Basal Ganglia Flashcards

1
Q

What is tbe primary function of the basal nuclei?

A
  1. Stop motor movement
  2. Start motor movment
  3. Modulate motor movement
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2
Q

Explain the basic steps of the interaction between the basal nuclei, thalamus and motor cortex

A
  1. The cortex plans and decides movement and sends a signal to the basal nuclei
  2. The basal nuclei receive and interprets information on the direction and amplitude of the movement and decides what package of movement is appropriate
  3. Basal nuclei relay the decision to the thalamus
  4. The thalamus decides to either:
    • Excites the cerebral cortex to facilitate wanted movement
    • Dampens the cerebral cortex to inhibit unwanted movement
  5. Information then relayed to motor cortex
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3
Q

What are the 2 effects that the thalamus can have on information going from the basal nuclei to the cortex?

A

Can either:

  1. Excites the cerebral cortex to facilitate wanted movement
  2. Dampens the cerebral cortex to inhibit unwanted movement
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4
Q

How would lesions of the basal ganglia present?

A

Dyskinesia (abnormal, involuntary movements)

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5
Q

What is an excitatory neuron?

A

Releases neurotransmitter that has an excitatory effect; activating/enhancing structure

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6
Q

What is an inhibitory neuron?

A

Releases inhibitory neurotransmitters; inhibit/dampen down activity of structure

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7
Q

What is the overall effect of an excitatory neuron exciting an excitatory neuron?

A

Enhanced activation effect on structure

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8
Q

What is the overall effect of an excitatory neuron exciting an inhibitory neuron?

A

Enhanced inhibition effect on structure

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9
Q

What is the overall effect of an inhibitory neuron inhibiting an inhibitory neuron?

A

Decreased/removal of inhibition (i.e. activation)

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10
Q

Anatomically, what are the basal nuclei?

A

Closely related (anatomically and embryologically) masses of grey matter in the forebrain

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11
Q

What are the 5 important individual structures of the basal nuclei?

A
  1. Caudate nucleus
  2. Putamen
  3. Globus pallidus
  4. Substantia nigra
  5. Subthalamic nucleus
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12
Q

From which 2ary vesicle does each structure develop from;

a) caudate nucleus
b) putamen
c) globus pallidus
d) substantia nigra
e) subthalamic nucleus

A

a) telencephalon
b) telencephalon
c) telencephalon
d) mesencephalon
e) diencephalon

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13
Q

What makes up the ‘neostriatum’?

A

Caudate nucleus + putamen

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14
Q

Why can the caudate nucleus & putamen be grouped together as the neostriatum?

A

Develop embryologically from the same origin

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15
Q

What makes up the corpus striatum?

A

Putamen + globus pallidus + caudate nucleus

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16
Q

What makes up the lentiform nucleus?

A

Putamen + globus pallidus

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17
Q

The globus pallidus has 2 segments. What are these?

A
  1. Internal
  2. External
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18
Q

What is the globus pallidus also known as?

A

Paleostriatum

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19
Q

The substantia nigra has 2 parts. What are these?

A
  1. a reticular (pars reticulata)
  2. a compact part (pars compacta)
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20
Q

Which part of the globus pallidus does the pars reticulata of the substantia nigra ‘act as one’ with?

A

Internal globus pallidus and pars reticulata are functionally similar –> act as one

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21
Q

Which part of the basal nuclei is responsible for the release of dopamine?

A

Pars compacta of substantia nigra; The compact part has many melanin containing cells which release dopamine.

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22
Q

Location of basal ganglia

A
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23
Q

Shape of caudate nucleus?

A

C-shaped

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24
Q

The caudate and putamen are fused in some areas but separated in others.

a) what are they fused by?
b) what are they separated by?

A

a) fused by ‘cellular bridges’
b) separated by fibres of internal capsule

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25
Q

Location of external vs internal segments of globus pallidus in relation to putamen and internal capsule?

A

a) external segment closer to putamen
b) internal segment closer to internal capulse

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26
Q

4 divisions of the diencephalon?

A
  1. Thalamus (orange)
  2. Hypothalamus (pink)
  3. Epithalamus (green)
  4. Subthalamus (red) –> this part contains the subthalamic nucleus
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27
Q

Anatomical location of subthalamic nucleus:

A

Subthalamic nucleus is below the thalamus and slightly lateral to it

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28
Q

Anatomical location of substantia nigra:

A
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29
Q

Why does the pars compacta of the substantia nigra stain dark?

