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Brain & behaviour > Lecture 3 - Motor Control, Dopamine and Basal Ganglia > Flashcards

Lecture 3 - Motor Control, Dopamine and Basal Ganglia Flashcards

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1
Q

What are the 4 motor Related structures in CNS

A

Key structures involved in movement and motor control:

  1. Motor Cortices
  2. Basal Ganglia (also known as striatul complex)
  3. Cerebellum
  4. Spinal Cord
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2
Q

What makes up the motor cortices?

A

Cortical Motor Areas:

  1. Primary Motor Cortex (M1)
  2. Premotor Cortex (PMC)
  3. Supplementary Motor area/ cortex (SMA)
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3
Q

Outline the Primary Motor Cortex

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A
  • Known as the M1
  • Large Pryamidal output neurons (Betz cells)
  • Most of the axons (85%) go into contralateral spinal cord for direct motor control
  • associated with fine, discrete movements
  • contralateral means to the other side
  • Direct motor control via spinal cord efferents
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4
Q

Outline the Premotor Cortex/ Area

A
  • Also known as the PMC/ PMA
  • Helps you respond to stimuli
  • Output mainly to M1
  • These neurons are to do with ANTICIPATED MOVEMENTS - planning movements
  • Prepares M1 for planned movements
  • lesion lead to slowing of anticipated movements but not paralysis
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5
Q

Outline Somatotropic Organisation of M1

A
  • For each different party of body, there is a different area of the motor cortex activated (from brain scans)
  • Disproportionate amount of motor cortex devoted to fingers and speech muscles (lips, larynx etc)
  • More neurons and more energy required = larger area dedicated to it
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6
Q

Outline the Supplementary Motor Area

A
  • Ouput again mainly to M1
  • For Complex movements, like the ones that use several muscles or which cross the sides of the body
  • Complex voluntary movements (playing piano) but not for simple acts
  • even if that movement is just imagined its activated
  • Lesions inhibit ability to perform complex movements

Complex motor plan rehersal

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7
Q

What do SMA and PMA do then?

A

Prepare M1 for complex movements

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8
Q

What other information does the SMA & PMA use

A

Whilst doing a complex movement like running down the wing in footbal, SMA & PMA use:

  • Visual information: looking when pass is coming
  • Auditory: someone shouting your name
  • Where we are in space and time

SMA & PMA constantly monitoring this and feeding it back to the M1

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9
Q

Outline the roles (4) of the cerrebellum

******

A

Basically takes all this information and relays it to the spinal cord, where the instructions are sent to
- so it can do these quick reflexes but also skilled movements

  1. Postural reflexes - if you dont have time to loop all this information around the brain, it just goes straight from here to spinal cord
  2. Rapid skilled limb movements
  3. Integration of movement sequences
  4. Motor Learning
    - from comparing expected sensory feedback to actual feedback
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10
Q

What are the damage effects on the cerrebellum

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A

Cerebellar Ataxia

  • Posture and balance disturbance
  • Limb rigidity (smooth movement of seperate joints, but it is staccato and not integrated)
  • Poor timing of ballistic (rapid, aimed) movements (throwing ball, kick ball etc)
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11
Q

What are the 4 components of the Basal Ganglia or (Straitul complex)
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A
  1. Caudate Nucleus - these first two overlay everthing
  2. Putamen -
  3. Globus Pallidus (has a lateral and medial (outside and inside))
  4. Substantia Nigra (at bottom, feeds DA into the system)

Thalamus is between 2 tails of the caudate

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12
Q

What is the Basal Ganglia important for?

*******

A

Critical for selecting motor plans and initiating movement

- planning and initiating movements

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13
Q

What are the inputs to the Basal Ganglia

*******

A
  1. Primary Motor + Somatosensory Cortex (using glutamate)

2. Substantia Nigra (Dopamine)

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14
Q

What are the outputs to the Basal Ganglia

A
  1. Back to M1, PMA and SMA (Via thalamus)

2. brainstem motor nuclei via ventrodmedial pathway - for automated movements

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15
Q

What are the 2 processing routes involved in the Basal ganglia

A
  1. Direct (excitatory)
  2. Indirect (inhibitory)

Movement requires a balance of excitatory and inhibitory stuff

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16
Q

Outline the Direct basal Ganglia processing route

A
  1. Cortex (glutamate - excitatory)
  2. Putamen (GABA - inhibitory)
  3. Globus Pallidus Internal (GABA - inhibitory)
  4. Thalamus (Glutamate - excitatory)
  5. Back to Cortex

Overall the direct route is excitatory

Stimulated by dopamine input to the Putamen from substantia nigra, via D1 Receptors
- D1 receptors are an excitatory family, they accept excitatory input

17
Q

Outline the indirect basal Ganglia processing route

A
  1. Cortex (gluatmate - excitatory)
  2. Putamen (GABA- inhibitory)
  3. Globus Pallidus External (GABA - inhibitory)
  4. SUB-THALAMIC NUCLUES (glutamate - excitatory)

At this point rejoins the direct route:

  1. Back to the Globus Pallidus Internal (GABA)
  2. Thalamus (Glutamate)
  3. Back to cortex

Overall the indirect route is inhibitory

Suppressed by dopamine input to putamen, from substantia nigra, via inhibitory D2 Receptors
- longe route, Dopamine suppresses the routes with D2 receptors

18
Q

What controls the balance between these two routes?

