<p><strong>Short answer</strong><br>
To start my post with a cliche - correlation (between raphe activity and movement) does not imply causality. More importantly, the complete absence of the raphe nucleus does not negate movement. </p>

<p><strong>Background</strong><br>
Although I cannot disprove your hypotheses, I do wish to express a word of caution (6 years after your post :-)</p>

<blockquote>
  <p>Can I reverse this statement to say that movement indicates DRN activity?</p>
</blockquote>

<p>I would be careful with this statement. Activity in the raphe nucleus is positively correlated with behavioral arousal, yes <a href="http://www.physiology.org/doi/full/10.1152/jn.00507.2009" rel="nofollow noreferrer">(Ranade &amp; Mainen, 2009)</a>. Further, raphe activity is thought to be related to the level of tonic motor activity associated with gross motor activity and repetitive, central pattern generator mediated responses <a href="https://www.sciencedirect.com/science/article/pii/S0959438897801419" rel="nofollow noreferrer">(Jacobs &amp; Fomal, 1997)</a>. Yet, to couple these findings in reverse, and state that one can measure raphe activity through movement detection is tricky. Importantly, there are hosts of studies <strong>where the raphe nucleus was ablated and animals still showed (quite normal) motor activity</strong> (<em>e.g.</em> <a href="https://www.sciencedirect.com/science/article/pii/S1877042812000626" rel="nofollow noreferrer">Ghaderi <em>et al</em>. (2012)</a>). </p>

<blockquote>
  <p>I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days. </p>
</blockquote>

<p>It has been shown that successful treatment of depression results in an increase of motor activity. As depression is strongly linked to serotonin signaling this may be an interesting side track. However, increased motor activity was only found for day-time level of movements; clinical improvement was not reflected by night-time measurements. In case of depression, it is thought that activity in the frontal lobe is associated with motor impairments in depression and is related more top dopamine transmission than<br>
serotonin <a href="https://www.tandfonline.com/doi/pdf/10.3109/15622970701403081?needAccess=true" rel="nofollow noreferrer">(Todder <em>et al</em>., 2009)</a>. Indeed, the motor system is regulated more directly through dopaminergic neurons (think Parkinson).</p>

<blockquote>
  <p>what are your thoughts on the train of thought above? Is there any merit to the hypothesis? </p>
</blockquote>

<p>I think there is merit, but using movement detection with an iphone app, and thinking that a correlation between movement and serotonin signalling implies a causal relation between raphe activity and movement is dodgy. You have to prove this first, either by a solid literature search or through experimental investigation and find support for your hypothesis.</p>

<p><sub><strong>References</strong><br>
<strong>-</strong> <a href="https://www.sciencedirect.com/science/article/pii/S1877042812000626" rel="nofollow noreferrer">Ghaderi <em>et al</em>. <em>Procedia - Social Behav Sci</em> (2012); <strong>32</strong>: 403-10</a><br>
<strong>-</strong> <a href="https://www.sciencedirect.com/science/article/pii/S0959438897801419" rel="nofollow noreferrer">Jacobs &amp; Fomal, <em>Curr Opinion Neurobiol</em> (1997); 7(6): 820-5</a><br>
<strong>-</strong> <a href="http://www.physiology.org/doi/full/10.1152/jn.00507.2009" rel="nofollow noreferrer">Ranade &amp; Mainen, <em>J Physiol</em> (2009); <strong>102</strong>(5): 3026-37</a><br>
<strong>-</strong> <a href="https://www.tandfonline.com/doi/pdf/10.3109/15622970701403081?needAccess=true" rel="nofollow noreferrer">Todder <em>et al</em>., <em>World J Biol Psych</em> (2009); <strong>10</strong>(4): 276-84</a></sub></p>

CC BY-SA 3.0
2018-03-05T09:37:38.560Z
2018-03-05T19:20:06.423Z
2018-03-05T19:20:06.423Z
AliceD
<p>I'm reading this paper, which discusses Serotonin activity in the Dorsal Ralphe Nucleus(DRN), and even includes some mathematical models of how serotonin is released and reabsorbed. The paper states that depressed patients show significant decreases in serotonin both in DRN and outside. The thing that impressed me about this paper is that it gives examples of the <strong>serotonin concentration in DRN in normal person, compared to depressed patient, and the difference is about 80%</strong></p>

