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Action > Task 3: Basal Ganglia > Flashcards

Task 3: Basal Ganglia Flashcards

1
Q

A1: Revise the anatomical & basic functional organization of the Basal Ganglia (BG)

A

Striatum: Caudate + putamen, divided by internal capsule
- Major input structure of BG

Globus pallidus: internal (GPi) + external (GPe)

  • GPi: major output structure to thalamus
  • GPe: part of indirect pathway

Substantia Nigra: pars compacta (SNc) + pars reticulata (SNr)

  • SNc: DA pathways to striatum
  • SNr: major output structure to thalamus with GPi
Subthalamic Nucleus (STN):
- indirect & hyperdirect pathway
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2
Q

What are Medium Spiny Neurons (MSNs)?

A

MSNs:

  • form 95% of neurons in striatum
  • mostly GABAergic
  • modulated by DA from SNc/VTA
  • receive information from cortex integrated by interneurons
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3
Q

What structures form the ventral Striatum?

A

Nucleus Accumbens (NA)
Medial & ventral portions of caudate & putamen
Cells of olfactory tubercle & anterior perforated substance

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4
Q

A1: What neurotransmitters play a role in the BG?

A

GABA (transient & tonic inhibitory signal)
Glutamate (transient, excitatory signal)

DA (transient & tonic, excitatory & inhibitory modulation)

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5
Q

A1: Give an overview of the direct pathway

A

Direct: Disinhibition/movement initiation

Cortex     -> more transient glutamate
  • > striatum -> more transient GABA
  • > GPi -> less tonic GABA
  • > thalamus -> more transient glutamate (disinhibited)
  • > frontal motor neurons
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6
Q

A1: Give an overview of the indirect pathway

A

Indirect: Inhibition of motor initiation

Cortex     -> more transient glutamate -> striatum   -> more transient GABA -> GPe         -> less tonic GABA    (-> STN   -> more transient glutamate) -> GPi -> more tonic GABA -> thalamus -> less transient glutamate (inhibited)
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7
Q

A1: Give an overview of the hyperdirect pathway

A

Hyperdirect: Fast inhibition of motor initiation

Cortex   -> more transient glutamate
  • > STN -> more transient glutamate
  • > GPi -> more tonic inhibition
  • > thalamus (inhibited) -> less transient glutamate -> motor areas
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8
Q

A2: Describe the loop-structure of BG & the similarities and differences between the loops

A

Similarities:

  • Cortex -> striatum -> thalamus
  • dorsal to ventral
  • Principle of disinhibition
  • direct, indirect & hyperdirect pathways
  • signal returns back to original place in cortex (hence, loop)
  • all receive input from Primary Sensory/Motor Cortex (+ their individual regions)

Differences:

  • Function & specific areas
    1) Motor (limb)
    2) Oculomotor
    3) Executive/associative
    4) Emotion/motivaiton (limbic)
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9
Q

A2: For each loop name the function & cortical input regions

A

1) Motor (limb) -> movement
- Stimulus-response learning (S-R)
- M1, SMA, PreMC, CMA (cingulate motor area)

2) Oculomotor -> saccades
- Similar to motor/limb
- FEF, SEF

3) Executive/associative
- Action-outcome learning (A-O)
- dlPFC -> executive function
- lOFC -> empathic/socially appropriate behaviour

4) Emotion/motivation (limbic) -> mood/motivated behaviour/reward
- Stimulus-outcome learning (S-O)
- ACC, mOFC

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10
Q

A2: Explain the 2 anatomical observations of interaction between the BG loops (Haber (2016)):
1) Topographical & integrative connectivity of corticostriatal projections

A
  • Different cortical inputs are topographically organized in the dorsomedial striatum
  • > form cortico-striatal hubs
    1) mPFC/ACC -> reward/emotion/motivation
    2) vmPFC -> visceral/emotional functions/monitoring/flexibility
    3) dlPFC -> higher/executive functions/cognition
    4) OFC -> S-O representations
    5) dACC -> reward & action network/working memory
  • The different corticostriatal paths converge in the rostral striatum
    -> integration of motivational, reward & cognitive control information
    (think back to striatal MSNs which receive integrated information from interneurons)
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11
Q

A2: Explain the 2 anatomical observations of interaction between the BG loops (Haber (2016)):
2) Inverse striato-nigro-striatal projections

A

Inverse dorsal-ventral relationship between topographically matching parts of striatum and midbrain DA regions
1) midbrain –> striatum
Dorsal tier (VTA, dSNc) –> DA cells –> ventral striatum
Ventral tier (SNr) –> DA cells –> dorsal(lateral) striatum
2) striatum –> midbrain
Dorsal striatum –> dorsal midbrain
Ventral striatum –> ventral midbrain

VTA & medial SN –> related to limbic system
lateral midbrain –> associative striatal regions
ventral midbrain –> motor striatal regions

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12
Q

A2: Summarize the flow of information through the BG loops by giving an example for meaningful behaviour

A

Striatum-midbrain connections are organized in an ascending spiral

  • -> connect different functional regions of striatum
  • -> signal for meaningful behaviour moves through loops

Example:
Stimulus: dickhead ex boyfriend
Action: slap him
Outcome: he suffers

1) Limbic loop (S-O): I see my ex boyfriend and I want him to suffer
2) Associative loop (A-O): If I slap him, he will suffer
3) Motor (S-A): When I see my ex boyfriend, I will slap him

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13
Q

A3: What is the role of Tonic Dopamine (DA) in the BG?