A

Dark appearance due to melanin-containing neurones (melanin stains dark) which release dopamine

(pars reticula does NOT stain dark)

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30
Q

Cortical output is modulated via multiple, parallel looping circuits from the cerebral cortex back to the cerebral cortex. Where must ALL relays occur through? through the thalamus.

A

Through the thalamus

31
Q

What makes up the ‘input nuclei’? Where do they receive/send information from/to?

A
  • N.B. This is also known as striatum
  • Made up of: Caudate nucleus + Putamen
  • Function: Receive information from cortex (afferent fibres) and send information to the output nuclei
32
Q

What makes up the ‘output nuclei’? Where does it receive information from/send information to?

A
  • Made up by; Globus pallidus internal (Gpi) + Substantia nigra pars reticulata (Snr)
  • Recevies info from: Input nuclei
  • Sends info to: Thalamus
33
Q

What is the ‘default state’ of the thalamus?

A

Excitatory –> always trying to excite cortex (unless inhibited)

34
Q

What is the ‘default state’ of the output nuclei?

A

Inhibitory - to ensure we are not constantly moving

35
Q

What is the ‘default state’ of the input nuclei?

A

Inhibitory

36
Q

What is the default state of fibres going from cortex to input nuclei?

A

Excitatory

37
Q

After the thalamus has received information from the output nuclei, what are the 2 ways in which it can influence the cortex?

A
  1. Enhance inhibition (N.B. default connection between output nuclei and thalamus is inhibitory) –> prevent unwanted movement
  2. Prevent inhibition –> allow movement to happen
38
Q

What are the 2 types of afferents received by the basal nuclei?

A
  1. Corticostriatal fibres
  2. Nigrostriatal fibres
39
Q

Where do corticostriatal fibres come from? Go to?

A
  • Come from cortex (hence cortico-)
  • Go to striatum (input nuclei) (hence -striatum)
40
Q

Where do nigrostriatal fibres come from? Go to?

A
  • Come from; pars compacta of substantia nigra (hence nigro-)
  • Go to; striatum (hence -striatum)
41
Q

Do corticostriatal fibres have excitatory or inhibitory effects?

A

Excitatory information about movement

42
Q

Do nigrostriatal fibres have excitatory or inhibitory effects? What do they bring with them?

A

Can have excitatory or inhibitory effects, depending on the type of receptor on the postsynaptic neurone. Bring dopamine to the striatum.

43
Q

There are 2 routes that neurons can take after synapsing at the striatum. What are these?

A
  1. Direct route; neuron from striatum goes directly to the Gpi (internal) of the globus pallidus (output nuclei)
  2. Indirect route; neuron goes through the Gpe (external) of the globus pallidus
44
Q

Afferent connections pathway:

A

N.B. In the following pathways, afferent inputs are shown projecting only to the putamen. In reality, inputs project to the caudate as well.

45
Q

Efferent signals of the basal nuclei pathway can be sent which which 2 structures?

A
  1. Globus pallidus internus
  2. Pars reticula of the substantia nigra

N.B. they pass here AFTER the input nuclei (putamen/caudate)

46
Q

What type of fibres does the Gpi always send to the thalamus (i.e. default state)? Why?

A

Inhibitory (pallido-thalamic) fibres –> to prevent the constant activation that the thalamus sends to the cortex by default

47
Q

Are the thalamocortical fibres excitatory or inhibitory?

A

Excitatory (default state) - facilitating movement

48
Q

What is the thalamus under chronic inhibition by?

A

The thalamus is under chronic inhibition by pallidothalamic fibres from the GPi+SNr neurones

49
Q

Efferent pathway:

A

N.B. Efferent inputs are shown projecting only from the GPi. outputs project from SNr as well.

50
Q

Describe the basic overall steps of the direct pathway of the basal ganglia

A
  1. Cortico-striatal fibres (excitatory default) pass from cortex to striatum; synapse in striatum
  2. Fibres (inhibitory default) pass from striatum to GPi; synapse in GPi
  3. Pallidothalamic fibres (default inhibitory) pass from GPi to thalamus; synapse in thalamus) – there is disinhibition of thalamus (prevention of unwanted movement)
  4. Thalamocortical fibres (default excitatory) pass from thalamus to cortex
51
Q

What is the overall fucntion of the direct pathway of the basal ganglia?

A

Enhances movement

52
Q

Explain how the steps of the direct pathway of the basal ganglia enhances movement

A
  1. Cortico-striatal afferent fibres (always excitatory) go from cortex to striatum
  2. These neurones synapse to an inhibitory neurone going directly to the GPi; this enhances the inhibition (excitatory neuron exciting inhibitory neuron)
  3. These neurons then synapse to an inhibitory neuron (pallidothalamic fibre) in the GPi; this decreases the inhibition (inhibitory neuron inhibiting inhibitory neuron)
  4. Inhibitory effects of the pallidothalamic fibres are decreased; these fibres then pass to the thalamus from the GPi
  5. Decreased inhibition of thalamocortical fibres; travel from the thalamus to the cortex to stimulate the cortex to facilitate movement
53
Q

What is the overall function of the indirect pathway of the basal ganglia?

A

Overall effect of indirect pathway is a dampening of the excitatory thalamo-cortical pathway, and this decreased movement

54
Q

Explain how the steps of the indirect pathway decreases movement

A
  1. Cortico-striatal afferent fibres (always excitatory) go from cortex to striatum; synapse in striatum
  2. These neurons synapse to inhibitory neurones that go to the Globus Pallidus externa (GPe) where they sypapse –> activity of inhibitory neuron is increased (more inhibition) due to excitatory neuron exciting an inhibitory neuron
  3. Inhibitory neuron then travel to reaches the subthalamic nucleus where it synapses –> activity of inhibitory neuron is decreased (less inhibition) due to inhibitory neuron inhibiting inhibitory neuron
  4. Subthalamic nucleus then talks back to the GPi; sends excitatory neuron (default) to the GPi where it synapses –> activity of this excitatory neuron is increased (due to reduced inhibition of previous inhibitory neuron)
  5. Fibre then passes from GPi to the thalamus (default inhibitory) where they synapse –> leads to increased inhibition due to excitatory neuron exciting an inhibitory neuron
  6. Thalamocortical neurons (excitatory) then pass from the thalamus to the cortex –> the activity of these neurons is then under inhibition (due to inhibition from previous fibres)
55
Q

Are these fibres always excitatory or inhibitory?

a) corticostriatal
b) pallidothalamic (from GPi to thalamus)
c) thalamocortical
d) fibres from striatum to GPi
e) fibres from striatum to GPe
f) fibres from GPe to subthalamic nucleus
g) fibres from subthalamic nucleus to GPi

A

a) excitatory
b) inhibitory
c) excitatory
d) inhibitory
e) inhibitory
f) inhibitory
g) excitatory

56
Q

Key points 1:

A

To influence movement, the basal nuclei function primarily through balancing between inhibition and disinhibition (release from inhibition) of thalamocortical pathways.

Basal ganglia:

  • Facilitate ongoing movements that are required and appropriate.
    • = Direct pathway: leads to excitation of the cortex from the thalamus
  • Inhibit unwanted movements.
    • = Indirect pathway: leads to inhibition of the cortex from the thalamus
57
Q

How can the substantia nigra modulate the direct/indirect pathway?

A

Releases dopamine –> main function is to INITIATE movement (i.e. excite direct pathway and inhibit indirect pathway)

58
Q

Nigrostriatal fibres can be excitatory or inhibitory. How is this decided?

A

Depending on if dopamine binds to D1 or D2 receptors.

59
Q

What is the effect of dopamine (released from nigrostriatal fibres) binding to D1 receptor (located in the striatum)?

A

Dopamine + D1 receptor = activation

This leads to enhanced activation of the thalamus and then cortex (go back and see path) –> activates direct pathway and movement is initiated

60
Q

What is the effect of dopamine (released from nigrostriatal fibres) binding to D2 receptor (located in the striatum)?

A

Dopamine + D2 receptor = inhibition

  • This leads to disinhibition of the indirect pathway, so thalamus is activated and cortex is activated
  • Movement is initiated
61
Q

In what condition can you see the degerenation of substantia nigra?

A

Parkinson’s

62
Q

Explain the steps of how the degeneration of substantia nigra can result in failure to initiate movement

A
  1. Loss of dopamine producing neurons (nigrostriatal)
  2. Less activation of D1 neurons through direct pathway
  3. This decreases inhibition of next neuron (increases activity)
  4. This inhibits thalamocortical fibres to a greater extent (decreases activity)

OVERALL EFFECT: Increased inhibition of thalamocortical fibres

63
Q

What are hypokinetic disorders? Presentation?

A

Hypokinesia is a type of movement disorder. It specifically means that your movements have a “decreased amplitude” or aren’t as big as you’d expect them to be.

