r/visualsnow • u/Jatzor24 • Feb 10 '25
Research Why I think it's GABA!
A reduction in GABAergic inhibition in thalamic relay cells is more likely to cause palinopsia than 5-HT2A receptor overactivity due to the essential role of the thalamus in visual processing and its reliance on inhibitory control for proper sensory gating.
The lateral geniculate nucleus (LGN) of the thalamus is the key relay for visual information traveling from the retina to the primary visual cortex. Thalamic relay cells depend on both tonic and phasic GABAergic inhibition, primarily from the reticular thalamic nucleus (RTN) and intrinsic interneurons, to prevent excessive or prolonged visual signals. Phasic inhibition, in particular, plays a critical role in the rapid modulation of sensory information, allowing the thalamus to filter out unnecessary or redundant visual input. When GABAergic inhibition—both tonic and phasic—is reduced in the LGN, the normal suppression of irrelevant visual information is impaired, leading to prolonged visual persistence. This manifests as afterimages and trailing effects, which are characteristic of palinopsia.
In certain conditions where NKCC1 is overactive or KCC2 is downregulated, GABA can shift from being inhibitory to excitatory. This alteration leads to hyperexcitability of thalamic relay neurons, increasing visual persistence and contributing to palinopsia-like symptoms.
While 5-HT2A receptor overactivation is known to influence sensory perception, particularly in hallucinogenic states, it does not directly affect thalamic relay gating in the same way as GABAergic inhibition. 5-HT2A receptors are highly expressed in layer V pyramidal neurons of the cortex, especially in association areas such as the visual cortex. Although overactivation of these receptors can contribute to visual distortions, it is unlikely to be the primary cause of afterimage persistence seen in palinopsia.
There is supporting evidence for this theory, as benzodiazepines, which enhance GABAergic activity, have been reported to reduce palinopsia symptoms, reinforcing the importance of GABAergic inhibition in preventing visual persistence. Additionally, patients with thalamic lesions or dysfunction, such as those resulting from strokes affecting the LGN, sometimes report persistent afterimages, further supporting the critical role of the thalamus in visual processing.
5-HT2A overactivation may contribute to perceptual distortions, a reduction in GABAergic inhibition within thalamic relay cells is more likely to be the primary mechanism underlying palinopsia. This is because thalamic GABAergic inhibition, including both tonic and phasic inhibition, is crucial for sensory filtering. When this inhibition is impaired, excessive or prolonged visual signals can lead to persistent afterimages, trailing effects, and other visual phenomena associated with palinopsia.
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u/No_Arachnid_9699 Feb 10 '25
But then when I take gabapentin and other GABA increasing drugs it doesn’t change anything for us?
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u/nothings_right6962 Feb 11 '25
It makes the symptoms go away for me, just saying(with gabapentin) , but I'm not taking it regularly bcuz I kind of feel dumber on it
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u/deadly_fungi lifelong mild-moderate VSS Feb 11 '25
i take spravato and my visual snow gets more noticeable during sessions, and spravato causes an increase in glutamate as well as GABA. i don't think VSS has a single cause, like low GABA for example.
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u/Independent-Bug5457 Feb 10 '25
I don't think it can be reduced to a single neurotransmitter. There are probably parameters that affect each other like dominoes.
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u/cmcalgary Feb 10 '25
Tossed this into chatgpt, then asked if taking GABA supplements could theoretically help ease symptoms:
In theory, increasing GABA activity might help with Visual Snow and Palinopsia if they are caused by reduced GABAergic inhibition in the thalamus. However, simply taking a GABA supplement is unlikely to be effective because:
GABA Can’t Easily Cross the Blood-Brain Barrier – Most GABA supplements don’t enter the brain in significant amounts, so they may not directly increase GABA levels where they’re needed.
GABA Regulation is Complex – Even if you increase GABA levels, the brain has mechanisms to maintain balance, and simply adding more GABA doesn’t guarantee it will improve filtering in the thalamus.
Medications That Boost GABA Activity Exist – Drugs like benzodiazepines (e.g., clonazepam), gabapentin, or lamotrigine enhance GABAergic activity and have been reported to help some people with Visual Snow or Palinopsia. However, these medications can have side effects and are usually prescribed by a doctor.
Alternatives
Magnesium and Taurine – These can indirectly support GABA activity. Some people with Visual Snow report mild benefits from magnesium.
Lifestyle Factors – Reducing stress, improving sleep, and avoiding stimulants (caffeine, excess screen time) may help reduce overactive visual processing.
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u/MaintenanceOk7855 Feb 10 '25
There is a acetylated version, magnesium Acetyl taurinate. We can try that I guess
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u/Firm-Equivalent4971 Feb 10 '25
I used to take 4g of taurine nearly every day. It was in a product I consumed for probably a decade or more. Oddly, though probably coincidental, I developed VSS not long after stopping that product.
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u/deadly_fungi lifelong mild-moderate VSS Feb 11 '25
genuinely, why on earth are you asking chatGPT this?
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u/imoffthecouch Feb 10 '25
I think there’ll probably be a few different reasons why people get VS(S), this is definitely one of them. I find Etifoxine gets rid of a lot of my symptoms over time. I can’t understand all the science behind it, but I believe it works like a benzodiazepine but without the sedation & addiction. Taking a GABA supplement does zilch. Am also autistic, have found so many ND people have VS.
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u/jedr___ Feb 10 '25
Do u have to keep taking erifoxine ?
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u/imoffthecouch Feb 10 '25
I took it for a few weeks, and the effects stuck for quite some time before coming back (after a period of extreme stress).
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u/Lux_Caelorum Solution Seeker Feb 11 '25
its GABAergic inhibitory inputs on 5ht2a receptors. Its why both serotonergic agonists *and* antagonists make it worse for a lot of us. Also why palinopsia is so dam tricky to treat.
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u/Jatzor24 Feb 11 '25
Thalamic relay neurons that's why , Palinopsia can be cause by Both id say that 5ht2a is in indirect effect of from as you said GABAergic inhibitory inputs on 5ht2a receptors but if that were the case of 5ht2a causing it then antagonist to 5ht2a should work , i don't think people understand how GABA in the Thalamus Works
- GABA in RTN: Inhibits thalamocortical relay neurons, controls sensory flow.
- GABA_A Receptors: Chloride influx → hyperpolarization → less excitability.
- GABA_B Receptors: Opens K⁺ channels or inhibits Ca²⁺ channels → reduces excitability.
Ion Channels:
- Cl⁻ (GABA_A): Influx → hyperpolarization.
- K⁺ (GABA_B): Efflux → hyperpolarization.
- Ca²⁺ (GABA_B): Inhibition → less neurotransmitter release
it so complex its insane
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u/renjazid7 Feb 15 '25
GABAergic supplements and agonists reduce my symptoms considerably.
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u/Jatzor24 Feb 15 '25
you might wanna try add a supplement called Honokiol pure, expensive shit but its very good for upregulating GABA-A receptor sensitivity in the brain
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u/HuschelPuschel Feb 11 '25
Sounds interesting maybe this is the case why people with PERM often have same visual disturbances. In their case it is often caused by GlyR Antibodies who block heteropentameric receptors for GABA.
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u/Mara355 Feb 10 '25
This makes sense to me, GABA levels have been found to be lower in autistic people, and autistic people have trouble with sensory filtering (and a disproportionate amount of them has visual snow). So, yeah