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basal ganglia Flashcards

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1
Q

what are the cortical inputs to the striatum? what cues do neurons fire related to?

A

input from primary motor and somatosensory cortex via glutamatergic neurons

to GABAergic medium spiny neurons (MSNs) in putamen that receive most of afferent input and fire related to cues for movement/intended movement

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2
Q

what are the non-cortical inputs to the striatum?

A

negrostriatal dopamine input from SNc

inhibitory or excitatory

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3
Q

what are the 2 types of neuron in the striatum?

A

D1: enriched in dopamine D1 receptors and substance P receptors (dynorphin opioid)
D2: enriched in dopamine D2 receptors, A2A receptors (enkephalin opioid)

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4
Q

what are the outputs of the basal ganglia and where do they go?

A

also GABAergic, leave SNr/GPi to inhibit the VLo/VA of thalamus (thalamocortical relay)

or leave SNr/GPi to upper brainstem, regulating nuclei for balance and gait

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5
Q

how does the modulation of BG outputs work?

A

striatal neurons to SNr/GPi disinhibit thalamocortical relay

GABAergic striatal input to SNr/GPi inhibits them, meaning they don’t fire tonically and their inhibition of the thalamus ceases : disinhibition

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6
Q

describe the direct pathway

A

Striatal output inhibits SNr/GPi and so
reduces GPi inhibition on thalamus
→ Disinhibition of thalamocortical relay
Overall, it facilitates movement

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7
Q

describe the indirect pathway

A

Striatal output inhibits GPe and so reduces GPe inhibition of STN.
Increased activity in STN increases
GPi inhibition on thalamus
→ Inhibition of thalamocortical relay
Overall, it inhibits movements

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8
Q

how does dopamine modulate the direct pathway?

A

D1 receptors on direct striatal projections to SNr/GPi facilitate the pathway

DA facilitates movement

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9
Q

how does dopamine modulate the indirect pathway?

A

D2 receptors on indirect strial projections to GPe, STN then SNr/GPi inhibit pathway, inhibiting the STOP signal

DA facilitates movement

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10
Q

what does decreases DA in parkinson’s disease lead to?

A

akinesia

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11
Q

what are the broad symptoms of basal ganglia diseases?

A

deficiency of movement: akinesia, bradykinesia

involuntary movements: tremor at rest, chorea, dystonia (spasms), ticks, dyskinesia, ballismus (violent involuntary movements)

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12
Q

what are some diseases affecting the basal ganglia?

A

Parkinson’s
Huntington’s
Hemiballismus
Tourette’s
Manganism + Hatters Disease

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13
Q

what are some things that cause basal ganglia disease?

A

toxins + heavy metals (Manganese, Mercury)
addiction disorders
ageing

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14
Q

what are the primary motor symptoms of Parkinson’s?

A

Tremor at rest
Rigidity (resistance to movement)
Akinesia
Postural instability (poor righting reflexes + balance, results in hunching and small shuffling gait)

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15
Q

what are the non-motor symptoms of Parkinson’s?

A

dysfunction: bowels, olfaction, depression, pain, cognition, dementia
REM behaviour sleep disorder (RBD): movement in these sleep states (70% progress to Parkinsons)

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16
Q

what happens to Parkinson’s tremors when patients carry out a reflex or common action?

A

disappear

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17
Q

what is the pathology of Parkinson’s?

A

progressive loss of SNc DA neurons

proteinaceous aggregations (Lewy bodies)

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18
Q

F-dopa PET images show innervation loss in where in particular in Parkinson’s?

A

putamen

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19
Q

why does progressive loss of SNc DA neurons lead to PD?

A

causes loss of nigrostriatal pathway supplying dopamine to the striatum
(need to lose more than half of DA for symptoms to appear)

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20
Q

what are Lewy bodies and why do they cause PD?

A

intraneuronal cytoplasmic inclusions in SNc neurons + axons

major insoluble components = alpha-synuclein and ubiquitin

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21
Q

what is the comparable activity of the BG flow diagram in PD?

A

sporadic input from DA from SNc
much less output from striatum to SNr through direct pathway
much more output through indirect pathway
thalamus inhibited much more, therefore cortex less stimulated: sporadic output to brainstem + spinal cord

22
Q

what causes parkinson’s disease?

A

genetic components: ~15% PARK genes 1-23

intrinsic biochemistry + physiology promotes selective vulnerability: high metabolic demand, DA oxidation + oxidative stress, neuroinflammation

acquired/environmental contributions: pesticides, toxin exposure (MPTP parkinsonism)

23
Q

describe MPTP toxicity

A

can cross BBB, becomes MPP+ in glial cells, enters DA neurons via DA transporter

sequestered into mitochondria, inhibIt complex I, less ATP, increases downstream reactive oxygen species

oxidative species cause death of DA neurons?

24
Q

does MPTP toxicity provide a good model for sporadic PD?

A

ish: explains degeneration of SNc DA neurons
but no
not progressive
no Lewy bodies

25
Q

which models better reproduce progressive PD?

A

other toxins
trasngenic
alpha-synuclein aggregation

26
Q

how can you treat PD?

A

dopamine replacement

tyrosine -> l-DOPA (DOPA decarboxylase) -> dopamine
+ inhibit peripheral decarboxylase (use carbidopa)

27
Q

why is L-DOPA problematic?

A

on/off effects and gait freezing
induced dyskinesias after 5-10 years

28
Q

what are alternative treatments for PD?

A

other DA replacement strategies

non-DA pharm

molecular antibody therapies/gene therapy

surgery: deep brain stimulation

29
Q

how does DBS work?

A

stimulating electrode placed within BG nuclei e.g. STN, GP

creates electrical field when turned on that prevents nearby neurons firing, stops STN stimulating GPi/SNr to inhibit thalamus so strongly

may act through modifying axon tracts of afferent inputs [Gradinaru]

30
Q

what are the symptoms of Huntington’s disease?

A

hyperkinetic, dystonia (spasms), rigidity, cognitive decline

31
Q

what is the pathology of HD?

A

striatal atrophy + loss of caudate nucleus GABAergic MSNs (indirect D2 particularly)

favours direct pathway: excessive activation of motor programmes: chorea

cortical atrophy

32
Q

what is aetiology?

A

study of causation or origin

33
Q

what are the causes of HD?

A

genetic: highly inherited autosomal dominant
‘codon-repeat disease’ : encodes consecutive CAGs (>36) in protein product of huntingtin gene
mutant protein aggregates

age of presentation depends inversely on no. repeats

34
Q

what is the method of action of HD?

A

direct pathway > indirect pathway = decreased overall inhibition of thalamus = hyperkinetic phenotype

35
Q

what are the treatments for HD?

A

antidopaminergics: tetrabenazine, benzodiazepines

36
Q

so summarise the role of the BG

A

selects volunatry motor programmes and motivationally driven behaviours depending on cortical + subcortical inputs (incl. from DA)

calibrated by cerebellum

37
Q

how does the BG operate?

A

through the disinhibition of thalamocortical relay to motor cortex

DA changes balance of inhibition vs disinhibition

38
Q

how does the direct + indirect neuronal circuity link to the actions of the BG?

A

section of cortex controlling movement projects to BG, projects to thalamus and back to cortex

if direct pathway most strongly excited, that section of cortex excited and motor programme it encodes is activated, sending impulses to muscles resulting in movement

39
Q

how does tetrabenezine work?

A

prevents DA being loaded into vesicles, so when they fuse w cell membrane, no DA is released into the synapse

40
Q

which cortical loops deal with executive functions?

A

originate in PFC

41
Q

where do ‘effective’/’emotional’ loops originate?

A

limbic areas

42
Q

why do all the loops flow through the BG?

A

so it can perform action selection
“decide what to do next”

43
Q

how does the BG achieve action selection?

A

inhibits many of the loops that flow through it, and when action is relevant, BG removes inhibition of its circuits, allowing action to be carried out

44
Q

what is the hyperdirect pathway?

A

direct, stimulatory pathway from cortex to STN

45
Q

what is salience?

A

an action’s relevance to the current situation
appropriate behaviour = high salience value

level of activation of a loop reflects its salience

46
Q

what is the selection pathway in the Gurney et al. model?

A

inputs from cortex excites striatum, inhibits GPi/SNr, reduces inhib of thalamus, excites cortex.

inputs from cortex also excites STN, excites inhibitory neuron output of other loops in GPe/SNr.

47
Q

why is the control pathway needed in the Gurney et al. model?

A

to balance the excitation of the STN with the inhibition of the striatum (of salient loops)

as number of loops increases, sheer volume of excitatory input from STN will excite GPi more than striatum can inhibit it

48
Q

which neuron will fire at the greatest rate?

A

the one with the highest salience

49
Q

how does the selection pathway work?

A

e.g. 3 competing loops, middle loop connects cortical areas most relevant to the current situation to the BG: has the greatest salience: its neurons fire at the greatest rate

connects to and excites middle loop the most in STN and striatum, striatum can therefore inhibit middle GPi/SNr output loop most strongly and STN can excite output nuclei of competing loops most strongly

therefore there is reduced inhibition of thalamus at middle loop, and cortex excites the most salient loop, allowing that action to be selected and occur

50
Q

how does the control pathway work?

A

cortex excites striatum, inhibits GPe, inhibits STN and SNr, GPe receives diffuse excitation from STN

as more loops are added there is also increased activation of inhibitory neurons in GPe, inhibit STN and GPi, preventing runaway excitation of salient loops

51
Q

so in summary what do the loops in the BG do?

A

compete to reduce inhibition placed on themselves and increase inhibition placed on other loops to ensure most salient action is selected

brain and behaviour (4 decks)

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