<p><a href="http://metabolism.math.duke.edu/docs/SSRIsJ7.pdf" rel="nofollow noreferrer">Bursts and the Efficacy of Selective Serotonin Reuptake
Inhibitors</a></p>

<p>The paper above referenced this excellent paper on how DRN is involved in the regulation of motor activity, and even includes some references to how <strong>DRN is involved in the sleep/wake cycle</strong>. </p>

<p><a href="http://www.princeton.edu/~sswang/awake_cerebellar_ms_refs/jacobs_fornal93_TINS.pdf" rel="nofollow noreferrer">5-HT and motor control: a hypothesis</a></p>

<p>Here's an example of a graph from the article above. It shows how the firing rate of the DRN increases in response to cat's grooming, compared to quiet wakefulness. DRN firing pattern changes in response to movement. Can I reverse this statement to say that <strong>movement indicates DRN activity?</strong> </p>

<p><img src="https://i.sstatic.net/s0wWs.png" alt="Cat DRN activation during waking and grooming"></p>

<p><strong>The hypothesis that I have is that if less Serotonin is available in the DRN as a result of depression, the activity of the DRN as related to motion at night would be different from the normal person.</strong> I hypothesize that by observing the motion of human in bed at night, it may be possible to quantify the activity of DRN, potentially using this information to predict mood fluctuations. </p>

<p>Here's my train of thought - DRN fires differently in response to motion, and motion is accompanied by DRN firing, while muscle atonia is accompanied by total lack of firing. An actigraph has shown that a person (myself and others) moves over the course of the night, in bursts with episodes of total stillness and episodes of burst activity. People move differently in different sleep stages. In cats without atonia (see figure below), DRN gets activated when Rapid Eye Movement(REM) sleep is detected, in response to the cat's actions within the dream, similar to the waking state.. Normally, DRN shows absolutely no firing pattern during REM sleep. <strong>I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days</strong>, where depression can be linked to decreased levels of Serotonin in DRN cells.  </p>

<p>If I understand the <a href="http://metabolism.math.duke.edu/docs/SSRIsJ7.pdf" rel="nofollow noreferrer">Bursts and the Efficacy of Selective Serotonin Reuptake
Inhibitors</a> paper correctly, bursts of electrical activity within the DRN alter Serotonin concentrations for some time after the burst. As such, it seems to me that bursts of electrical activity associated with motion (a typical motion at night is 3-10 seconds) with a large motion observed every 2-3 minutes over the 20 or so minute period that preceedes awakening would have an impact on the Serotonin concentration in the DRN.  </p>

<p><img src="https://i.sstatic.net/n0RBP.png" alt="Cat without atonia"></p>

<p>I'm trying to understand if activation of Dorsal Raphe Nucleus during Rapid Eye Movement sleep can be detected with an <strong>iPhone actigraph</strong>, and if this activation can be quantified, measured and correlated to behavior in the preceeding and subsequent few days. I'm looking to correlate activation of DRN or lack of thereof with the normal, elevated or depressed moods and activity patterns. </p>

<p>An iPhone actigraph measures gross motor activity, which I guess would roughly compare to the EMG from the images above. In this case, the plot is logarithmic, with taller redder bars being orders of magnitude bigger than the baseline "noise" observed by the device. 
<img src="https://i.sstatic.net/QlJKN.png" alt="iPhone actigraph"></p>

<p>Over the past year I've been working on an iPhone actigraph - an app that analyzes user's motion and can be used for sleep studies. On that actigraph, I'm seeing spikes in motion (my sleep) at different sleep phases. The device allows marking of events over night - midnight awakenings, and dream awakenings. </p>

<p>Here's an example of a sleep cycle graph that is drawn based on the observed motion at night. In this case, the deeper the graph, the more still the person is. Red circles indicate insomnia, green circles indicate subsequent dream awakenings. 
<img src="https://i.sstatic.net/IIifN.png" alt="enter image description here"></p>

<p>The device also allows the user to track moods over the course of the day with a very cool Pick A Mood scale and add different events, such as meals, exercise and over 80 other types of events. </p>

