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NBoVA > W8 - Basal Ganglia > Flashcards

W8 - Basal Ganglia Flashcards

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1
Q

What is the basal ganglia and why is it considered evolutionarily “old”?

A

It’s a group of subcortical nuclei that predates the neocortex and plays a key role in motor control, motivation, and action selection.

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2
Q

Which brain regions does the basal ganglia interact with?

A

It interacts with motor and prefrontal cortical areas via the thalamus, and with the limbic system affecting emotion and motivation.

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3
Q

What are the main input nuclei of the basal ganglia?

A

The striatum (caudate, putamen, nucleus accumbens), which receives input from the cortex.

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4
Q

What are the output structures of the basal ganglia?

A

GPi (globus pallidus internal) and SNr (substantia nigra pars reticulata).

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5
Q

Where is the basal ganglia located?

A

It is a subcortical structure lateral to the thalamus and deep within the cerebral hemispheres.

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6
Q

What is the role of the direct pathway?

A

It facilitates movement by disinhibiting the thalamus.

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7
Q

Describe the direct pathway.

A

Cortex → Striatum → GPi/SNr → Thalamus → Cortex.

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8
Q

What is the role of the indirect pathway?

A

It inhibits movement by increasing inhibition to the thalamus via the STN.

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9
Q

Describe the indirect pathway.

A

Cortex → Striatum → GPe → STN → GPi/SNr → Thalamus → Cortex.

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10
Q

What determines the balance between movement facilitation and inhibition in the basal ganglia?

A

Dopamine release from the substantia nigra pars compacta (SNc), which modulates activity in the striatum.

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11
Q

Where is dopamine in the basal ganglia produced?

A

In the substantia nigra pars compacta (SNc).

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12
Q

What are the two main dopamine receptor types in the striatum, and what do they do?

A

D1: Excitatory to the direct pathway. D2: Inhibitory to the indirect pathway.

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13
Q

What is the overall effect of dopamine on movement?

A

It facilitates movement by activating the direct pathway and inhibiting the indirect pathway.

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14
Q

What causes Parkinson’s Disease?

A

Progressive loss of dopaminergic neurons in the SNc, leading to striatal dopamine depletion.

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15
Q

How does Parkinson’s disease affect basal ganglia pathways?

A

Weakens the direct pathway and strengthens the indirect pathway, reducing movement.

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16
Q

What motor symptoms are typical in Parkinson’s Disease?

A

Akinesia, bradykinesia, resting tremor, rigidity.

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17
Q

What non-motor symptoms are common in Parkinson’s?

A

Postural instability, gait abnormalities, depression, sleep issues, loss of smell, cognitive dysfunction, and speech/swallowing difficulties.

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18
Q

Why is Parkinson’s considered a unique neurological condition?

A

It’s caused primarily by a single neurochemical disruption (dopamine loss), and responds well to targeted chemical therapies like L-DOPA.

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19
Q

What is L-DOPA and how does it help?

A

It’s a dopamine precursor that crosses the blood-brain barrier to temporarily restore dopamine levels.

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20
Q

What are potential long-term issues with L-DOPA therapy?

A

Motor fluctuations and dyskinesia.

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21
Q

What surgical treatments exist for Parkinson’s?

A
  1. Deep brain stimulation (DBS), typically in the STN or GPi. 2. Thalamotomy or pallidotomy (lesioning overactive nuclei).
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22
Q

What experimental therapies are being explored?

A

Stem cell transplants (embryonic/adult), bone marrow-derived cells.

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23
Q

What causes hyperkinetic movement disorders?

A

Excess activity in the direct pathway and/or reduced activity in the indirect pathway.

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24
Q

Name three hyperkinetic disorders linked to basal ganglia dysfunction.

