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Action & Perception > 11. Motor Control 2 > Flashcards

11. Motor Control 2 Flashcards

1
Q

What is the role of the basal Ganglia?

A
  • control of movement - helps release movements at the right time.
  • Different BG loops project to different cortical areas – cognitive as well as motor functions.
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2
Q

Neurotransmitter between the Substantia Nigra pars compacta (SNc) and the Putamen.

A

Glutamate

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3
Q

Neurotranmitter between the Putamen and the Lateral Globus Pallidus (GPl), Medial Globus Pallidus (GPm) and Subthalamic nucleus (STN).

A

GABA

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4
Q

Neurotranmitter between the Medial Globus Pallidus (GPm) and the Thalamus.

A

GABA

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5
Q

Neurotransmitter between Subthalamic nucleus (STN) and the Medial Globus Pallidus (GPm).

A

Glutamate

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6
Q

Neurotransmitter between the Thalamus and the Motor Cortex.

A

Glutamate

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7
Q

Neurotransmitter between the motor cortex and the Putamen

A

Glutamate

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8
Q

Is Glutamate excitatory or inhibitory?

A

excitatory

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9
Q

Is GABA excitatory or inhibitory?

A

inhibitory

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10
Q

Is Dopamine excitatory or inhibitory?

A
  • excitatory for BG direct pathway

- inhibitory for BG indirect pathway

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11
Q

What is the direct basal ganglia pathway?

A
  • It’s an excitatory pathway.

- It allows desired movements to occur

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12
Q

What is the indirect basal ganglia pathway?

A

Putamen → Lateral Globus Pallidus (external) (GPl) → Subthalamic nucleus (STN)

  • longer than the direct pathway.
  • It prevents undesired movement occurring
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13
Q

Putamen (Striatum) receives input from what?

A

The cortical areas of the motor cortex.

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14
Q

What does the GPm do in the basal ganglia circuit?

A

projects back to the cortex.

GPm → Thalamus → Motor cortex

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15
Q

What are the stages in the Direct BG Pathway?

A
  1. Excitatory signal from cortex
  2. Increased inhibitory signal from Putamen to GPm
  3. Reduced inhibitory signal from GPm to Thalmus
  4. Increased excitatory signal from thalamus to motor cortex
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16
Q

What are the stages in the Indirect Pathway?

A
  1. Increased inhibitory signal from Putamen to GPl
  2. Reduced inhibitory signal from GPl to STN
  3. Increased excitatory input to GPm
  4. Increased inhibitory output to thalamus
  5. Reduced excitatory output to cortex
17
Q

Describe the movement selection mechanism in the basal ganglia.

A
  • Different possible movements
  • Desired movement is ‘disinhibited’ (or released)
  • Competing movements are inhibited (and prevented from occurring)
18
Q

What are the main 3 disorders associated with the basal ganglia?

A
  • Parkinson’s disease
  • Huntington’s disease
  • Tourrette syndrome
19
Q

What is the effect of the lack of dopamine in Parkinson’s disease on the basal ganglia pathways?

A

○ Underactive direct pathway (increased GPm activity)
○ Overactive indirect pathway (increased GPm activity)

Both lead to increased inhibition of the thalamus and reduced excitation of the cortex

20
Q

What is the treatment for Parkinson’s disease?

A
  • L-dopa but drug induced dyskinesias
    ○ Newer dopaminergic drugs
  • Surgery – lesions and deep brain stimulation
21
Q

What is DBS?

A

Deep brain stimulation

  • Battery-operated stimulator delivers electrical stimulation to targeted areas
  • Targets - thalamus, subthalamic nucleus, and globus pallidus
22
Q

What does Deep brain stimulation do to help Parkinsons?

A
  • Reduces effect of indirect pathway
  • Reduced activity in the STN
  • Reduced excitation of the GPm
  • Reduced inhibition of the thalamus
  • Greater excitation of the motor cortex
23
Q

Describe Huntington’s Disease.

A
  • inherited, autosomal dominant condition
  • Onset in 30’s or 40’s
  • Chorea – uncontrolled movements
  • Degeneration of putamen and caudate
  • Death from complications
  • No treatment at present
24
Q

What happens in the brain in people with Huntington’s disease?

A
  • enlarged lateral ventricles

- Cortical degeneration

25
Q

What happens to the basal ganglia circuitry in people with Huntington’s disease?

A
  • Underactivity of Indirect pathway
  • Reduced inhibition of GPl
  • Increased inhibition of STN
  • Reduced activity of GPm
    ==>Too much movement
26
Q

What are the cognitive impairments associated with Huntington’s disease?

A 
○ Attention
○ Executive function 
○ Speed of processing
○ Prospective memory 
○ Emotion recognition
27
Q

What are the symptoms seen in Tourette’s sysndrome?

A
  • Simple tics e.g. eye blinking, nose twitching
  • Complex tics e.g. scratching, gestures, utterances
  • May increase during times of stress and decrease when concentrating
28
Q

What is Tourette’s Syndrome?

A
  • > 1000 per 100,000 children (greater than 1 in 1000)
  • Hereditary
  • Links to obsessive-compulsive behaviours
  • Developmental
  • 4x more common in boys tha girls
29
Q

What occurs in the basal ganglia to cause Tourette’s syndrome?

A
  • Increased dopamine from substantia nigra

- Overactivity of the direct pathway – leads to ‘disinhibition’ of an unwanted movement

30
Q

Describe the aberrant selection of movement in the Basal Ganglia in people with Tourette’s Syndrome.

A
  • ‘Aberrant focus’ of activity in striatum leads to activity in the direct pathway
  • And disinhibition of undesired movement
  • May also explain obsessive compulsive behaviours

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