<p>The phenomenon you are referring to is called <strong><a href="http://www.scientificamerican.com/article/what-is-synesthesia/" rel="nofollow noreferrer">synesthesia</a></strong>, which can be defined as <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>:</p>
<blockquote>
<p>Synesthesia (Greek: <em>syn</em> = together; <em>aesthesis</em> = perception) is [...] a crossing of sensory perceptions, where stimulation within one sensory modality/stream leads to an internally generated perceptual experience of another sensory modality/stream.</p>
</blockquote>
<p>Synesthesia does not have to be drug-induced; there are people that experience it always (<a href="http://www.scientificamerican.com/article/what-is-synesthesia/" rel="nofollow noreferrer">synesthetes</a>). Their perceptions are often quite subtle, for example, specific written characters assume specific colors <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>.</p>
<p>There are no explicit models for drug-induced synesthesia <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797969/" rel="nofollow noreferrer">(Luke &amp; Turhune, 2013)</a>. Nevertheless, the neurophysiological changes brought about by them can provide models for why hallucinogens can induce a synesthetic state.</p>
<p>The two major classes of <strong>psychedelic hallucinogens</strong>, the indoleamines (e.g., LSD) and the phenethylamines (e.g., mescaline), have a common site of action, namely <strong>activation of serotine (5-HT) receptors</strong>. Specifically, they are <strong>partial agonists</strong> of the <strong><a href="http://www.ncbi.nlm.nih.gov/books/NBK1853/" rel="nofollow noreferrer">5-HT<sub>2</sub>A</a></strong> and other 5-HT<sub>2</sub> receptors in the central nervous system. The noradrenergic locus coeruleus and the cerebral cortex are among the regions where hallucinogens have prominent effects through their actions upon a 5-HT<sub>2</sub>A receptors.</p>
<p>In general, hallucinogens like LSD are thought to inhibit serotonergic neuron transduction, referred to as the <strong>disinhibited feedback model</strong>. Serotonin (5-HT) is mainly produced in the <strong><a href="http://www.ncbi.nlm.nih.gov/pubmed/14729135" rel="nofollow noreferrer">raphne nuclei</a></strong> (RN) of the midbrain. The RN extends its projections into the brainstem and up into the higher cortex. It has been suggested that neurons of the RN may inhibit sensation, thus protecting the brain from sensory overload. Thus, 5-HT may be labeled to be primarily an inhibitory neurotransmitter. A decrease in 5-HT activity hence leads to disinhibition of the next neuron in the chain (e.g., neurons in the cortex) and becomes more active <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>. This increased activity of the cortex may in turn explain the hallucinogenic activity of LSD and related drugs <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>.</p>
<p>However, a few 5-HT receptors are excitatory ion channels (5-HT3), and some 5-HT receptor subtypes may have excitatory effects <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>. Specifically, <strong>5-HT<sub>2</sub>A receptor activation</strong> has been shown to directly mediate an <strong>enhancement</strong> of nonsynchronous, late components of <strong>glutamatergic excitatory postsynaptic potentials at apical dendrites of <a href="http://www.scholarpedia.org/article/Pyramidal_neuron" rel="nofollow noreferrer">layer V cortical pyramidal cells</a></strong>. Hallucinogens indeed increase cortical excitability and activate large areas of the cortex. It has been proposed that this effect of hallucinogens on cerebral glutamatergic transmission may in fact be responsible for the higher-level cognitive, perceptual, and affective distortions produced by these drugs <a href="http://www.nature.com/npp/journal/v21/n1s/full/1395318a.html" rel="nofollow noreferrer">(Aghajanian &amp; Marek, 1999)</a>. Along the lines of these observations, the effect is quite similar to the disinhibited feedback model, in that the effects of drug intoxication are due to enhanced activation of brain regions. With regard to synesthetic effects, it is proposed that this abnormal activity <strong>spreads to neighboring sensory areas that, in turn, lead to cross-modal sensory activations and hence synesthesia</strong> <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>.</p>
<p>Since serotonergic systems appear to be intimately involved in the control of sensation, sleep, attention, and mood, it may be possible to explain the actions of LSD and other hallucinogens by their disinhibition of these critical systems <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">(Sinke <em>et al</em>., 2012)</a>.</p>
<p><sub><strong>References</strong><br />
<strong>-</strong> <a href="http://www.nature.com/npp/journal/v21/n1s/full/1395318a.html" rel="nofollow noreferrer">Aghajanian &amp; Marek, Neuropsychopharmacology (1999) <strong>21</strong>: 16S–23S</a><br />
<strong>-</strong> <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797969/" rel="nofollow noreferrer">Luke &amp; Turhune. Frontiers in Psychology (2013); <strong>4</strong>: 753</a><br />
<strong>-</strong> <a href="http://www.daysyn.com/Sinkeetal2012.pdf" rel="nofollow noreferrer">Sinke <em>et al</em>., Consciousness and Cognition (2012); <strong>21</strong>: 1419–34</a></sub></p>