A
  1. Huntington’s disease – degeneration of striatal neurons. 2. Hemiballismus – damage to the subthalamic nucleus (STN). 3. Tourette’s syndrome – linked to dopaminergic imbalance and BG circuitry.
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25
What functional loop do the basal ganglia participate in?
The cortico-striatal-thalamo-cortical loop.
26
What roles do the direct and indirect pathways play in action selection?
Direct = initiates action ("Go"). Indirect = suppresses action ("Stop")
27
How does dopamine influence action selection?
By exciting the direct pathway and inhibiting the indirect, it biases selection toward initiating action.
28
How do basal ganglia connect to emotion and motivation?
Through interactions with the limbic system, particularly via the nucleus accumbens.
29
What is the main focus of Part 2 of the basal ganglia lecture?
Understanding how the basal ganglia contribute to learning and behaviour, especially through reinforcement learning and dopamine signalling.
30
Which brain systems does the basal ganglia integrate with?
The cortical, limbic, and motor systems.
31
What types of cortical input does the basal ganglia receive?
Motor cortex (movement), prefrontal cortex (cognition), and limbic cortex (emotion/motivation).
32
What is the function of these parallel loops?
To integrate sensory, cognitive, and emotional inputs for action selection and behaviour control.
33
How do the basal ganglia influence eye movements?
They inhibit the superior colliculus generally, but release this inhibition for target-specific saccades, enabling focused gaze and suppression of distractions.
34
What is the basal ganglia’s core function in behaviour?
A selector and filter of behavioural outputs, especially for self-initiated actions.
35
What areas does it modulate to perform this role?
The thalamus and cortical areas like the Supplementary Motor Area (SMA).
36
How do the cortex, basal ganglia, and cerebellum differ in their learning roles?
1. Cortex learns relationships and contingencies. 2. Basal ganglia learn via reinforcement (reward/punishment). 3. Cerebellum learns via error correction for motor accuracy.
37
What is reinforcement learning?
A learning system based on rewards and punishments, with feedback that is qualitative rather than instructive.
38
Does reinforcement learning provide error signals?
No — learning is based on trial and error, not explicit correction.
39
Why does reinforcement learning take time?
Associations form slowly (e.g. a baby takes about a year to learn to walk).
40
How does the Skinner Box demonstrate reinforcement learning?
A rat accidentally presses a lever and receives food, reinforcing the lever-pressing behaviour.
41
What is the explore vs. exploit dilemma in RL?
Balancing trying new behaviours (exploration) vs. repeating successful ones (exploitation).
42
What natural rewards release dopamine?
Food, water, sex.
43
What is the effect of addictive substances on dopamine?
They increase dopamine release, especially in the nucleus accumbens (NAcc).
44
What is dopamine’s nickname and why?
The "reward chemical" — it reinforces motivated behaviour and habit formation.
45
Name the three key dopamine pathways and their targets.
Mesolimbic: VTA → Nucleus accumbens. Mesocortical: VTA → Prefrontal cortex. Nigrostriatal: SNc → Dorsal striatum
46
What happens during intra-cortical stimulation (ICS) of DA neurons?
DA is released in NAcc, striatum, and cortex, enhancing glutamate signalling and inducing LTP in corticostriatal synapses.
47
What does dopamine release cause at the synaptic level?
1. Enhances glutamatergic input 2. Strengthens synaptic connections 3. Induces long-term potentiation (LTP)
48
What behavioural outcomes result from this process?
Reinforced and persistent behaviours — underlying habit formation and addiction.
49
What did Frank et al. (2004, Science) find about learning in Parkinson’s patients?
ON medication: better reward learning (via direct pathway) OFF medication: better punishment learning (via indirect pathway)
50
What does this suggest about dopamine's role in learning?
Dopamine affects both the ability to learn and the type of learning style (reward vs. punishment).
51
What basal ganglia pathways are involved in this difference?
Reward learning = direct pathway (D1) Punishment learning = indirect pathway (D2)
52
What are the main behavioural roles of the basal ganglia?
Action selection, behavioural adaptation, and self-initiated movement.
53
How does dopamine contribute to these processes?
It modulates reinforcement learning and supports the formation of habits and goal-directed behaviours.
54
What happens when these systems malfunction?
Movement disorders (e.g. Parkinson’s) and motivation-related conditions (e.g. addiction).
55
What is the main focus of Part 3 of the basal ganglia lecture?
Understanding how the brain selects actions through cognitive control, reward evaluation, and motor planning, using parallel systems that compete to guide behaviour.
56
Where is the dlPFC located and why is it important?
At the top part of the brain; it’s a recently evolved area involved in executive functions like planning and decision-making.
57
What is unique about the development of the dlPFC?
It matures late (into early adulthood), mirroring the development of abstract thinking and long-term planning.
58
Which systems is the dlPFC strongly connected to?
The basal ganglia and dopaminergic systems.
59
When is the dlPFC most active?
When evaluating the cost-benefit trade-offs of different actions.
60
What cognitive functions is the dlPFC associated with?
Decision-making, cognitive flexibility, and inhibitory control.
61
How does the Wisconsin Card Sorting Test (WCST) assess executive function?
By requiring participants to deduce and adapt to an unseen sorting rule based on feedback.
62
What types of errors are common in patients with dlPFC lesions?
