asaaal
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I have the WORST lecture notes for the pathophysiology !! its a massive complicated flow chart involving dopamine, Glu, GABA.

Can someone link me to an easy website because I cannot find anything which mentions all three neurotransmitters. (No luck in the books I always use for this lecturer either)

Thank you!!!
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riglerssign
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(Original post by asaaal)
I have the WORST lecture notes for the pathophysiology !! its a massive complicated flow chart involving dopamine, Glu, GABA.

Can someone link me to an easy website because I cannot find anything which mentions all three neurotransmitters. (No luck in the books I always use for this lecturer either)

Thank you!!!
I found this video explained it very well:

https://youtu.be/Mz_tEu835Yg


It animates it well and talks about how all the drugs work at the different receptors
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courvoisier
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(Original post by riglerssign)
I found this video explained it very well:

https://youtu.be/Mz_tEu835Yg


It animates it well and talks about how all the drugs work at the different receptors
Thanks for this, it's very useful!
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asaaal
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(Original post by riglerssign)
I found this video explained it very well:

https://youtu.be/Mz_tEu835Yg


It animates it well and talks about how all the drugs work at the different receptors
sorry stupid question but is dopamine purely excitatory?
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asaaal
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'Loss of the inhibitory effect of dopamine results in more production of acetylcholine, which triggers a chain of abnormal signalling leading to impaired mobility'

I thought dopamine was excitatory therefore as lower levels are present in parkinsons it causes slowed movement etc. - The orange text suggests its inhibitory?


Also, acetylcholine is excitatory?
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thegodofgod
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(Original post by asaaal)
sorry stupid question but is dopamine purely excitatory?
Not to my knowledge; I know it is inhibitory with regards to lactation, it inhibits the release of prolactin from the PP, and this effect is reversed by administering a dopamine antagonist, which induces lactation (Guillaume et al. Reprod Domest Anim 2003; 38(5): 394-400).
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asaaal
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(Original post by thegodofgod)
Not to my knowledge; I know it is inhibitory with regards to lactation, it inhibits the release of prolactin from the PP, and this effect is reversed by administering a dopamine antagonist, which induces lactation (Guillaume et al. Reprod Domest Anim 2003; 38(5): 394-400).
so why does it cause slowed movement if its inhibitory? :confused:
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thegodofgod
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(Original post by asaaal)
so why does it cause slowed movement if its inhibitory? :confused:
It is not just inhibitory, it can be excitatory too - I was under the impression that it is one of the rare neurotransmitters that exhibit both excitatory and inhibitory actions.

EDIT:

Akaike et al. Brain Res 1987; 418(2): 262-72.
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Letournel
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http://www.neuroanatomy.wisc.edu/coursebook/motor2.pdf
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purplefrog
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Dopamine is both excitatory and inhibitory in the basal ganglia. It depends on the receptor. Broadly speaking, the D1 receptors are excitatory for the direct pathway and D2 receptors are inhibitory for the indirect pathway.
I'm sure somebody with more detailed neuroscience knowledge or with a neuro BSc may wish to elaborate on this or refine my generalisation.
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asaaal
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(Original post by riglerssign)
I found this video explained it very well:

https://youtu.be/Mz_tEu835Yg


It animates it well and talks about how all the drugs work at the different receptors

(Original post by thegodofgod)
Not to my knowledge; I know it is inhibitory with regards to lactation, it inhibits the release of prolactin from the PP, and this effect is reversed by administering a dopamine antagonist, which induces lactation (Guillaume et al. Reprod Domest Anim 2003; 38(5): 394-400).



okay so my question is trying to sort out the dopamine-acetylcholine balance in my head.

Dopamine and acetylcholine are both excitatory. Parkinson's disease = dopamine reduction and normal amount of excitatory acetylcholine.
Direct pathway dopamine = increases movement and indirect pathway dopamine = decreases movement

How does all of this come together?

Provided me with some great sources here guys, thanks !
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Letournel
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(Original post by asaaal)
okay so my question is trying to sort out the dopamine-acetylcholine balance in my head.

Dopamine and acetylcholine are both excitatory. Parkinson's disease = dopamine reduction and normal amount of excitatory acetylcholine.
Direct pathway dopamine = increases movement and indirect pathway dopamine = decreases movement

How does all of this come together?

Provided me with some great sources here guys, thanks !
Take some time to read the resource i linked you, it explains this and was invaluable to me back in 2nd year.

The action of dopamine on the indirect pathway doesn't inhibit movement. In the striatum dopamine acts on D2 receptors which are associated with the indirect pathway and inhibits. The result is inhibition of the indirect pathway which means less inhibition to the thalamus. At the same time it excited D1 receptors. D1 receptors are associated with the direct pathway portion of the striatum which means more excitation to the thalamus. Inhibition of indirect + excitation of the direct = more movement.

Ach is basically the opposite. It inhibits the direct pathway and excited the indirect pathway
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Letournel
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(Original post by asaaal)
okay so my question is trying to sort out the dopamine-acetylcholine balance in my head.

Dopamine and acetylcholine are both excitatory. Parkinson's disease = dopamine reduction and normal amount of excitatory acetylcholine.
Direct pathway dopamine = increases movement and indirect pathway dopamine = decreases movement

How does all of this come together?

