Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Action (Neuroscience) > Task 3 > Flashcards

Task 3 Flashcards

1
Q

3.1: What are the functions of the basal ganglia (=BG) loops?

A

movement, cognition & emotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3.1: What are the structures of the BG?

A

Striatum (caudaute nucleus & putamen), substantia nigra pars compacta & pars reticulata (SNc&SNr), Globus pallidus internal&external (GPi&GPe) + subthalamic nucleus (STN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3.1. What are the main input & output structures of the BG?

A
  • Input: Striatum

- Output: GPi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3.1: Which areas does the striatum get its input from?

A

Thalamus, cortex & brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3.1: Direct BG pathway

A

-Cortex transiently excites striatum (GLU) –> Striatum transiently inhibit GPi (GABA) –> tonic inhibition of GPi on thalamus released (DISINHIBITION) –> Thalamus transiently excites cortex (GLU)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3.1: Role of SNc in direct pathway

A

D1 receptor –> transiently excites striatum as well (like cortex) but with DOPAMINE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3.1: Direct pathway of BG leads to what?

A

Movement (GO-pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

3.1: Indirect BG pathway

A

-Cortex transiently excites striatum (GLU) –> transiently inhibits GPe (GABA) –> GPe usually tonically inhibts STN (GABA) –> STN disinhibited (because GPe inhibited) –> STN transiently excites GPi (GLU) –> GPi tonically inhibits thalamus (GABA) –> so thalamus CANNOT excite cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3.1: SNc: D1 &D2 receptors

A
  • D1: DOPA excites
  • D2: DOPA inhibits
  • -> both have effect on striatum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3.1: Indirect pathway of BG leads to what?

A

NO movement (NO-GO pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3.1: What are the 4 different BG loops?

A

Motor, occulomotor, executive/associative & emotional/motivational loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3.2: What are the two anatomical observations by Haber (2016)?

A

(1) Cortical inputs to striatum from functionally different regions of PFC strongly overlap in dorsal-medial striatum
(2) Spiral of connections between functionally matching topographical parts of striatum & midbrain dopamine region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3.2: What is seen in the striatum in terms of projections from other areas?

A
  • great overlap of projections of cortex to striatum
  • overlap of projections from vmPFC, OFC & dACC ==> hubs for integrating reward value, predictability & salience
  • also functionally diverse projections overlap in striatum (e.g. input from dPFC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3.2: Where in the striatum is there the most convergence of input?

A

anterior (rostral) striatum (see figure 1 in Haber (2016))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3.2: What do both the DA-striatal pathway & the striatal input to the DA neurons show in terms of their organization?

A

general inverse dorsal-ventral topographic organization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3.2: What does the spiraling of information faciliate in DA-striatal pathway?

A

through this spiral, information can flow from limbic to cognitive to motor circuits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3.2: How is info always channeled (from where to where?)

A

from limbic to cognitive to motor circuits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3.2: Is there strictly parallel processing in BG?

A

no, there are many interconnections

19
Q

3.2: What does motivation trigger in BG (limbic loop)?

A
  • Triggers cognitive considerations (rules that apply in the situation, do’s and dont’s)
  • Triggers attentional priorities (what objects, stimuli, are relevant to realize this goal; are all the conditions met?
  • Triggers action patterns (which actions can accomplish my goal?)
20
Q

3.3: Where does DOPA originate from?

A

Substantia nigra (midbrain)

21
Q

3.3: What’s the role of DOPA in the direct pathway?

A
  • D1 receptors (stimulates)
  • Stimulating stimulation
  • Striatum more inhibitory – disinhibiting Thalamus
  • Learning: LTP/ strengthening connection

-‚Pressing gas‘
= stronger go-signal 🡪 increases trigger readiness

22
Q

3.3: What’s the role of DOPA in the indirect pathway?

A
  • D2 receptors (inhibits)
  • Inhibiting inhibition (disinhibition) = less inhibition
  • Striatum less inhibitory –-> unable to completely inhibit Thalamus
  • Learning: LTD / weakening inhibitory connections (if no dopamine, LTD converts to LTP)

-`Releasing brake‘
= weaker no-go signal 🡪 increases trigger readiness

23
Q

3.3: Which NTs are drivers?

A
  • Glutamate (+) & GABA (-)

- in/decreases likelihood of firing of neurons

24
Q

3.3: Which NTs are modulators?

