Basal Ganglia Flashcards
(73 cards)
1
Q
What is tbe primary function of the basal nuclei?
A
- Stop motor movement
- Start motor movment
- Modulate motor movement
2
Q
Explain the basic steps of the interaction between the basal nuclei, thalamus and motor cortex
A
- The cortex plans and decides movement and sends a signal to the basal nuclei
- The basal nuclei receive and interprets information on the direction and amplitude of the movement and decides what package of movement is appropriate
- Basal nuclei relay the decision to the thalamus
- The thalamus decides to either:
- Excites the cerebral cortex to facilitate wanted movement
- Dampens the cerebral cortex to inhibit unwanted movement
- Information then relayed to motor cortex
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:
- Excites the cerebral cortex to facilitate wanted movement
- Dampens the cerebral cortex to inhibit unwanted movement
4
Q
How would lesions of the basal ganglia present?
A
Dyskinesia (abnormal, involuntary movements)
5
Q
What is an excitatory neuron?
A
Releases neurotransmitter that has an excitatory effect; activating/enhancing structure
6
Q
What is an inhibitory neuron?
A
Releases inhibitory neurotransmitters; inhibit/dampen down activity of structure
7
Q
What is the overall effect of an excitatory neuron exciting an excitatory neuron?
A
Enhanced activation effect on structure
8
Q
What is the overall effect of an excitatory neuron exciting an inhibitory neuron?
A
Enhanced inhibition effect on structure
9
Q
What is the overall effect of an inhibitory neuron inhibiting an inhibitory neuron?
A
Decreased/removal of inhibition (i.e. activation)
10
Q
Anatomically, what are the basal nuclei?
A
Closely related (anatomically and embryologically) masses of grey matter in the forebrain
11
Q
What are the 5 important individual structures of the basal nuclei?
A
- Caudate nucleus
- Putamen
- Globus pallidus
- Substantia nigra
- Subthalamic nucleus
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
13
Q
What makes up the ‘neostriatum’?
A
Caudate nucleus + putamen
14
Q
Why can the caudate nucleus & putamen be grouped together as the neostriatum?
A
Develop embryologically from the same origin
15
Q
What makes up the corpus striatum?
A
Putamen + globus pallidus + caudate nucleus
16
Q
What makes up the lentiform nucleus?
A
Putamen + globus pallidus
17
Q
The globus pallidus has 2 segments. What are these?
A
- Internal
- External
18
Q
What is the globus pallidus also known as?
A
Paleostriatum
19
Q
The substantia nigra has 2 parts. What are these?
A
- a reticular (pars reticulata)
- a compact part (pars compacta)
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
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.
22
Q
Location of basal ganglia
A
23
Q
Shape of caudate nucleus?
A
C-shaped
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
25
Location of external vs internal segments of globus pallidus in relation to putamen and internal capsule?
a) external segment closer to putamen
b) **internal** segment closer to **internal** capulse
26
4 divisions of the diencephalon?
1. Thalamus (orange)
2. Hypothalamus (pink)
3. Epithalamus (green)
4. Subthalamus (red) --\> this part contains the **subthalamic nucleus**
27
Anatomical location of subthalamic nucleus:
Subthalamic nucleus is below the thalamus and slightly lateral to it
28
Anatomical location of substantia nigra:
29
Why does the pars compacta of the substantia nigra stain dark?
Dark appearance due to **melanin**-containing neurones (melanin stains dark) which release **dopamine**
(pars reticula does NOT stain dark)
30
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.
Through the thalamus
31
What makes up the 'input nuclei'? Where do they receive/send information from/to?
* 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
What makes up the 'output nuclei'? Where does it receive information from/send information to?
* Made up by; Globus pallidus internal (Gpi) + Substantia nigra pars reticulata (Snr)
* Recevies info from: Input nuclei
* Sends info to: Thalamus
33
What is the 'default state' of the thalamus?
Excitatory --\> always trying to excite cortex (unless inhibited)
34
What is the 'default state' of the output nuclei?
Inhibitory - to ensure we are not constantly moving
35
What is the 'default state' of the input nuclei?
Inhibitory
36
What is the default state of fibres going from cortex to input nuclei?
Excitatory
37
After the thalamus has received information from the output nuclei, what are the 2 ways in which it can influence the cortex?