A

Dopamine input to the Putamen from the Substantia Nigra control balance

Need a balance because if we had too much excitatory input (direct), we would move all the time
- need the indrect route to return movements to resting states

19
Q

What type of receptor are dopamine receptors

*******

A

Metabotropic receptors

  • G-protein coupled
  • not directly linked to Ion channels
20
Q

Outline the D1 Family of dopamine receptors

A

D1 family is made up of:

  1. D1 Receptors
  2. D5 Receptors

These are excitatory

  1. Coupled to Gsa (Second messenger protein) GS ALpha
  2. this activates the process of ADENYLYL CYLCASE
  3. This increases intracellular second messenger cAMP (Cyclic Adenosie Monophosphate)
21
Q

Outline the D2 Family of dopamine receptors

****

A

D2 Family is made up of:

  1. D2 Receptors
  2. D3 Receptors
  3. D4 Receptors

These are inhibitory

  1. Coupled to Gia (second messenger protein) Gi alpha
  2. This inhibits adenyly cyclase
  3. Reduces intracellular second messenger cAMP
22
Q

Which part of the Basal Ganglia Processing route is most important?

A

Dopamine Goes from :

  1. Substantia nigra to
  2. putamen

Putamen is very important, because it has both D1 receptors and D2 receptors

  • At this point it can go either way
  • can be excitatory (direct route) or inhibitory (indirect route)

We can use the same neurotransmitter to inhibit or excite the system

23
Q

What are the motor symptoms of Parksinsons Disease

A

• Resting tremor, ‘pill rolling’ hands
- old people may have a tremor, but this is pill rolling
•Muscular rigidity and stiff limbs
• poor balance, slow movement
- e.g. writing becomes spider like, cant control fine movements
• Problems initiating/ regulating movement sequence
- starting/ stopping movement, and postural balance
- might be able to initiate but not regulate or not be initiate at all

24
Q

What are the mood/cognitive symptoms of Parksinsons Disease

****

A 
• Can often start with a depression (40-50% of cases)
• Anxiety disorder also common, 1 in 4
- perhaps hallucinations
•Cognitive problems, memory, attention
- can have 'Parkinsons with dementia'
25
Q

What is cause of Parkinsons?

A

Caused by neuron loss in Substantia Nigra

- leads to a lack of dopamine in the putamen

26
Q

What is treatment for Parksinsons?

A

L-dopa (DA precursor)

27
Q

What are side effects of L-Dopa

A

•Dyskensia/ Dystonia

- involuntary movements and postures due to too much DA in putamen, similar to Huntingtons

28
Q

Outline Lewy Body Dementia

**

A
  • Flucuating attention, not always alert, concious seems to fluctuate
  • Second most common dementia
  • Lewy bodies in CNS cells, predominantly in brain
  • Hallucinations
  • issues with language and planning
  • Shown by Trail Making Test B
29
Q

What are symptoms of huntingdons disease?

******

A

•Uncontrollable movements

  • not planned, coordinated or controlled
  • jerky limbs:CHorea
  • often mistaken for being drunk/ mad
  • cant stay seated
  • Usually starts around 20-40
  • progressive, eventually fatal after around 20 years
30
Q

What are causes of huntingtons?

******

A

• Rare genetic mutation in huntington gene
• Cell loss in caudate nuclues & Putamen
- means the indirect route is weaker, and the direct route is stronger
- weak indirect means you cannot inhibit movements
- much more activation in Basal Ganglia - leading to involuntary movements

31
Q

What are treatments for huntingtons?

A
  • Various drugs to manage symptoms

- no long term cure: its progressive

32
Q

What is the difference in where things are wrong in Parkinsons compared to huntingtons?
******

A

Parkinsons:

  • Substantia Nigra is broken - not sending dopamine to either inhibitory or excitatory systems
  • not much dopamine going to Putamen
  • no dopamine mean input = cant initiate movement
  • lack of movement

huntingtons:

  • Caudate and Putamen is broken
  • making excitatory route much stronger
  • Link between D2 and Gpe is broken too
  • D1 route is much stronger - cant control it
33
Q

What is Dopamine Critical for?

A

Motor regulation

  • critical in regulating movement
  • in the basal ganglia
  • Produced in Substania Nigra
34
Q

What are the other roles in the brain of Dopamine?

*******

A
  • Cognitive function & memory (ageing)
  • Mood
  • Hallucinations, psychosis, Sz
  • Reward Systems (VTA -> Nuclues Accumbens)
  • Target for recreational drugs - because of reward systems, its the happy NT
35
Q

What can too much dopamine cause?

*******

A

Over time, the body becomes used to it, and doesnt produce any

  • so you get ticks/ tardive dyskenisia and chorea type movements
  • have to lower Da down but the person returns to parkinsons symptoms
36
Q

Outline Dopamine Synthesis

A
  1. Phenylalanine
  2. Tyrosine (starts as an amino acid)
  3. Dopa (now a neurotransmitter)
  4. Dopamine
  5. Norepinephrine
  6. Epinephrine
37
Q

Why do you have to give a parkinsons patient L-dopa

A
  • Dopamine cant pass the blood brain barrier
  • have to give a precursos that can - l-dopa
  • Have to hope it will be converted into dopamine, but if their system is so broken, it might not happen
38
Q

Whats bad about synthesis/ giving l-dopa

A

1: Free Radicals
- Synthesis generates other stuff as well as Dopamine, compounds that can damage DNA// damage cells are a byproduct
- these are called free radicals
- can cause Az or accelerate ageing

2: Oxidative stress
- too much dopamine/ L-Dopa and brain gets stressed trying to use it all
- Might accelerate ageing
- or worsen Parkinsons symptoms

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