<p>I'm also self-studying Neuroscience, and my understanding of the topic you're asking about is the following:</p>
<p>You're correct to assume that it's more about neuronal pathways than specific neurotransmitters. This is because you can stimulate neurons via electric current, or by pharmaceuticals to achieve equivalent effect without a particular neurotransmitter.</p>
<p>One example that's easy for me to reason about is Nicotine that mimics neurotransmitter Acetylcholine in nACh receptors. These receptors on a post-synaptic neuron won't tell the difference whether the presynaptic neuron released Acetylcholine, or if you smoked a cigarette and inhaled some Nicotine. It will generate EPSP the same way, and if the action potential is generated, the pathways down the road will take care of the rest to generate improvements in attention, working memory and so on (<a href="https://www.cell.com/trends/neurosciences/fulltext/S0166-2236(20)30125-9" rel="nofollow noreferrer">Do Nicotinic Receptors Modulate High-Order Cognitive Processing?</a>). So <strong>theoretically</strong> you can get rid of the neurotransmitter (Acetylcholine) altogether, fake it with some other substance (Nicotine), and the system overall should work the same.</p>
<p>And from another angle:<br />
To transmit information from neuron to neuron in a specific pathway, you can't just beam electric signal from presynaptic neuron to stimulate postsynaptic neuron. You need to use some neurotransmitter to traverse the space between neurons (synaptic cleft) - presynaptic neuron releases some neurotransmitter, then receptors on the postsynaptic neuron pick it up, open ion channels, and the current causing action potential is generated. With Dopamine, people just figured out that it was a neurotransmitter that happened to be at the synaptic cleft in pathways related to motivation.</p>

CC BY-SA 4.0
2024-08-13T23:26:20.370Z
2024-08-13T23:26:20.370Z
Amade
<p>Sorry very basic question incoming, if you still had time for answering I'd be very happy:)</p>
<p>I'm self studying Neuroscience and I'm confused by the fact that neurotransmitters only make the communication between two neurons, but at the same time have very clear effects in the big scheme of things.</p>
<p>Let's take Dopamin as an example. Before I researched neurotransmitters I intuitively thought that there is some sort of 'Dopamin-gland' and when released into the brain, the Dopamin that is floating around activates some chain reactions.</p>
<p>Now I've learned that in fact dopamin and all other transmitters only act between two neurons. How comes that for certain functions (e.g. motivation) there is a specific transmitter? Why isn't it more about the paths of neurons that get activated instead of the transmitters (That's what I would have expected intuitively)?</p>

<neuroscience><neurophysiology>
How can neurotransmitters have a big-scheme effect when their influence is in fact only between two neurons?
Sven
# How can neurotransmitters have a big-scheme effect when their influence is in fact only between two neurons?

(Asked by: username_0 on 2024-08-10)

Sorry very basic question incoming, if you still had time for answering I'd be very happy:)

I'm self studying Neuroscience and I'm confused by the fact that neurotransmitters only make the communication between two neurons, but at the same time have very clear effects in the big scheme of things.

Let's take Dopamin as an example. Before I researched neurotransmitters I intuitively thought that there is some sort of 'Dopamin-gland' and when released into the brain, the Dopamin that is floating around activates some chain reactions.

Now I've learned that in fact dopamin and all other transmitters only act between two neurons. How comes that for certain functions (e.g. motivation) there is a specific transmitter? Why isn't it more about the paths of neurons that get activated instead of the transmitters (That's what I would have expected intuitively)?

**Tags:** neuroscience, neurophysiology


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## 1 answers

### Answer by username_1 on 2024-08-13. Score: 2 | Accepted answer

I'm also self-studying Neuroscience, and my understanding of the topic you're asking about is the following:

You're correct to assume that it's more about neuronal pathways than specific neurotransmitters. This is because you can stimulate neurons via electric current, or by pharmaceuticals to achieve equivalent effect without a particular neurotransmitter.

One example that's easy for me to reason about is Nicotine that mimics neurotransmitter Acetylcholine in nACh receptors. These receptors on a post-synaptic neuron won't tell the difference whether the presynaptic neuron released Acetylcholine, or if you smoked a cigarette and inhaled some Nicotine. It will generate EPSP the same way, and if the action potential is generated, the pathways down the road will take care of the rest to generate improvements in attention, working memory and so on ([Do Nicotinic Receptors Modulate High-Order Cognitive Processing?](https://www.cell.com/trends/neurosciences/fulltext/S0166-2236(20)30125-9)). So **theoretically** you can get rid of the neurotransmitter (Acetylcholine) altogether, fake it with some other substance (Nicotine), and the system overall should work the same.

And from another angle:  
To transmit information from neuron to neuron in a specific pathway, you can't just beam electric signal from presynaptic neuron to stimulate postsynaptic neuron. You need to use some neurotransmitter to traverse the space between neurons (synaptic cleft) - presynaptic neuron releases some neurotransmitter, then receptors on the postsynaptic neuron pick it up, open ion channels, and the current causing action potential is generated. With Dopamine, people just figured out that it was a neurotransmitter that happened to be at the synaptic cleft in pathways related to motivation.


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