I should know this but, can someone clarify dopamine vs acetylcholine?

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Knicks

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When it comes to these 2 neurotransmitters and motor movement, is dopamine needed to initiate movement or Ach?

Because I know that dopamine stimulates the direct pathway in the basal ganglia, and thus PROMOTES movement.

But what about Ach? Does it promote movement as well?

I thought dopamine promotes/initiates movement and Ach stops the movement.


HaLp 😀

EDIT: In myesthenia gravis, you have muscle weakness because there are antibodies that attack post-synaptic Ach receptors, thereby preventing Ach from binding to these receptors.

So I still wanna know the difference between Dopamine and Ach in regards to muscle motor movement.
 
I should probably go look this up, but I think Ach inhibits movement or at least suppresses dopamine's promotion of movement. That's why they give people with Parkinson's anticholinergics.

I just googled this, and apparently Ach stimulates GABA.

http://www.med.howard.edu/pharmacology/handouts/parkinsons.htm
 
ACh is the transmitter present at the neuromuscular junction which initiates the actual muscle contraction. Dopamine in the CNS regulates central production of movement. Hope that helps.
 
When it comes to these 2 neurotransmitters and motor movement, is dopamine needed to initiate movement or Ach?

Because I know that dopamine stimulates the direct pathway in the basal ganglia, and thus PROMOTES movement.

But what about Ach? Does it promote movement as well?

I thought dopamine promotes/initiates movement and Ach stops the movement.


HaLp 😀

EDIT: In myesthenia gravis, you have muscle weakness because there are antibodies that attack post-synaptic Ach receptors, thereby preventing Ach from binding to these receptors.

So I still wanna know the difference between Dopamine and Ach in regards to muscle motor movement.

If you're talking about the basal ganglia, I find this pretty confusing as well, but my understanding is that dopamine stimulates the direct pathway, thus increasing movement, as mentioned above. The indirect pathway has an inhibitory effect on movement and is stimulated via interneurons using acetylcholine as the neurotransmitter. Thus, when you block Ach with a drug like benztropine and and inhibit the indirect pathway, you shift the balance to the direct pathway and improve symptoms.

If you have a copy of Blumenfield handy, this book has the best discussion I've seen of this; check out p700-701.
 
ACh is the transmitter present at the neuromuscular junction which initiates the actual muscle contraction. Dopamine in the CNS regulates central production of movement. Hope that helps.

What's the difference between "central production of movement" and peripheral production of movement?

Because, doesn't your arm move because your brain tells your arm to move? So shouldn't all movement intiated by dopamine?

What's this "central" talk?
 
I don't feel like getting into all the details, but I'll point out that there is the pyramidal motor system and the extra-pyramidal motor system. Each has distinctive functions and pathways, with some common components and feedback loops. But the biggest thing to remember is that neurotransmitters wear many different hats depending on where in the body they are being used... NO, Ach, Dopamine, etc.

Very, very grossly speaking, Ach is the neurotransmitter in the pyramidal system that communicate actions from the cortex to the muscle fiber, and it is the neurotransmitter in the extrapyramidal system that puts the brakes on the actions of Dopamine.

Again, very grossly, think of the pyramidal system as stuff like purposefully touching your finger to your nose (though there is a lot of fine control exhibited by the extrapyramidal system), and the extrapyramidal system as stuff like "instinctively" batting away something thrown at your head (edit: well, that's probably as much cerebellar as extrapyramidal... neuro is one area where I can answer the question right, but probably shouldn't teach it!).
 
.....still lost 🙁 lol

Maybe it's cuz I'm extremely tired at the moment. 😳
 
EDIT: In myesthenia gravis, you have muscle weakness because there are antibodies that attack post-synaptic Ach receptors, thereby preventing Ach from binding to these receptors.

So I still wanna know the difference between Dopamine and Ach in regards to muscle motor movement.

myasthenia gravis is a neuromuscular junction disorder.

------------
What does it do?

The basal ganglia is responsible for:
1) maintaining muscle tone
2) initiating and stopping movement

Think of it as an inhibitory system that keeps movement under control.

What happens when its damaged/impaired?
1) increased muscle tone
2) problem initiating and stopping movement


When you want to move:
Caudate + Putamen --> GP --> Thalamus (VA/VL) --> pre-motor cortex --> motor cortex --> brainstem, spinal cord, etc etc

(Mood Disorders are also common in patient's with movement disorders, commonly depression)
 
What's the difference between "central production of movement" and peripheral production of movement?

