<p>The ability of dopamine to work on different time scales is discussed by <a href="http://www.ncbi.nlm.nih.gov/pubmed/17600522" rel="nofollow">Schultz</a>. More generally, the <a href="http://www.behavioralandbrainfunctions.com/content/1/1/6" rel="nofollow">basic idea of prediction error reinforcement based learning and DA is that the prediction error signal "propagates back in time"</a>. There is <a href="http://www.ncbi.nlm.nih.gov/pubmed/18789964" rel="nofollow">some doubt for how temporally precise this DA signal actually is, and if DA is fast enough to support RPE TD learning.</a></p>

<p>Does that answer the question?</p>

CC BY-SA 3.0
2014-07-09T13:06:47.033Z
2014-07-09T13:06:47.033Z
jona
<p>I just recently learned (indirectly from <a href="http://cnl.salk.edu/~terry/BGGN/reynolds.NN.02.pdf" rel="nofollow">this source</a>) that long-term potentiation/depression only takes place when you have large/small amounts of dopamine present at the relevant synapse. However, my understanding is that early in the process of learning behavior, dopamine isn't released until after a reward is received. If I'm a monkey who has to look one way or the other to get some juice, by the time I drink the juice and get the resulting dopamine, the neurons I used to move my eye are presumably not firing any more, right? So then how does this work? Is it that:</p>

<ol>
<li>There's a slow bootstrapping process. Something like: first the
monkey has to learn that the taste of juice leads to the reward of
sugar. Then the monkey has to learn that the sight of juice
correlates to the taste, and extend the chain one step further,
etc., etc., such that by the time you actually have the monkey in
the lab there's a very small inferential step needed to plug into a
larger reward chain.</li>
<li>The neurons don't actually stop firing. There is some sort of
system in play that keeps the neurons firing afterwards, waiting for
fluctuations in dopamine level to tell it whether or not it should
increase or decrease long term potentiation.</li>
<li>Something I haven't thought of?</li>
</ol>

CC BY-SA 3.0
2014-07-09T11:11:24.217Z
Just a comment to point out that crediting dopamine for neuroplasticity is a tremendous reduction. Does this affect your question at all?
anongoodnurse
CC BY-SA 3.0
2014-07-09T12:56:35.317Z
In a similar vein, much of the cortex doesn't even get any dopaminergic enervation, at least in non-human animals. Yet, plasticity happens.
jona
CC BY-SA 3.0
2014-08-04T17:32:32.240Z
This is generally known as the temporal credit assignment problem (see http://scholarworks.umass.edu/dissertations/AAI8410337/ ) and many different models attempt to explain how it might be solved in various brain systems.
Tim
<plasticity><ltp><dopamine>
How does the timing work out for dopamine to affect the development of long-term potentiation?
Adam Strandberg
# How does the timing work out for dopamine to affect the development of long-term potentiation?

(Asked by: username_0 on 2014-07-09)

I just recently learned (indirectly from [this source](http://cnl.salk.edu/~terry/BGGN/reynolds.NN.02.pdf)) that long-term potentiation/depression only takes place when you have large/small amounts of dopamine present at the relevant synapse. However, my understanding is that early in the process of learning behavior, dopamine isn't released until after a reward is received. If I'm a monkey who has to look one way or the other to get some juice, by the time I drink the juice and get the resulting dopamine, the neurons I used to move my eye are presumably not firing any more, right? So then how does this work? Is it that:

1. There's a slow bootstrapping process. Something like: first the
   monkey has to learn that the taste of juice leads to the reward of
   sugar. Then the monkey has to learn that the sight of juice
   correlates to the taste, and extend the chain one step further,
   etc., etc., such that by the time you actually have the monkey in
   the lab there's a very small inferential step needed to plug into a
   larger reward chain.
2. The neurons don't actually stop firing. There is some sort of
   system in play that keeps the neurons firing afterwards, waiting for
   fluctuations in dopamine level to tell it whether or not it should
   increase or decrease long term potentiation.
3. Something I haven't thought of?

**Tags:** plasticity, ltp, dopamine

> **Comments:**
> **username_1**: Just a comment to point out that crediting dopamine for neuroplasticity is a tremendous reduction. Does this affect your question at all?  
> **username_2**: In a similar vein, much of the cortex doesn't even get any dopaminergic enervation, at least in non-human animals. Yet, plasticity happens.  
> **username_3**: This is generally known as the temporal credit assignment problem (see http://scholarworks.umass.edu/dissertations/AAI8410337/ ) and many different models attempt to explain how it might be solved in various brain systems.  

---

## 1 answers

### Answer by username_2 on 2014-07-09. Score: 1 | Accepted answer

The ability of dopamine to work on different time scales is discussed by [Schultz](http://www.ncbi.nlm.nih.gov/pubmed/17600522). More generally, the [basic idea of prediction error reinforcement based learning and DA is that the prediction error signal "propagates back in time"](http://www.behavioralandbrainfunctions.com/content/1/1/6). There is [some doubt for how temporally precise this DA signal actually is, and if DA is fast enough to support RPE TD learning.](http://www.ncbi.nlm.nih.gov/pubmed/18789964)

Does that answer the question?


---