<p>Since I'm only an amateur at science and sleep studies, <strong>what are your thoughts on the train of thought above? Is there any merit to the hypothesis?</strong> How would I go about testing it with the technology I outlined?</p>

<p>Thank you for your input!</p>

CC BY-SA 3.0
2012-10-31T00:17:28.903Z
The raphe is only half of the story, unfortunately, as a large proportion of its regulation of mood is through indirect effects on frontal dopaminergic neurons.  Also, the advantage of the study above is that it was done invasively, with electrodes in the brain of the animal, along with invasive EMG electrodes, which pick up a lot more activity from twitches and small movements that an actigraph would never in a million years recognize.  The disadvantage of your system is that it is even further removed from the situation than these recordings are.
Chuck Sherrington
CC BY-SA 3.0
2012-10-31T00:23:07.950Z
I think your project is a neat idea, don't get me wrong, but getting information from the nervous system without interacting with it in a more direct fashion somehow (EEGs, EMGs - even surface ones measuring legs or chin muscles, or some sort of implantable array) is largely guessing, IMO.
Chuck Sherrington
CC BY-SA 3.0
2012-10-31T23:45:59.753Z
Chuck, you are very right, I've been looking at actigraphic output, and even when I know that something is happening (for example, I just woke up from a dream, can estimate the dream's duration), looking at the records is baffling. This is why I was hoping that combining this output with user-reported events would result in a slightly clearer picture.
Alex Stone
CC BY-SA 3.0
2012-10-31T23:47:40.360Z
The only advantage of this study that I can think of if that it that this study can be done over a very long time - my previous attempts at sleep study have 9 months of data night after night.
Alex Stone
CC BY-SA 3.0
2012-10-31T23:55:25.597Z
I haven't read [this article](http://www.ncbi.nlm.nih.gov/pubmed/22078731), but it talks about (with respect to a clinical symptom, but that's not at issue here) alternative methods of detecting REM onset.  You wouldn't have to go all out, but even just recording chin EMG would give you more info than no physiological signals.  If you placed electrodes in a consistent spot that you measure in from some facial feature, it might give you the kind of reproducibility that you want.
Chuck Sherrington
CC BY-SA 3.0
2012-11-01T01:25:19.553Z
One day I will graduate to real xxGram tools. For now I have my actigraph and a commericially available EEG headband (Zeo). I had some success with REM detection - for example in the sleep graph above, blue lines indicate when my app would think the person is dreaming, while Green markers indicate dream awakenings. In many cases the app can predict when the person is dreaming based on the analysis of observed motion.
Alex Stone
CC BY-SA 3.0
2012-11-01T01:40:47.560Z
The thing about commercially available headbands is that they don't use any sort of gel to interface with the scalp, so you really end up with EMGs of the forehead muscles.
Chuck Sherrington
CC BY-SA 3.0
2012-12-30T07:44:16.513Z
Could you use something like fMRI (on the humans) with support from homology studies (in other primates/mammals) that are more invasive?
Keegan Keplinger
<neuroscience><theoretical-neuroscience><mood>
How can I test whether Dorsal Raphe Nucleus (DRN) activity at night is related to variations in mood?
Alex Stone
# How can I test whether Dorsal Raphe Nucleus (DRN) activity at night is related to variations in mood?

(Asked by: username_0 on 2012-10-30)

I'm reading this paper, which discusses Serotonin activity in the Dorsal Ralphe Nucleus(DRN), and even includes some mathematical models of how serotonin is released and reabsorbed. The paper states that depressed patients show significant decreases in serotonin both in DRN and outside. The thing that impressed me about this paper is that it gives examples of the **serotonin concentration in DRN in normal person, compared to depressed patient, and the difference is about 80%**

[Bursts and the Efficacy of Selective Serotonin Reuptake
Inhibitors](http://metabolism.math.duke.edu/docs/SSRIsJ7.pdf)

The paper above referenced this excellent paper on how DRN is involved in the regulation of motor activity, and even includes some references to how **DRN is involved in the sleep/wake cycle**.

