Voluntary Motion - Basal Ganglia Flashcards

1
Q

We do not understand a fair amount about the function of the _______ _______, but will focus on these aspects:

– They are involved in the planning and programming of movement.

– Their input is particularly important in the initiation of movement.

A

Basal Ganglia

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2
Q

Basal Ganglia control the beginning and (to a lesser extent) the end of the movement. They work by inhibition and withdrawal of that inhibition (to start the movement). Frequently descried as an “excess of _______”.

A

GABA

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3
Q

The Basal Ganglia have a direct and indirect pathway. When activated, the direct pathway is ________ to motion.

A

Permissive

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4
Q

Put the following steps of the Striatonigal GABA-ergic pathway (direct pathway) in order:

A. Inhibition of the neurons in the SNPR and GPi

B. Axons from the striatum project to the SNPR and GPi

C. Presynaptic terminal releases GABA in the SNPR and GPi

A

1) B.
2) C.
3) A.

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5
Q

The Basal Ganglia have a direct and indirect pathway. When activated, the the indirect pathway is _________ to motion.

A

Inhibitory

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6
Q

Put the following steps of the basal ganglia indirect pathway in order:

A. Axons from the subthalamic nucleus travel to the SNPR and GPi and release EAA.

B. Axons from the SNPR and GPi travel to the thalamus and release GABA.

C. Axons from the striatum project to the external segment of the Globus Pallidus and release GABA.

D. Axons from the GPe travel to the subthalamic nucleus and release GABA.

A

1) C.
2) D.
3) A.
4) B.

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7
Q

The (D1/D2) dopamine receptor is involved in the indirect pathway, while the (D1/D2) dopamine receptor is involved in the direct pathway.

A

D2

D1

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8
Q

This is what produces the dopamine to be released in the striatum and attach to either D1 or D2 receptors.

A

Substantia Nigra pars compacta (SNPC)

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9
Q

Describe the direct pathway once dopamine has bound to D1.

A

The binding of dopamine to D1 creates an EPSP, which depolarizes the neurons going from the striatum to the SNPR/GPi. The depolarization causes increased GABA release at the SNPR/GPi, which in turn creates an IPSP. This IPSP hyperpolarizes the neurons going to the Thalamic Nucleus, causing there to be decreased levels of GABA. Since there is less GABA, the Thalamic Nucleus is able to send out EAA via its Thalamocortical Neurons.

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10
Q

Describe the indirect pathway once dopamine has bound to D2.

A

The binding of dopamine to D2 creates an IPSP, which hyperpolarizes the neurons and decreases the release of GABA going to the GPe neuron. This decrease in GABA allows the GPe neuron to depolarize and increase the release of GABA at the Subthalamic neuron. The increased GABA at the Subthalamic neuron creates an IPSP, which decreases the amount of action potentials and the EAAs going to the SNPR/GPi. The decreased APs and EAAs help create the IPSP at the SNPR/GPi, which then goes on to follow the exact same path through the thalamus as in the direct pathway.

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11
Q

By activating the direct pathway and inactivating the indirect pathway, dopamine is ________ to motion.

A

Permissive

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12
Q

Describe how Parkinson’s disease works with dopamine/

A

In Parkinson’s, there is an inability to initiate motion. This is because the SNPC input is abolished. This has two effects:

1) The direct pathway becomes difficult to activate.
2) The indirect pathway becomes overactive (due to loss of inhibition).

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13
Q

To produce motion we must:

    • (INACTIVATE/ACTIVATE) the direct pathway
    • (INACTIVATE/ACTIVATE) the indirect pathway
A

Activate

Inactivate

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14
Q

Explain how we suppress motion via the indirect pathway.

A

EAA (from the cortex) and ACh (from intrastriatal cholinergic pathway) cause an EPSP at the start of the pathway in the Striatum. This EPSP causes the neurons to depolarize and allow an increase of GABA at the GPe neurons. This increased GABA creates an IPSP at the GPe neurons, which decreases the release of GABA at the Subthalamic Neurons. Decreased GABA at the Subthalamic Neurons causes the neurons to depolarize, increasing the action potentials and release of EAA at the SNPR/GPi. This causes an EPSP at the SNPR/GPi, which increases GABA release at the Thalamic Nucleus, making an IPSP. This IPSP decreases the release of EAA from the Thalamic Nucleus, thus suppressing motion.

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15
Q

In this disease, the indirect pathway can’t be turned on to suppress motion.

A

Huntington’s Chorea

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16
Q

This cortex has two major functions, including planning of complex motor actions and carrying out of “thought” processes.

A

Prefrontal cortex

17
Q

T/F. Interactions between the frontal, premotor, SMC, and the basal ganglia (dopamine) determine IF the motion will occur.

A

True

18
Q

Once the motion is planned, sequenced, and ‘approved’, the appropriate columns in the _______ _______ _______ are activated.

A

Primary motor cortex

19
Q

Once the columns are activated, action potentials then travel down the axons of the pyramidal (Betz) cells and activate the ________ ________ that innervate the muscles needed to complete the motion.

A

Alpha-motor Neurons

20
Q

The problem with the alpha-motor neurons being activated is the muscle spindle, because it will oppose every motion we make unless we do something about it. This happens because…

A

Every motion we make stretches one or more muscles!

***Remember, the muscle spindle (specifically intrafusal fibers) are sensitive to the change in length from stretching

21
Q

How does the brain solve the problem of the muscle spindles when activating alpha-motor neurons?

A

By using the gamma-motor neurons to reduce the sensitivity of the muscle spindles in the antagonist muscle.

***Remember, by activating the gamma-motor neurons, it contracts the ends of the intrafusal fibers and stretches the sensory portions (nuclear chain and bag). Stretching the sensory portion keeps it sensitive to stretch and allows it to work along with the extrafusal fibers so you don’t get hurt.

22
Q

To make motion occur, if the brain activates the alpha-motor neurons then it also activates the gamma-motor neurons for spindles in the contracting (_______) msucle. This is called alpha-gamma coactivation.

A

Agonist

***Active, sensitive to length change (without the gamma-motor neurons, the spindles would be limp and not pulled taut to assist the extrafusal fibers)

23
Q

To make motion occur, if the brain inhibits the alpha-motor neuron, it also inhibits the gamma-motor neurons for spindles in the stretching (________) muscle.

A

Antagonist

***Inactive, not sensitive to stretch (because we need this muscle to be stretching)

24
Q

Once the motion has started, the _________ is called upon to make sure the motion is correct!

A

Spinocerebellum