Provided me with some great sources here guys, thanks !
My above comment is a little unclear, it was written at pace. Basically:

D1 receptor - Located in striatum associated with the direct pathway. Dopamine excites. Results in increased excitation of direct pathway and as a result thalamus and therefore excitation.

D2 receptor - Located in striatum associated with indirect pathway. Dopamine inhibits. Results in increased in inhibition of the indirect pathway and as a result decreased inhibition of the thalamus. This leads to 'unapposed' excitation by direct and therefore movement
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Sinatrafan
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My take on it that I wrote during my neuroscience masters.

"Neuronal loss in the subtantia ***** pars compacta (SNc) occurs in PD. Along with the striatum, pallidum and subthalamic nucleus (STN), these nuclei make up the basal ganglia (BG); the group of nuclei involved in the initiation of movement. How the basal ganglia co-ordinates movement is typically described by the direct/indirect pathway model. In this model the direct pathway stimulates movement and the indirect pathway inhibits movement.

In the direct pathway, the ventral striatum receives excitatory glutamatergic signals from the motor cortex. The ventral striatum then sends GABAergic signals to the globus pallidus interna (GPi) and substantia ***** reticulata (SNr). These two nuclei then relay GABAergic signals to the thalamus, which stimulates the thalamus into sending excitatory glutamatergic signals back to the motor cortex. The motor cortex is therefore stimulated into sending motor commands to the rest of the body and inducing movement. This pathway is largely under tonic GABAergic inhibition, so stimulating the nuclei with more inhibitory GABAergic signals decreases inhibition and has an excitatory effect on nuclei output.

The indirect pathway also begins with excitatory input into the ventral striatum from the motor cortex. In this pathway however, GABAergic signals are then sent to the globus pallidus externa (GPe) rather than the GPi. This frees the STN from inhibition and promotes STN output. The STN's output inhibits the GPi and SNr, and stops excitatory motor commands being sent to the thalamus and then on to the motor cortex.

Within this model, the SNc acts directly on the ventral striatum to regulate its output through dopaminergic neurons. Dopamine stimulates the direct pathway through D1 receptors and inhibits the indirect pathway through D2 receptors. In PD, loss of dopaminergic neurons means that direct stimulation of movement is reduced and inhibition of movement from the indirect pathway goes unopposed. This leads to a reduction of motor output."
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asaaal
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(Original post by Sinatrafan)
My take on it that I wrote during my neuroscience masters.

"Neuronal loss in the subtantia ***** pars compacta (SNc) occurs in PD. Along with the striatum, pallidum and subthalamic nucleus (STN), these nuclei make up the basal ganglia (BG); the group of nuclei involved in the initiation of movement. How the basal ganglia co-ordinates movement is typically described by the direct/indirect pathway model. In this model the direct pathway stimulates movement and the indirect pathway inhibits movement.

In the direct pathway, the ventral striatum receives excitatory glutamatergic signals from the motor cortex. The ventral striatum then sends GABAergic signals to the globus pallidus interna (GPi) and substantia ***** reticulata (SNr). These two nuclei then relay GABAergic signals to the thalamus, which stimulates the thalamus into sending excitatory glutamatergic signals back to the motor cortex. The motor cortex is therefore stimulated into sending motor commands to the rest of the body and inducing movement. This pathway is largely under tonic GABAergic inhibition, so stimulating the nuclei with more inhibitory GABAergic signals decreases inhibition and has an excitatory effect on nuclei output.

The indirect pathway also begins with excitatory input into the ventral striatum from the motor cortex. In this pathway however, GABAergic signals are then sent to the globus pallidus externa (GPe) rather than the GPi. This frees the STN from inhibition and promotes STN output. The STN's output inhibits the GPi and SNr, and stops excitatory motor commands being sent to the thalamus and then on to the motor cortex.

Within this model, the SNc acts directly on the ventral striatum to regulate its output through dopaminergic neurons. Dopamine stimulates the direct pathway through D1 receptors and inhibits the indirect pathway through D2 receptors. In PD, loss of dopaminergic neurons means that direct stimulation of movement is reduced and inhibition of movement from the indirect pathway goes unopposed. This leads to a reduction of motor output."

(Original post by plrodham1)
My above comment is a little unclear, it was written at pace. Basically:

D1 receptor - Located in striatum associated with the direct pathway. Dopamine excites. Results in increased excitation of direct pathway and as a result thalamus and therefore excitation.

D2 receptor - Located in striatum associated with indirect pathway. Dopamine inhibits. Results in increased in inhibition of the indirect pathway and as a result decreased inhibition of the thalamus. This leads to 'unapposed' excitation by direct and therefore movement

(Original post by plrodham1)
Take some time to read the resource i linked you, it explains this and was invaluable to me back in 2nd year.

The action of dopamine on the indirect pathway doesn't inhibit movement. In the striatum dopamine acts on D2 receptors which are associated with the indirect pathway and inhibits. The result is inhibition of the indirect pathway which means less inhibition to the thalamus. At the same time it excited D1 receptors. D1 receptors are associated with the direct pathway portion of the striatum which means more excitation to the thalamus. Inhibition of indirect + excitation of the direct = more movement.

Ach is basically the opposite. It inhibits the direct pathway and excited the indirect pathway

How can you get tremors and get slow muscle movement and increased tone all with PD. They contradict each other right?

Also low dopamine reduces dopamine in direct excitatory pathway and indirect excitatory pathway, so how is the excitatory pathway favoured?
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asaaal
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anyone?
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