A
  • DOPA & serotonin

- able to effect large number of neurons at the same time 🡪 affect strength of signal between the neurons

25
Q

3.3: Cools et al study w/ Parkinsons: AIM

A

Observing set-shifting deficit in Parkinson‘s by using a switch task in a non-learning context

26
Q

3.3: Cools et al study w/ Parkinsons: METHOD

A
  • Task-switching: naming digits or letters
  • 2 conditions
  • -> No-cross talk: only relevant stimuli (only letter or only digit)
  • -> Cross-talk: irrelevant stimuli included (letter and digit simultaneously)
27
Q

3.3: Cools et al study w/ Parkinsons: RESULTS

A
  • Evidence for deficit in cognitive set shifting in PD

- -> Independent from impairments in rule learning, WM etc

28
Q

3.3: Cools et al study w/ Parkinsons: only when was there a deficit in set shifting?

A

Shifting deficit only in cross-talk condition –> only apparent when irrelevant information presented

29
Q

3.3: Cools et al study w/ Parkinsons –> Conclusions about role of BG

A
  • BG: selection & inhibition of competing cognitive & motor programs
  • -> Evidence that BG has also role in cognition
30
Q

3.3: Cools et al study w/ Parkinsons –> Conclusions about role of DOPA

A

DOPA facilitates focusing function by disinhibiting task-relevant corticostriatal projections & inhibiting task-irrelevant ones

31
Q

3.4: Evidence BG makes decisions- What was Grillner’s (2005) observation?

A

-Decorticated cats: could still search for food & eat , move around & display goal-directed locomotion/behaviour

32
Q

3.4: Evidence BG makes decisions- LEE ET AL (2014)

A
  • evolutionary evidence

- evolving role of striatum in decision making

33
Q
  1. 4: Evidence BG makes decisions- LEE ET AL (2014)

- -> ‘Ballot Box’ model

A
  • Striatum as “ballot box”: various sensory modalities, motivation networks & cognitive systems are able to ‘vote’ for a limited set of behavioral responses
  • -> Direct (= votes for) & indirect pathway (=votes against)
34
Q
  1. 4: Evidence BG makes decisions- Cools et al (2001)

- -> Parkinson’s disease

A

Parkinson’s disease –> cognitive impairments even in its early stages, resembling those seen in frontal lobe patients
–> Deficits in the ability to shift set

35
Q
  1. 5: How does BG contribute to WM?

- -> Input gating

A

Input gating of WM

  • -> Useful info in environment => D1: gate open & WM updated
  • -> Gating mediated by cortico-striatal mechanism
  • -> Causes a go cell to fire & facilitates thalamic-PFC info flow for WM updating
  • -> Distracting info triggers No-go cells
36
Q
  1. 5: How does BG contribute to WM?

- -> Input gating ==> fMRI EVIDENCE

A
  • striatal activation –> WM tasks that require updating (D1 receptors active)
  • D2 –> no go cells ==> limit WM update
37
Q
  1. 5: How does BG contribute to WM?

- -> Output gating

A
  • Single out or select relevant representation stored within WM
  • Higher order plans can select motor plans via corticostriatal circuits
38
Q

3.5: How does BG contribute to WM?
–> Output gating
==> fMRI EVIDENCE

A

-used a task: 3 sequentially presented stimuli (2 items, 1 context)
-if context appears last –> output gating
==> BOLD response in pre-motor cortex

39
Q
  1. 5: Reallocation of WM & BG
    - -> What is tracked by BG?
    - -> study
A
  • Utility of WM for future behaviour is tracked possibly by BG
  • PP required more time to reallocate
40
Q

3.6: Ballot box model of striatum

A

o Striatum: like ballot box
o Massive convergence of input onto striatum
o All of sensory & motivation systems etc: can all vote
o Movement with most votes –> will be executed

41
Q
  1. 6: Ballot box model of striatum

- -> comparison with go/no-go model (Chatham)

A

xxx

42
Q
  1. 6: Ballot box model of striatum & go/no-go model

- -> Can both pathways be active at same time?

A

o Ballot model: two pathways can be activated at same time

o Go-no go signal (classical model) –> two pathways cannot be activated at same time!

43
Q

3.6: Chatham’s go/no-go model: How does this model place BG at the core of all forms of cognition?

A
  • all cognition (implicit as well as explicit) requires WM activity, which is regulated by BG
  • BG regulates initiation & termination of cognitive processes = i.e. planning, attention etc. (which all affect WM)
44
Q

What changes in Parkinson’s disease regarding the direct & indirect pathway of the BG?

A
  • Go-pathway: disappears
  • No-go pathway: turns into LTP ==> reverses effect
    o Strengthens the indirect one
    –> More difficult to initiate movements

Action (Neuroscience) (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions