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PBL SEM 3 > 7 - the basal ganglia > Flashcards

7 - the basal ganglia Flashcards

1
Q

what makes up the striatum?

A

putamen and caudate nucleus

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2
Q

what does the lentiform nucleus consist of?

A

putamen and globus pallidus

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3
Q

what separates the lentiform nucleus from the caudate and thalamus?

A

internal capsule

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4
Q

what can basal ganglia dysfunction cause?

A

movement disorders

  • hypokinetic — too little movement eg. Parkinson’s
  • hyperkinetic — too much movement, often abnormal involuntary movements
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5
Q

what is the input region of the basal ganglia?

A

striatum

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6
Q

what are the output regions of the basal ganglia?

A

globus pallidus internal and SNr

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7
Q

what is the main inhibitory neurotransmitter?

A

GABA

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8
Q

what are the main neurones in the striatum? describe them

A

medium spiny neurones — have a number of dendritic spines — vastly increases SA of neurones (lots of spines) allowing very fine tuning of signal in those neurones

= projection neurones

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9
Q

what neurotransmitter do medium spiny neurones use?

A

GABA +/- neuropeptides

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10
Q

what are the other type of neurone in the striatum?

A

interneurons
- modulate transmission withi the neural networks of the striatum
- there are GABAergic interneurons and cholinergic (large aspiny neurones)

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11
Q

what input does the striatum have?

A
  1. glutamatergic cortciostriatal pathway = input from all regions of cerebral cortex
  2. dopaminergic nigrostriatal pathway = from SNc
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12
Q

what pathway is damaged in parkinson’s?

A

nigrostriatal pathway

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13
Q

the interaction between what controls the level of activity within the striatum?

A

dopamine and glutamate

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14
Q

what kind of input is striatal input?

A

excitatory

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15
Q

what does the input from the whole cerebral cortex excite?

A

medium spiny neurons

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16
Q

DA regulates the activity of what?

A

medium spiny neuroens

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17
Q

where is DA produced?

A

SNc

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18
Q

what type of output is the output from medium spiny neurones?

A

inhibitory

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19
Q

glutamate from corticostrial neurone acts on what receptors?

A

ionotropic AMPAR and NMDAR receptors and metatrobic receptors mGluR on tip of spine of MSN

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20
Q

what interact to modulate synaptic strength?

A

dopamine and glutamate

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21
Q

what is key to long term potentiation?

A

dopamine — without dopamine the long-term enhancement of synaptic strength doesnt happen

dopamine alters level of activity in the neuron

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22
Q

what neuropeptide is in the direct pathway?

A

dynorphin substance P

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23
Q

what neuropeptide is used in the indirect pathway?

A

enkephalin

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24
Q

what receptors are used in the 2 pathways?

A

direct = D1
indirect = D2

25
Q

the output of the basal ganglia is overall what?

A

inhibitory

26
Q

how does D1 receptor enhance neuronal activity?

A

G protein coupled with GaS — activates adenylyl cyclase to convert ATP —> cAMP which allows the phosphorylation/activation of intracellular substances

27
Q

how does the D2 receptor decrease neuronal activity?

A

coupled with Gi/o which inhibits adenylyl cyclase

28
Q

direct vs indirect pathway functions

A

D1 = facilitation of desired movements

D2 = suppression of unwanted movements

29
Q

how is dopamine released in resting conditions?

A

tonic dopamine release — low synaptic levels and extra synaptic levels — preferential D2R activation indirect pathway neuroens higher excitability at rest — action inhibiton “no-go” long term depression

indirect pathway overactive at rest

30
Q

how is dopamine released in active movement?

A

phasic dopamine release — preferential D1R activation — motor initiation, enhances motor learning via long-term potentiation

31
Q

what is the hyper direct pathway?

A
  • from cortex to STN
  • additional role in inhibitory control (enhance fine tuning of inhibition)
32
Q

describe the dorso lateral to ventromedial in terms of function in the basal ganglia?

A

dorslolateal = more motor
ventromedial = more limbic

33
Q

there are parallel loops in the basal ganglia subserving different functions such as what?

A

eye movements, limbic

34
Q

what happens in parkinson’s to the 2 pathways?

A
  • degeneration of SNc — loss of dopamine
  • reduced D1 activation — reduced excitation
  • reduced D2 activation — less (-) stimulation
35
Q

there is the relative overactivity of what in parkinson’s? what is the result?

A

indirect pathway — reduced voluntary movement (bradykinesia), rigidity

36
Q

why is there impaired motor learning in parkinson’s?

A

loss of long term potentiation as dopamine and glutamate don’t interact to facilitate motor learning

37
Q

what is the subthalamus like in parkinson’s?

A

over active — lesion of STN alleviates experimental parkinsonism

38
Q

what are cognitive disturbances in PD linked to?

A
  • linked to changes in DA handling in basal ganglia loops
39
Q

what is later dementia in PD related to?

A

cortical spread of Lewy body pathology

40
Q

what impulsive behaviour are there in PD?

A

pathological gambling, hyper sexuality, compulsive eating

41
Q

what is impulsive behaviour in PD linked to?

A

more severe dopaminergic deficit in ventral (limbic) striatal area

42
Q

what is depression and anxiety in PD linked to?

A

monoamine cell loss in brainstem

43
Q

what may improve depression in PD?

A

dopamine agonists

44
Q

what are 2 choreiform disorders?

A

Huntingtons disease and levodopa-induced dyskinesia

45
Q

what is chorea?

A
  • rapid, multi focal irregular movements
  • flitting between various muscle groups and body parts
  • motor impersistence
46
Q

pathophysiology of chorea

A
  • imbalance between direct and indirect pathways
  • relative overactivity of direct pathway — excessive movement
  • underactivity of indirect pathway — no suppression of unwanted movements
47
Q

pathophysiology of Huntingtons disease

A
  • selective loss of D2 receptor-bearing indirect pathway neurones —> involuntary movements
  • later loss of direct pathway neurons —> hypokinetic movement disorders
48
Q

in Huntington’s disease there is loss of neuroens in what layers of the cortex?

A

layers V and VI

49
Q

striatal pathology in Huntington’s disease

A

degeneration in caudate and indirect pathway D2 receptor-bearing medium spiny neurones

50
Q

what neuropsychiatric disturbances are there in Huntington’s disease?

A
  • anxiety, depression
  • impulsivity, apathy
51
Q

what is a potential treatment to Huntington’s disease?

A

cell transplantation — replace MSNs

52
Q

what is enkephalin like in huntington’s disease?

A

rapidly reduced

53
Q

describe tourette syndrome

A
  • tic disorder
  • usually onset age <20
  • rapid, repetitive, stereotyped movements or vocalisations
  • frequent comorbid neuropsychiatric illness
54
Q

pathophysiology of tourette syndrome

A
  • loss of cholinergic and GABAergic striatal interneurones — reduced basal ganglia inhibition
  • increased striatal dopamine D2 receptor binding in patients with TS
55
Q

how a tic disorders treated?

A
  • anti dopaminergic therapy
  • alpha receptor agonists - clonidine, helpful for ADHD symptoms too
  • deep brain stimulation (GPm/thalamic DBS may help in some cases)
56
Q
A
57
Q
A
58
Q

what is hemiballismus?

A

Hemiballismus is a hyperkinetic involuntary movement disorder characterized by intermittent, sudden, violent, involuntary, flinging, or ballistic high amplitude movements involving the ipsilateral arm and leg caused by dysfunction in the central nervous system of the contralateral side

thrashing movement contralaterally. caused by a subthalamic stroke

PBL SEM 3 (49 decks)

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