[5-HT and motor control: a hypothesis](http://www.princeton.edu/~sswang/awake_cerebellar_ms_refs/jacobs_fornal93_TINS.pdf)

Here's an example of a graph from the article above. It shows how the firing rate of the DRN increases in response to cat's grooming, compared to quiet wakefulness. DRN firing pattern changes in response to movement. Can I reverse this statement to say that **movement indicates DRN activity?**

![Cat DRN activation during waking and grooming](https://i.sstatic.net/s0wWs.png)

**The hypothesis that I have is that if less Serotonin is available in the DRN as a result of depression, the activity of the DRN as related to motion at night would be different from the normal person.** I hypothesize that by observing the motion of human in bed at night, it may be possible to quantify the activity of DRN, potentially using this information to predict mood fluctuations.

Here's my train of thought - DRN fires differently in response to motion, and motion is accompanied by DRN firing, while muscle atonia is accompanied by total lack of firing. An actigraph has shown that a person (myself and others) moves over the course of the night, in bursts with episodes of total stillness and episodes of burst activity. People move differently in different sleep stages. In cats without atonia (see figure below), DRN gets activated when Rapid Eye Movement(REM) sleep is detected, in response to the cat's actions within the dream, similar to the waking state.. Normally, DRN shows absolutely no firing pattern during REM sleep. **I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days**, where depression can be linked to decreased levels of Serotonin in DRN cells.

If I understand the [Bursts and the Efficacy of Selective Serotonin Reuptake
Inhibitors](http://metabolism.math.duke.edu/docs/SSRIsJ7.pdf) paper correctly, bursts of electrical activity within the DRN alter Serotonin concentrations for some time after the burst. As such, it seems to me that bursts of electrical activity associated with motion (a typical motion at night is 3-10 seconds) with a large motion observed every 2-3 minutes over the 20 or so minute period that preceedes awakening would have an impact on the Serotonin concentration in the DRN.

![Cat without atonia](https://i.sstatic.net/n0RBP.png)

I'm trying to understand if activation of Dorsal Raphe Nucleus during Rapid Eye Movement sleep can be detected with an **iPhone actigraph**, and if this activation can be quantified, measured and correlated to behavior in the preceeding and subsequent few days. I'm looking to correlate activation of DRN or lack of thereof with the normal, elevated or depressed moods and activity patterns.

An iPhone actigraph measures gross motor activity, which I guess would roughly compare to the EMG from the images above. In this case, the plot is logarithmic, with taller redder bars being orders of magnitude bigger than the baseline "noise" observed by the device.
![iPhone actigraph](https://i.sstatic.net/QlJKN.png)

Over the past year I've been working on an iPhone actigraph - an app that analyzes user's motion and can be used for sleep studies. On that actigraph, I'm seeing spikes in motion (my sleep) at different sleep phases. The device allows marking of events over night - midnight awakenings, and dream awakenings.

Here's an example of a sleep cycle graph that is drawn based on the observed motion at night. In this case, the deeper the graph, the more still the person is. Red circles indicate insomnia, green circles indicate subsequent dream awakenings.
![enter image description here](https://i.sstatic.net/IIifN.png)

The device also allows the user to track moods over the course of the day with a very cool Pick A Mood scale and add different events, such as meals, exercise and over 80 other types of events.

Since I'm only an amateur at science and sleep studies, **what are your thoughts on the train of thought above? Is there any merit to the hypothesis?** How would I go about testing it with the technology I outlined?

Thank you for your input!

