influences to depolarize snd excite motorneurons. For example, hallucinogens have been shown to enhance the excitatory influence of norepinephrine on motor neurons. So it makes sense that a more promiscuous releaser such as MDMA would produce more bruxism than selective compounds, eg MDAI or 25I-NBOMe.
In other words, 5-HT2A (and potentially other serotonin receptors) enhance the excitability of the motor neurons, but that action still depends on other influences to actually drive the neurons to fire. But when you combine that with additional norepinephrine then you are increasing the baseline excitatory input to the neurons, so you end up with synergistic effects.
http://www.ncbi.nlm.nih.gov/pubmed/7392
If 5HT2A is such a huge culprit, how come bruxism or 'tightness in the face' are mostly associated with stimulants (MDMA is an empathogenic stimulant which action on 5HT2A / or the MDA metabolite / are to be considered a side effect in this story not shared by lesser psychedelic empathogen analogues), while the majority of psychedelics show rather mild bruxism effect afaik?
I think 5HT2AR is - either direct or indirect - one of several possible causators ... demonstrated by the bruxism compounds like 25I-NBOMe can cause, but that does not prove it is a major one.
And 5HT2AR does not seem like it can be seen separate from the sympathomimetic CNS (massive overstimulation from NBOMe OD leads to toxic weirdness all over, in extreme cases). So I think Crook has given us a lot of information (as have you all) on it being multifactorial and CNS stimulation top-down, where 5HT2A also ties in but not as a major player.
If you delve quite deeply into the electrophysiology literature then there are some answers to the issue you raised. 5-HT2A activation facilitates the ability of other excitatory influences to depolarize snd excite motorneurons. For example, hallucinogens have been shown to enhance the excitatory influence of norepinephrine on motor neurons. So it makes sense that a more promiscuous releaser such as MDMA would produce more bruxism than selective compounds, eg MDAI or 25I-NBOMe.
In other words, 5-HT2A (and potentially other serotonin receptors) enhance the excitability of the motor neurons, but that action still depends on other influences to actually drive the neurons to fire. But when you combine that with additional norepinephrine then you are increasing the baseline excitatory input to the neurons, so you end up with synergistic effects.
http://www.ncbi.nlm.nih.gov/pubmed/7392
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Cotcha Yankinov
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Hey scolipsis I think part of the idea of not being able to compare MDMA's 5-HT2A activity and a psychedelic's 5-HT2A is that depending on what is binding to the 5-HT2Ar it will have different down stream effects, serotonin itself might signal differently than a 5-HT2A agonist like LSD.
I think part of the idea of not being able to compare MDMA's 5-HT2A activity and a psychedelic's 5-HT2A is that depending on what is binding to the 5-HT2Ar it will have different down stream effects, serotonin itself might signal differently than a 5-HT2A agonist like LSD.
Dresden
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I don't think anyone really knows the answer to the OP's question other than to say it is just what is observed when certain drugs which may share some of the same biochemical properties such as 5-HT2a agonism in vivo is given to a live and preferably human test subject. Although theories could be developed, they are all at this point equally speculative and thus worthless. Therefore coming up with an explanation is worse than a waste of time because it tells us nothing concretely true or factual that we can prove while propagating misinformation by those of us who will one day encounter it and not realize its author was utterly bullshitting us on a currently scientifically unanswerable question in order to appear erudite or important. Not to criticize, but such realities have been known to occur here on bluelight occasionally in the past, especially when the poster wanted to keep the title of most know it all naysayer for example. For example, I would suggest structure x, a novel structure that no one myself included knows anything about the effects of and hear a litany of well that could never work because <insert biochemical explanation with reference to some other related compound structurally>. It behooves even scientists to at certain times to admit to how little rather than how much they know, but I digress. Damn, I'm obviously freaking flying high on methamphetamine again apparently based on the amount of logorrhea I'm producing. All apologies, of course.
Cotcha Yankinov
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^^but don't you love theory crafting :D
I found in a textbook that some ligands bind to 5-HT2A and then signal to PLC from a G-q protein, and then some ligands bind 5-HT2A and through G-i/o (and possibly other G proteins) signal downstream via arachidonic acid metabolites. The text book is even giving 5HT2A specifically as its sole example. I wonder which pathway serotonin is and if that one seems to fit better with causing bruxism.
Recently discussed in the big and banging thread was why do different agonists at 5HT2A have different effects, I suppose this is very similar. It might ultimately be because of different downstream effects from ligand to ligand (or different receptor Heteromers vs. dimers as well?)
I found in a textbook that some ligands bind to 5-HT2A and then signal to PLC from a G-q protein, and then some ligands bind 5-HT2A and through G-i/o (and possibly other G proteins) signal downstream via arachidonic acid metabolites. The text book is even giving 5HT2A specifically as its sole example. I wonder which pathway serotonin is and if that one seems to fit better with causing bruxism.
Recently discussed in the big and banging thread was why do different agonists at 5HT2A have different effects, I suppose this is very similar. It might ultimately be because of different downstream effects from ligand to ligand (or different receptor Heteromers vs. dimers as well?)