  • Slow movement, poor initiation
    • Walk slowly, little steps
    • External initiation (can move if someone pushes them)
    • Mask face: cannot initiate facial expression (infrequent blink)
  • Rigidity
  • Tremor
64
Q

What does the most common disease of the basal ganglia involve?

A

Most common disease of the basal ganglia involved disruption of nigrostriatal (lesions of substantia nigra) input, leading to Parkinson’s disease (due to lack of dopamine release)

65
Q

What are hyperkinetic disorders?

A

Unwanted movements occur

66
Q

What type of disorder is Hemiballismus? What lesion does it result from?

A
  • WHAT: a rare hyperkinetic movement disorder, that is characterised by violent involuntary limb movements on one side of the body
  • LESION: degeneration of the subthalamic nucleus
67
Q

What is chorea?

A

Chorea is a movement disorder that causes involuntary, irregular, unpredictable muscle movements.

68
Q

What type of disorder is Huntington’s (chorea)? What lesion does it result from?

A
  • WHAT: hyperkinetic
  • LESION: degeneration of inhibitory fibres from striatum to globus pallidus
69
Q

Explained direct and indirect pathways:

A
  1. Excitatory neuron (corticostriatal) from cortex to striatum
  2. DIRECT:
    1. Inhibitory neuron from striatum to GPi
    2. Inhibitory neuron (pallidothalamic) from GPi to thalamus
    3. Excitatory neuron (thalamocortical) from thalamus to cortex
    4. OVERALL –> excitatory thalamocortical fibres NOT inhibited
  3. INDIRECT:
    1. Inhibitory neuron from striatum to GPe
    2. Inhibitory neuron from GPe to subthalamic nucleus
    3. Excitatory neuron from subthalamic nucleus to GPi
    4. Inhibitory neuron (pallidothalamic) from GPi to thalamus
    5. Excitatory neuron (thalamocortical) from thalamus to cortex
    6. OVERALL –> inhibition of excitatory thalamocortical fibres
70
Q

What type of disorder does a lesion to the subthalamic nucleus result in?

A

Hyperkinetic - Hemiballismus

71
Q

Explain how a lesion to the subthalamic nucleus can lead to hyperkinesia

A

This is a failure of the indirect pathway.

  • Normal indirect pathway:
    • Excitatory neuron (corticostriatal) from cortex to striatum
    • Inhibitory neuron from striatum to GPe
    • Inhibitory neuron from GPe to subthalamic nucleus
    • Excitatory neuron from subthalamic nucleus to GPi
    • Inhibitory neuron (pallidothalamic) from GPi to thalamus
    • Excitatory neuron (thalamocortical) from thalamus to cortex
    • OVERALL –> inhibition of excitatory thalamocortical fibres
  • Lesion to subthalamic nucleus:
    • Lesion to subthalamic nucleus
    • Excitatory neuron from subthalamic nucleus is not really working causing reduced inhibitory effect of pallidothalamic neuron (from GPi to thalamus)
    • Decreased inhibition (increased excitation) of thalamocortical fibre (from thalamus to cortex) –> hyperkinesia
72
Q

What type of disorder does a lesion to the inhibitory fibres from striatum to GPe result in?

A

Hyperkinesia; Huntington’s

73
Q

Explain how a lesion to the inhibitory fibres from the striatum to GPe can lead to hyperkinesia

A

This is a failure of the indirect pathway.

  • Normal indirect pathway:
    • Excitatory neuron (corticostriatal) from cortex to striatum
    • Inhibitory neuron from striatum to GPe
    • Inhibitory neuron from GPe to subthalamic nucleus
    • Excitatory neuron from subthalamic nucleus to GPi
    • Inhibitory neuron (pallidothalamic) from GPi to thalamus
    • Excitatory neuron (thalamocortical) from thalamus to cortex
    • OVERALL –> inhibition of excitatory thalamocortical fibres
  • Damage to inhibitory fibres from striatum to GPe:
    • Degeneration of inhibitory fibres from striatum to GPe
    • Loss of inhibition of inhibitory neuron from GPe to subthalamic –> increased inhibitory effect
    • Increased inhibition of excitatory neuron from subthalamic nucleus to GPi –> deceased activity of this neuron
    • Decreased excitation of inhibitory pallidothalamic neuron from GPi to thalamus –> decreased inhibitory effect of this neuron
    • Decreased inhibition of excitatory thalamocortical neuron from thalamus to cortex –> hyperkinesia