CC BY-SA 3.0
2016-05-25T14:44:41.653Z
It seems to me you know a lot about this subject. Do you know if some music composers based their compositions on the synesthesis of sound and vision (colours or forms)?
Deschele Schilder
CC BY-SA 3.0
2016-05-25T19:03:33.143Z
@descheleschilder - I have added additional neurophysiological data and the newly added  Aghajanian & Marek (1999) paper is highly recommended. My knowledge on music composers is limited, however.
AliceD
CC BY-SA 4.0
2016-05-20T14:41:04.653Z
2020-09-05T10:33:20.590Z
2020-09-05T10:33:20.590Z
AliceD
<p><a href="https://www.theguardian.com/science/2016/apr/11/lsd-impact-brain-revealed-groundbreaking-images" rel="noreferrer"><strong>In a recent study</strong></a>, brain scans revealed that people under the influence of LSD experience images through information drawn from many parts of their brains, and not just the visual cortex at the back of the head that normally processes visual information. While under influence, regions normally segregated spoke to one another. Further images showed that other brain regions that usually form a network became more separated.</p>

<p>Both alterations in your brain perfectly explain <a href="https://www.youtube.com/watch?v=XRV5NsyaRlU" rel="noreferrer"><strong>the many differences in one's perception</strong></a> while under the influence of LSD, which can include (but doesn't necessarilly include) <a href="https://en.wikipedia.org/wiki/Synesthesia" rel="noreferrer"><strong>synesthesia</strong></a>.</p>

<p><a href="https://i.sstatic.net/j5k8K.jpg" rel="noreferrer"><img src="https://i.sstatic.net/j5k8K.jpg" alt="enter image description here"></a></p>

CC BY-SA 3.0
2016-05-26T09:39:37.167Z
2016-05-26T09:39:37.167Z
John Slegers
<p><strong>How is it possible that after using LSD you can hear sounds and see colors?</strong></p>
<p>I have my own experience with this phenomenon. When I´m lying totally relaxed in bed and suddenly a door is closed loudly, I see an explosion of colors. Are the two brain regions responsible for hearing and seeing, if you´re totally relaxed (for example just before falling asleep), somehow more connected with each other?    Maybe the two regions are disconnected in a relaxed mode, but when a sudden sound (or maybe a flash of light in the other direction) occurs the neural network associated with hearing is suddenly &quot;scared&quot; and sends a &quot;cry for help&quot; to adjacent regions (resulting in a flash of light or in the other direction a sound, but I've never experienced this).</p>
<p>I edited because the new answer is always welcome, though the first answer is very clear about this &quot; tpo-cic&quot;.</p>

CC BY-SA 3.0
2016-05-01T19:48:21.560Z
Hi, I actually just read an article which was published recently. Researchers from Imperial College of London, explored the brain under MRI scans in people who have been taking LSD vs placebo. It was shown that actually the brain firing was very spread out, and that the underlying default network was dissolved. The fact that areas of the brain were firing together might explain de different hallucinations experimented under LSD.You might want to have a look at the article: http://www.pnas.org/content/113/17/4853
Elise
CC BY-SA 3.0
2016-05-01T22:08:17.510Z
@Elise Hi, I read with much interest the article (mainly written by men, while much brain research is executed also by women, but that aside), but it still isn´t that much clear to me why the two sensations of hearing and seeing can melt together as it were. Or are the very spread out firing of neurons and a dissolved network to wich you refer in your comment causing the effect? Anyhow, thanks!
Deschele Schilder
<cognitive-psychology><neuroscience><cognitive-neuroscience><neurophysiology><psychopharmacology>
Can LSD connect sensory regions in the brain?
Deschele Schilder
# Can LSD connect sensory regions in the brain?

(Asked by: username_0 on 2016-05-01)

**How is it possible that after using LSD you can hear sounds and see colors?**

I have my own experience with this phenomenon. When I´m lying totally relaxed in bed and suddenly a door is closed loudly, I see an explosion of colors. Are the two brain regions responsible for hearing and seeing, if you´re totally relaxed (for example just before falling asleep), somehow more connected with each other? Maybe the two regions are disconnected in a relaxed mode, but when a sudden sound (or maybe a flash of light in the other direction) occurs the neural network associated with hearing is suddenly "scared" and sends a "cry for help" to adjacent regions (resulting in a flash of light or in the other direction a sound, but I've never experienced this).

I edited because the new answer is always welcome, though the first answer is very clear about this " tpo-cic".

**Tags:** cognitive-psychology, neuroscience, cognitive-neuroscience, neurophysiology, psychopharmacology

> **Comments:**
> **username_1**: Hi, I actually just read an article which was published recently. Researchers from Imperial College of London, explored the brain under MRI scans in people who have been taking LSD vs placebo. It was shown that actually the brain firing was very spread out, and that the underlying default network was dissolved. The fact that areas of the brain were firing together might explain de different hallucinations experimented under LSD.You might want to have a look at the article: http://www.pnas.org/content/113/17/4853  
> **username_0**: @username_1 Hi, I read with much interest the article (mainly written by men, while much brain research is executed also by women, but that aside), but it still isn´t that much clear to me why the two sensations of hearing and seeing can melt together as it were. Or are the very spread out firing of neurons and a dissolved network to wich you refer in your comment causing the effect? Anyhow, thanks!  

---

## 2 answers

### Answer by username_2 on 2016-05-20. Score: 7

The phenomenon you are referring to is called **[synesthesia](http://www.scientificamerican.com/article/what-is-synesthesia/)**, which can be defined as [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf):

> Synesthesia (Greek: *syn* = together; *aesthesis* = perception) is [...] a crossing of sensory perceptions, where stimulation within one sensory modality/stream leads to an internally generated perceptual experience of another sensory modality/stream.

Synesthesia does not have to be drug-induced; there are people that experience it always ([synesthetes](http://www.scientificamerican.com/article/what-is-synesthesia/)). Their perceptions are often quite subtle, for example, specific written characters assume specific colors [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf).

There are no explicit models for drug-induced synesthesia [(Luke & Turhune, 2013)](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797969/). Nevertheless, the neurophysiological changes brought about by them can provide models for why hallucinogens can induce a synesthetic state.

The two major classes of **psychedelic hallucinogens**, the indoleamines (e.g., LSD) and the phenethylamines (e.g., mescaline), have a common site of action, namely **activation of serotine (5-HT) receptors**. Specifically, they are **partial agonists** of the **[5-HT2A](http://www.ncbi.nlm.nih.gov/books/NBK1853/)** and other 5-HT2 receptors in the central nervous system. The noradrenergic locus coeruleus and the cerebral cortex are among the regions where hallucinogens have prominent effects through their actions upon a 5-HT2A receptors.

In general, hallucinogens like LSD are thought to inhibit serotonergic neuron transduction, referred to as the **disinhibited feedback model**. Serotonin (5-HT) is mainly produced in the **[raphne nuclei](http://www.ncbi.nlm.nih.gov/pubmed/14729135)** (RN) of the midbrain. The RN extends its projections into the brainstem and up into the higher cortex. It has been suggested that neurons of the RN may inhibit sensation, thus protecting the brain from sensory overload. Thus, 5-HT may be labeled to be primarily an inhibitory neurotransmitter. A decrease in 5-HT activity hence leads to disinhibition of the next neuron in the chain (e.g., neurons in the cortex) and becomes more active [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf). This increased activity of the cortex may in turn explain the hallucinogenic activity of LSD and related drugs [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf).

However, a few 5-HT receptors are excitatory ion channels (5-HT3), and some 5-HT receptor subtypes may have excitatory effects [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf). Specifically, **5-HT2A receptor activation** has been shown to directly mediate an **enhancement** of nonsynchronous, late components of **glutamatergic excitatory postsynaptic potentials at apical dendrites of [layer V cortical pyramidal cells](http://www.scholarpedia.org/article/Pyramidal_neuron)**. Hallucinogens indeed increase cortical excitability and activate large areas of the cortex. It has been proposed that this effect of hallucinogens on cerebral glutamatergic transmission may in fact be responsible for the higher-level cognitive, perceptual, and affective distortions produced by these drugs [(Aghajanian & Marek, 1999)](http://www.nature.com/npp/journal/v21/n1s/full/1395318a.html). Along the lines of these observations, the effect is quite similar to the disinhibited feedback model, in that the effects of drug intoxication are due to enhanced activation of brain regions. With regard to synesthetic effects, it is proposed that this abnormal activity **spreads to neighboring sensory areas that, in turn, lead to cross-modal sensory activations and hence synesthesia** [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf).

Since serotonergic systems appear to be intimately involved in the control of sensation, sleep, attention, and mood, it may be possible to explain the actions of LSD and other hallucinogens by their disinhibition of these critical systems [(Sinke *et al*., 2012)](http://www.daysyn.com/Sinkeetal2012.pdf).

**References**  
**-** [Aghajanian & Marek, Neuropsychopharmacology (1999) **21**: 16S–23S](http://www.nature.com/npp/journal/v21/n1s/full/1395318a.html)  
**-** [Luke & Turhune. Frontiers in Psychology (2013); **4**: 753](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797969/)  
**-** [Sinke *et al*., Consciousness and Cognition (2012); **21**: 1419–34](http://www.daysyn.com/Sinkeetal2012.pdf)

> **Comments:**
> **username_0**: It seems to me you know a lot about this subject. Do you know if some music composers based their compositions on the synesthesis of sound and vision (colours or forms)?  
> **username_2**: @descheleschilder - I have added additional neurophysiological data and the newly added  Aghajanian & Marek (1999) paper is highly recommended. My knowledge on music composers is limited, however.  

---

### Answer by username_3 on 2016-05-26. Score: 5

[**In a recent study**](https://www.theguardian.com/science/2016/apr/11/lsd-impact-brain-revealed-groundbreaking-images), brain scans revealed that people under the influence of LSD experience images through information drawn from many parts of their brains, and not just the visual cortex at the back of the head that normally processes visual information. While under influence, regions normally segregated spoke to one another. Further images showed that other brain regions that usually form a network became more separated.

Both alterations in your brain perfectly explain [**the many differences in one's perception**](https://www.youtube.com/watch?v=XRV5NsyaRlU) while under the influence of LSD, which can include (but doesn't necessarilly include) [**synesthesia**](https://en.wikipedia.org/wiki/Synesthesia).

[![enter image description here](https://i.sstatic.net/j5k8K.jpg)](https://i.sstatic.net/j5k8K.jpg)


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