Perseverative errors: Persisting with the wrong strategy. Capricious errors: Abandoning the right rule too quickly.
63
What do these errors suggest about dlPFC function?
It’s essential for maintaining goals, suppressing distractions, and adapting strategies over time.
64
What did the case of Phineas Gage illustrate?
Damage to frontal brain areas like dlPFC can dramatically alter behaviour and decision-making despite intact cognition.
65
What are the steps in the classical motor control model?
Sense – perceive the environment. Think – select an action. Act – execute the movement
66
What role does the motor system play in this classical motor control model?
It’s a passive output stage, only acting after decisions are made.
67
How does the Central Executive model view action selection?
As a serial process where cognition happens first, followed by motor output.
68
What assumption underlies this Central Executive model?
That decision-making is separate from and precedes motor planning.
69
Who proposed the Affordance Competition Model?
Cisek & Kalaska (2005, 2010).
70
What is the central claim of the Affordance Model?
Motor control is decision-making — actions are represented and selected in parallel.
71
How does this Affordance model work?
Multiple potential actions are specified in parallel. They compete for selection based on inputs like: Rewards, Costs, Sensory input, Prior goals
72
What determines which action is selected?
A distributed consensus emerges from the competition — no central controller.
73
What did the monkey reaching experiment show?
Initial broad activation of multiple motor plans (~50 ms post-cue). Later narrowing to a selected target (~150 ms). Demonstrates parallel encoding and competition in motor areas.
74
What does this imply about motor areas?
They actively contribute to decision-making and are not just passive output systems.
75
What role does the basal ganglia play in this model?
It acts as a central hub that biases action selection based on cost, reward, and contextual factors.
76
What is the role of the dlPFC in action selection?
It helps evaluate options and maintain strategies, shaping action through executive control.
77
How do the basal ganglia support decision-making?
By integrating competing signals and facilitating goal-directed behaviour via action selection.
78
What does the Affordance Competition Model reveal about brain function?
That cognition, perception, and motor control are tightly integrated and operate in parallel rather than sequentially.
79
What does it mean that cognition "leaks" into the motor system?
It means that the brain starts preparing actions before we are consciously aware of deciding to act.
80
What does this suggest about the nature of free will?
That free will may be an illusion — the brain initiates actions unconsciously, and we become aware of the decision afterward.
81
What was the goal of Libet’s experiment?
To investigate the timing of conscious intention relative to brain activity.
82
What was the experimental setup?
Participants made spontaneous movements while watching a clock and reported when they felt the urge to move. Brain activity was recorded with EEG.
83
What is the “readiness potential” (RP)?
A buildup of motor cortex activity that occurs before voluntary movement.
84
What did Libet find about the timing of RP vs. conscious awareness?
RP started ~600 ms before movement, but conscious intention was reported only ~200 ms before.
85
What does this imply about the decision to act?
The brain begins preparing the movement before we are consciously aware of it — suggesting decisions originate unconsciously.
86
What happened with Soon et al.'s study?
They used fMRI and machine learning to monitor and decode whole-brain activity patterns.
87
What was their key finding?
They could predict a participant's choice (e.g., left or right hand) up to 10 seconds before the person was consciously aware of deciding.
88
What conclusion did this support?
That decisions are initiated unconsciously, and consciousness follows rather than causes them.
89
What happens in the brain during imagined movement?
Similar areas activate as during real movement, including the Premotor Cortex and SMA, though activation is typically weaker.
90
What are the practical uses of mental rehearsal?
Improves motor performance in sports. Aids rehabilitation after injury or stroke. Supports design of brain-controlled prosthetics
91
Which study supports the similarity between real and imagined movement?
Schalk et al. (2009, PNAS) — showed shared neural signatures between mental imagery and motor execution.
92
What is a Brain-Machine Interface?
A system that decodes brain signals to control external devices.
93
What types of signals can BMIs use?
EEG, ECoG, or implanted electrodes that detect patterns related to intended or imagined movements.
94
What are some examples of BMI applications?
Moving a robot or cursor by thought. Restoring movement to people with paralysis. Enhancing stroke therapy and motor recovery
95
How do BMIs “read” motor intention?
They decode brain activity linked to intended or imagined movements and translate it into commands for devices.
96
How might electrical stimulation assist rehabilitation?
By reactivating motor circuits in the brain or spinal cord to support recovery of function.
97
What major idea challenges the concept of free will in this lecture?
That the brain initiates actions before conscious awareness, suggesting that free will may not be the true origin of voluntary actions.
98
What neural processes underlie imagined and real movement?
Both activate overlapping motor circuits such as the premotor cortex and SMA.
99
What is the significance of BMIs in neuroscience and medicine?
They demonstrate how neural signals can control devices, offering insight into motor intention and therapeutic applications for paralysis and brain injury.

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