  • Where does it come from?
  • Where does it go? (direct/indirect)
  • Where does it come from, Cotton Eyed Joe?
A

glutamate & GABA are drivers in BG
Dopamine is a modulator in the BG

DA origin: SNc & SNr + VTA (mdibrain)

-> signals to striatum (inverse topographical organization)

D1 –> stimulatory signal into striatum

 - -> causes LTP in direct pathway
 - -> (more active GPi --> more disinhibition thalamus --> stronger GO)

D2 –> inhibitory signal into striatum
–> causes LTD in indirect pathway
–> (less active GPi –> more
inhibition of thalamus –> weaker NOGO)

  • > facilitates learning/movement initiation
  • > increased trigger-readiness in BG
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14
Q

A3: Describe common symptoms seen in Parkinson’s Disease

A

Parkinson’s Disease

  • Motor symptoms (tremor, rigidity, bradykinesia, akinesia, unstable posture)
  • Cognitive symptoms (set-shifting/cognitive flexibility, working memory, attention, problem-solving, impulse control)
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15
Q

A3: Explain how DA cell death in Parkinson’s Disease (PD) interferes with Basal Ganglia functioning
(Aberrant learning hypothesis)

A
  • loss of ~80% of DA neurons in SN and striatum
  • degeneration of both D1 and D2 receptors

DA influences corticostriatal plasticity –> learning
D1 –> stimulants GO pathway –> LTP
D2 –> inhibits NOGO pathway –> LTD

No DA:

  • Indirect pathway –> LTP for cortical inputs –> increased pathological behavioural inhibition(!) with every engagement in movement (it gets worse)
    - -> aberrant/impaired learning
  • Direct pathway –> no LTP (nothing really happens, which is also bad)

Reintroducing DA (e.g. via medication)

  • Indirect pathway –> aberrant learning (inappropriate LTP) needs to be reversed first before “normal” functioning can continue
  • Direct pathway –> no reversal needed, normal functioning resumes
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16
Q

A3: How can BG dysfunction in Parkinson’s Disease (PD) be extrapolated from motor to other problems?

A

Parkinson’s Disease (PD) affects DA modulation which plays a role in all functional BG loops, not just the motor loop.

(Hast du da noch was anderes an info?)

17
Q

A3: Explain the Cools et al. (2001) experiment on cognitive set flexibility
- Methods

A

Task: subjects had to switch between letter- and digit-naming task every 2nd trial as indicated by colour of stimulus window
Stimuli: two characters presented side by side, could be task-relevant or irrelevant
Conditions:
- No-cross-talk condition: irrelevant stimulus was neutral, easy to focus on relevant stimulus
- Cross-talk condition: irrelevant stimulus was related to irrelevant task in 67% of trials

18
Q

A3: Explain the Cools et al. (2001) experiment on cognitive set flexibility
- Results

A

Results:
PD –> slower RT/more errors vs. control
PD –> slower RT/more errors in cross-talk condition vs. no-cross-talk
PD –> in cross-talk condition, bigger RT increase due to switch vs. healthy (group x switch) –> PD had larger switch-costs

  • > difficulty focusing on one task when competing info is present
  • > difficulty switching between tasks despite clear cue on what task to do

PD patients have specific deficit for set-shifting when competing info is presented –> proof that BG function goes beyond motor selection –> apart from cognitive, also motivational/affective/eye movement impairments

19
Q

A4: Present evidence for the role of the BG in decision-making (vs. cerebral cortex)

  • Grillner et al.
  • Evolutionary evidence (Lee et al.)
  • Neuropsychological evidence (Cools et al)
A

Grillner:

  • Decorticated cats still showed goal-directed movement
  • > subcortical structures must be sufficient to process meaningful voluntary movement

Evolutionary evidence, Lee:

  • Species without fully developed neocortex can make decisions
  • BG is a non-cortical, old region of convergence (striatum, Haber 2016)
  • BG may be more important in dealing with environment than cortex

Neuropsychological evidence

  • Cools: Parkinson’s Disease –> deficit in focusing on one task & rule switching when 2 options are competing (part of decision-making)
  • BG lesion in rats: inability to make flexible, goal-directed decisions
  • Ballot Box model fits here
    BG pathways as votes for/against a decision
20
Q

A5: How might the BG contribute to working memory (WM)? Give biological evidence

A

WM is limited in capacity & needs constant updating; this requires:

  • input control (processes to store relevant info in WM)
  • output control (select output to perform a task)
  • reallocation (remove irrelevant information if its utility/relevance decreases)

BG: “gate” for motor control & possibly also WM

Evidence from striatum
- 2 classes of MSN
Go cells –> D1 receptor –> open gate –> open information flow –> WM is updated for useful information
Nogo cells –> D2 receptor –> close gate –> blocks information flow –> WM updating is limited in the face of distracting information

21
Q

A5: Explain the Chatman & Badre (2015) experiment which studied the role of the BG in working memory (WM)

A

Task: 2 item stimuli (one is task-relevant) + 1 context stimulus (which task to do?)
Conditions:
- Context before items –> selective input gating
- Context after items –> selective output gating
- Context between items –> WM reallocation

Results
- All trials showed activation in PMd (dPreMC)

  • Context before items
  • > related to D1/D2 receptor effect on WM -> Input gating
  • Context after items
  • > More activity in rostral PMd (= PrePMd) -> Output gating
  • > Part of this area increased coupling with BG
    - Bilateral PrePMd activity predicted efficiency of selective output gating
    - Bilateral coupling with BG predicted response variability
  • Context between items
  • > New information given -> large benefit to behaviour performance but only after sufficient time passed
  • > Subjects need some time to reallocate WM capacity occupied by the now irrelevant info
  • Activity in ventral striatum related to encoding value of task-irrelevant stimuli
22
Q

A6: Explain the classic models of direct-indirect pathway interaction:

  • Go-Nogo
  • Co-activation
  • Competition
  • Co-activation 2
  • Current evidence
A

Classical Go-Nogo (Lee)

  • Direct pathway activates behaviour A
  • Indirect pathway stops it
  • Serial actication -> 2 pathways cannot be active at the same time
  • But evidence for coactivation

Co-activation model

  • Direct pathway activates behaviour A
  • Indirect pathway inhibits competing behaviour B
  • Parallel activation -> both benefit the same behaviour

Competition model

  • Direct pathway activates behaviour A
  • Indirect pathway stops it
  • Parallel activation -> both pathways are now activated at same time but in competition

Co-activation 2 model

  • Direct pathway activates behaviour A
  • Indirect pathway releases tonic inhibition on behaviour A
  • Parallel activation -> both benefit the same behaviour

Current evidence: combination of co-activation & competition

23
Q

A6: Present the Ballot Box Model of BG functioning

A

Ballot model
- Cortex/thalamus/HC/AMY
Represent states of the world
Each send 1 signal = 1 representation = 1 vote for a certain action

  • (dorsal) striatum
    Integrates states & compares them
    Finds common value of “votes” –> used to active direct and indirect pathway accordingly
24
Q

A6: Ballot Model: Explain the Principle of contralateral & ipsilateral biases in the pathways

A
  • Both pathways are active at the same time in both hemispheres and compete for action

Activity in direct pathway: contralateral bias

  • Pro contralateral vote
  • Against ipsilateral vote

Activity in indirect pathway: ipsilateral bias

  • Anti contralateral vote
  • Pro ipsilateral vote
25
Q

A6: Present evidence for the Ballot model in mice from Lee et al.

A 
Part 1: Value-based Probabilistic Task
Methods:
- Stimulation of either direct or indirect pathway + 2-alternatives choice task
- Choice made via nose pokes
- Feedback given 75% of time
- Reward-side switched every 7-23 trials

Results

  • Stimulation of direct pathway
  • -> induced contralateral bias
  • Stimulation of indirect pathway
  • -> induced ipsilateral bias

Part 2: Auditory Sensory Discrimination Task
Methods
- also choice task but using auditory sense, nose pokes & stimulation

Results

  • Stimulation of neuron A1 –> behavioural bias
  • Inactivation of neuron A1 –> “anti-bias”

Conclusion

  • > Activation of corticostriatal pathway is sufficient to bias choices
  • > Inactivation of corticostriatal pathway created an “anti-bias”
26
Q

A6: Compare the Ballot Box Model to the Go-Nogo model (Chatham & Badre) in relation to Working Memory (WM)

A

Go/NoGo

  • Direct pathway/Go cells/D1
  • -> open gates of WM –> support updating of WM
  • -> facilitates information flow
  • Indirect pathway/Nogo cells/D2
  • -> close gates of WM –> limit updating of WM
  • -> blocks information flow

Ballot Box

  • Activity in direct pathway
  • -> Contralateral bias vote
  • Activity in indirect pathway
  • -> Ipsilateral bias vote

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