**Tags:** neuroscience, theoretical-neuroscience, mood

> **Comments:**
> **username_1**: The raphe is only half of the story, unfortunately, as a large proportion of its regulation of mood is through indirect effects on frontal dopaminergic neurons.  Also, the advantage of the study above is that it was done invasively, with electrodes in the brain of the animal, along with invasive EMG electrodes, which pick up a lot more activity from twitches and small movements that an actigraph would never in a million years recognize.  The disadvantage of your system is that it is even further removed from the situation than these recordings are.  
> **username_1**: I think your project is a neat idea, don't get me wrong, but getting information from the nervous system without interacting with it in a more direct fashion somehow (EEGs, EMGs - even surface ones measuring legs or chin muscles, or some sort of implantable array) is largely guessing, IMO.  
> **username_0**: Chuck, you are very right, I've been looking at actigraphic output, and even when I know that something is happening (for example, I just woke up from a dream, can estimate the dream's duration), looking at the records is baffling. This is why I was hoping that combining this output with user-reported events would result in a slightly clearer picture.  
> **username_0**: The only advantage of this study that I can think of if that it that this study can be done over a very long time - my previous attempts at sleep study have 9 months of data night after night.  
> **username_1**: I haven't read [this article](http://www.ncbi.nlm.nih.gov/pubmed/22078731), but it talks about (with respect to a clinical symptom, but that's not at issue here) alternative methods of detecting REM onset.  You wouldn't have to go all out, but even just recording chin EMG would give you more info than no physiological signals.  If you placed electrodes in a consistent spot that you measure in from some facial feature, it might give you the kind of reproducibility that you want.  
> **username_0**: One day I will graduate to real xxGram tools. For now I have my actigraph and a commericially available EEG headband (Zeo). I had some success with REM detection - for example in the sleep graph above, blue lines indicate when my app would think the person is dreaming, while Green markers indicate dream awakenings. In many cases the app can predict when the person is dreaming based on the analysis of observed motion.  
> **username_1**: The thing about commercially available headbands is that they don't use any sort of gel to interface with the scalp, so you really end up with EMGs of the forehead muscles.  
> **username_2**: Could you use something like fMRI (on the humans) with support from homology studies (in other primates/mammals) that are more invasive?  

---

## 1 answers

### Answer by username_3 on 2018-03-05. Score: 2

**Short answer**  
To start my post with a cliche - correlation (between raphe activity and movement) does not imply causality. More importantly, the complete absence of the raphe nucleus does not negate movement.

**Background**  
Although I cannot disprove your hypotheses, I do wish to express a word of caution (6 years after your post :-)

> Can I reverse this statement to say that movement indicates DRN activity?

I would be careful with this statement. Activity in the raphe nucleus is positively correlated with behavioral arousal, yes [(Ranade & Mainen, 2009)](http://www.physiology.org/doi/full/10.1152/jn.00507.2009). Further, raphe activity is thought to be related to the level of tonic motor activity associated with gross motor activity and repetitive, central pattern generator mediated responses [(Jacobs & Fomal, 1997)](https://www.sciencedirect.com/science/article/pii/S0959438897801419). Yet, to couple these findings in reverse, and state that one can measure raphe activity through movement detection is tricky. Importantly, there are hosts of studies **where the raphe nucleus was ablated and animals still showed (quite normal) motor activity** (*e.g.* [Ghaderi *et al*. (2012)](https://www.sciencedirect.com/science/article/pii/S1877042812000626)).

> I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days.

It has been shown that successful treatment of depression results in an increase of motor activity. As depression is strongly linked to serotonin signaling this may be an interesting side track. However, increased motor activity was only found for day-time level of movements; clinical improvement was not reflected by night-time measurements. In case of depression, it is thought that activity in the frontal lobe is associated with motor impairments in depression and is related more top dopamine transmission than  
serotonin [(Todder *et al*., 2009)](https://www.tandfonline.com/doi/pdf/10.3109/15622970701403081?needAccess=true). Indeed, the motor system is regulated more directly through dopaminergic neurons (think Parkinson).

> what are your thoughts on the train of thought above? Is there any merit to the hypothesis?

I think there is merit, but using movement detection with an iphone app, and thinking that a correlation between movement and serotonin signalling implies a causal relation between raphe activity and movement is dodgy. You have to prove this first, either by a solid literature search or through experimental investigation and find support for your hypothesis.

**References**  
**-** [Ghaderi *et al*. *Procedia - Social Behav Sci* (2012); **32**: 403-10](https://www.sciencedirect.com/science/article/pii/S1877042812000626)  
**-** [Jacobs & Fomal, *Curr Opinion Neurobiol* (1997); 7(6): 820-5](https://www.sciencedirect.com/science/article/pii/S0959438897801419)  
**-** [Ranade & Mainen, *J Physiol* (2009); **102**(5): 3026-37](http://www.physiology.org/doi/full/10.1152/jn.00507.2009)  
**-** [Todder *et al*., *World J Biol Psych* (2009); **10**(4): 276-84](https://www.tandfonline.com/doi/pdf/10.3109/15622970701403081?needAccess=true)


---