Because, doesn't your arm move because your brain tells your arm to move? So shouldn't all movement intiated by dopamine?

What's this "central" talk?

There isn't one single neuron that goes from your brain right to your biceps. The nerve that actually activates the muscle releases ACh. Also, the DA pathways that are involved with movement deal more with a sub-cortical "fine tuning" of movement as opposed to the initiation of movement, which is done in the motor cortex. Hope that makes sense.
 
There isn't one single neuron that goes from your brain right to your biceps. The nerve that actually activates the muscle releases ACh. Also, the DA pathways that are involved with movement deal more with a sub-cortical "fine tuning" of movement as opposed to the initiation of movement, which is done in the motor cortex. Hope that makes sense.

I'd have to disagree. Cerebellum is involved in the fine tuning of movement. Basal ganglia is involved in initation/stopping movement, and muscle tone.

Hence, in Parkinson's Disease, patients have trouble initiating movement and often fall. They have a lack of facial expression due to the increased muscle tone.
 
I'd have to disagree. Cerebellum is involved in the fine tuning of movement. Basal ganglia is involved in initation/stopping movement, and muscle tone.

Hence, in Parkinson's Disease, patients have trouble initiating movement and often fall. They have a lack of facial expression due to the increased muscle tone.

Yes, the cerebellum is involved in fine-tuning, as well as balance and coordination. The basal ganglia also fine-tunes, in the sense that it receives input from the primary motor cortex and modulates this motor input through feedback loops so that the movement is appropriate. If you have Parkinson's disease and basal ganglia is malfunctioning, it is harder to initiate and stop movements, but not impossible. On the other hand, if the motor cortex is damaged, it would be impossible to move at all (on the opposite side of the body).
 
When it comes to these 2 neurotransmitters and motor movement, is dopamine needed to initiate movement or Ach?

Because I know that dopamine stimulates the direct pathway in the basal ganglia, and thus PROMOTES movement.

But what about Ach? Does it promote movement as well?

I thought dopamine promotes/initiates movement and Ach stops the movement.


HaLp 😀

EDIT: In myesthenia gravis, you have muscle weakness because there are antibodies that attack post-synaptic Ach receptors, thereby preventing Ach from binding to these receptors.

So I still wanna know the difference between Dopamine and Ach in regards to muscle motor movement.


.....still lost 🙁 lol

Maybe it's cuz I'm extremely tired at the moment. 😳

The reason why you are having difficulty in understanding the role of these neurotransmitters is that they work differently in different parts of the body and at different points along moter pathways - and you are trying to generalize.
 
P.S. For Step 1, you don't have to know about any neurotransmitter role in the basal ganglia OTHER than dopamine. Forget those insanely complex feedback loops, ACh, etc. Know dopamine's role in Parkinson's and Huntington's.
 
I don't feel like getting into all the details, but I'll point out that there is the pyramidal motor system and the extra-pyramidal motor system. Each has distinctive functions and pathways, with some common components and feedback loops. But the biggest thing to remember is that neurotransmitters wear many different hats depending on where in the body they are being used... NO, Ach, Dopamine, etc.

Very, very grossly speaking, Ach is the neurotransmitter in the pyramidal system that communicate actions from the cortex to the muscle fiber, and it is the neurotransmitter in the extrapyramidal system that puts the brakes on the actions of Dopamine.

Again, very grossly, think of the pyramidal system as stuff like purposefully touching your finger to your nose (though there is a lot of fine control exhibited by the extrapyramidal system), and the extrapyramidal system as stuff like "instinctively" batting away something thrown at your head (edit: well, that's probably as much cerebellar as extrapyramidal... neuro is one area where I can answer the question right, but probably shouldn't teach it!).

One of these days, when you have time, can you get into the details? Because I was just re-reading this stuff again and I remembered this thread I made.

P.S. For Step 1, you don't have to know about any neurotransmitter role in the basal ganglia OTHER than dopamine. Forget those insanely complex feedback loops, ACh, etc. Know dopamine's role in Parkinson's and Huntington's.
^^ You sure about that?
 
One of these days, when you have time, can you get into the details? Because I was just re-reading this stuff again and I remembered this thread I made.


^^ You sure about that?

Although the direct and indirect pathways are present in kaplan neuro and HY neuro, I tend to agree with the above poster that all you really need to know is dopamine's effect in disease states. The neuro on the exam was not as terribly in depth as you might expect from reading HY.
 
^^ But seeing as how each test is different, I always take statements like "so and so is/was not high yeild on the test" with a grain of salt.

Nothing against you personally. 🙂
 
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