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
What are the 2 types of afferents received by the basal nuclei?
1. Corticostriatal fibres
2. Nigrostriatal fibres
39
Where do corticostriatal fibres come from? Go to?
* Come from **cortex** (hence cortico-)
* Go to **striatum** (input nuclei) (hence -striatum)
40
Where do nigrostriatal fibres come from? Go to?
* Come from; **pars** **compacta** of substantia nigra (hence nigro-)
* Go to; **striatum** (hence -striatum)
41
Do corticostriatal fibres have excitatory or inhibitory effects?
**Excitatory** information about movement
42
Do nigrostriatal fibres have excitatory or inhibitory effects? What do they bring with them?
Can have **excitatory** or **inhibitory** effects, depending on the type of **receptor** on the postsynaptic neurone. Bring **dopamine** to the striatum.
43
There are 2 routes that neurons can take after synapsing at the striatum. What are these?
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
Afferent connections pathway:
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
Efferent signals of the basal nuclei pathway can be sent which which 2 structures?
1. Globus pallidus internus
2. Pars reticula of the substantia nigra
N.B. they pass here AFTER the input nuclei (putamen/caudate)
46
What type of fibres does the Gpi always send to the thalamus (i.e. default state)? Why?
Inhibitory (pallido-thalamic) fibres --\> to prevent the constant activation that the thalamus sends to the cortex by default
47
Are the thalamocortical fibres excitatory or inhibitory?
Excitatory (default state) - facilitating movement
48
What is the thalamus under chronic inhibition by?
The thalamus is under chronic inhibition by pallidothalamic fibres from the GPi+SNr neurones
49
Efferent pathway:
N.B. Efferent inputs are shown projecting only from the GPi. outputs project from SNr as well.
50
Describe the basic overall steps of the **direct** pathway of the basal ganglia
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
What is the overall fucntion of the direct pathway of the basal ganglia?
**Enhances** movement
52
Explain how the steps of the **direct** pathway of the basal ganglia **enhances** movement
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
What is the overall function of the **indirect pathway** of the basal ganglia?
Overall effect of indirect pathway is a dampening of the excitatory thalamo-cortical pathway, and this decreased movement
54
Explain how the steps of the **indirect** pathway **decreases** movement
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
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) excitatory
b) inhibitory
c) excitatory
d) inhibitory
e) inhibitory
f) inhibitory
g) excitatory
56
Key points 1:
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
How can the substantia nigra modulate the direct/indirect pathway?
Releases **dopamine** --\> main function is to INITIATE movement (i.e. excite direct pathway and inhibit indirect pathway)
58
Nigrostriatal fibres can be **excitatory** or **inhibitory**. How is this decided?
Depending on if dopamine binds to D1 or D2 receptors.
59
What is the effect of dopamine (released from nigrostriatal fibres) binding to D1 receptor (located in the striatum)?
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
What is the effect of dopamine (released from nigrostriatal fibres) binding to D2 receptor (located in the striatum)?
Dopamine + D2 receptor = inhibition
* This leads to **disinhibition** of the **indirect** **pathway**, so thalamus is **activated** and cortex is **activated**
* Movement is **initiated**
61
In what condition can you see the degerenation of substantia nigra?
Parkinson's
62
Explain the steps of how the degeneration of substantia nigra can result in failure to initiate movement
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
What are hypokinetic disorders? Presentation?
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
What does the most common disease of the basal ganglia involve?
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
What are hyperkinetic disorders?
Unwanted movements occur
66
What type of disorder is Hemiballismus? What lesion does it result from?
* 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
What is chorea?
Chorea is a movement disorder that causes involuntary, irregular, unpredictable muscle movements.
68
What type of disorder is Huntington's (chorea)? What lesion does it result from?
* WHAT: hyperkinetic
* LESION: degeneration of inhibitory fibres from **striatum** to **globus pallidus**
69
Explained direct and indirect pathways:
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
What type of disorder does a lesion to the subthalamic nucleus result in?
Hyperkinetic - Hemiballismus
71
Explain how a lesion to the subthalamic nucleus can lead to hyperkinesia
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
What type of disorder does a lesion to the inhibitory fibres from striatum to GPe result in?
Hyperkinesia; Huntington's
73
Explain how a lesion to the inhibitory fibres from the striatum to GPe can lead to hyperkinesia
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
