Lecture 13: Basal Ganglia Flashcards
What are the functions of Basal Ganglias?
1) Mood and movement 2) Initiation of movement 3) Execution of movement 4) Muscle Tone 5) Effects of Disease
What are the major ‘nuclear components’ of Basal Ganglia?
1) Striatum (caudate nucleus and putamen)
2) Globus Pallidus (GP; internal and external)
3) Subthalamus nucleus (SUT)
4) Substantia Nigra (SN)- midbrain -SN pars reticulata (SNR) -SN pars compacta (SNc- Pigmented cells/dopamine)
Describe the distinction in function between basal ganglia and cerebellium (roughly)
Basal ganglia is trying to plan motor movements Cerebellum is trying to correct the motor movements if they don’t go according to plan.
What does the caudate nucleus and the putamen together form?
Striatum The caudate nucleus and the putamen are separated by the Internal capsule
Name 4 structures that are found outside of the putamen.
1) External capsule (white matter)
2) Claustrum (large sheet of grey matter that sits on the side of the Basal Ganglia)
3) Extreme Capsule (white matter that separates the neocortex from the basal ganglia structures)
4) Insula cortex (important representation of GI system)
The external capsule and the extreme capsule carry white fibres that go from front to back. So some of the optic fibres go through these areas.
Label
1) (head of) Caudate Nucleus
2) Putamen
3) Thalamus
4) Hippocampus
5) Substantia Nigra
6) Red Nucleus
7) External Capsule
8) Corpus Callosum
Label
1) Crus Cerebrei
2) Corticospinal Fibres
3) Basilar Pons
4) Tigeminal Nerve
5) Internal Capusle
6) Fornix
Label
1) Caudate Nucleus
2) Internal Capsule
3) Putamen
4) Globus Pallidus
5) VA-VL (thalamus)
6) Caduate Nucleus
7) Thalamus
8) Claustrum
Describe the Indrect pathway Motor-planning-basal-ganglia circuit
1) The brain sends a fibre from the planning area of the cortex into the striatum (use glutamate EXCITATORY) fibres
2) The Striatum sends a fibre to Substantia Nigra, to GPE and/or GPI (use GABA INHIBITORY)
- if it goes to GPE = indirect pathway
3) From the GPE there’s a fibre which goes to the Subthalamic Nucleus (SUT) (use GABA INHIBITORY)
4) From the SUT, there is a fibre which goes to the GPI (use glutamate EXCITATORY)
5) From the GPI there is a fibre which goes to the VA-VL (use GABA INHIBITORY)
6) From the VA-VL there is a fibre which goes to the motor planning area of the cortex (use glutamate EXCITATORY)
7) The Primary Motor Cortex and the motor planning area talk to each other
Describe the connections of basal ganglia
1) The brain sends a fibre from the planning area of the cortex into the striatum (use glutamate EXCITATORY) fibres
2) The Striatum sends a fibre to Substantia Nigra, to GPE and/or GPI (use GABA INHIBITORY)
- if it goes to GPE = indirect pathway
- If it goes to the GPI = direct pathway (by-pass 3 and 4)
3) From the GPE there’s a fibre which goes to the Subthalamic Nucleus (SUT) (use GABA INHIBITORY)
4) From the SUT, there is a fibre which goes to the GPI (use glutamate EXCITATORY)
5) From the GPI there is a fibre which goes to the VA-VL (use GABA INHIBITORY)
6) From the VA-VL there is a fibre which goes to the motor planning area of the cortex (use glutamate EXCITATORY)
7) The Primary Motor Cortex and the motor planning area talk to each other
Describe the direct pathway Motor-planning-basal-ganglia circuit
1) The brain sends a fibre from the planning area of the cortex into the striatum (use glutamate EXCITATORY) fibres
2) The Striatum sends a fibre to Substantia Nigra, to GPE and/or GPI (use GABA INHIBITORY)
- if it goes to GPE = indirect pathway
- If it goes to the GPI = direct pathway (by-pass 3 and 4)
3) From the GPE there’s a fibre which goes to the Subthalamic Nucleus (SUT) (use GABA INHIBITORY)
4) From the SUT, there is a fibre which goes to the GPI (use glutamate EXCITATORY)
5) From the GPI there is a fibre which goes to the VA-VL (use GABA INHIBITORY)
6) From the VA-VL there is a fibre which goes to the motor planning area of the cortex (use glutamate EXCITATORY)
7) The Primary Motor Cortex and the motor planning area talk to each other
What part of the thalamus does the Basal Ganglia communicate with
VA-VL
What part of the Basal ganglia circuit is wiped out in Huntingtons?
the Inhibitory from Striatum to the GPE.
Describe the nigro-striatal pathway
Nigrostriatal pathway is the efferent connection between the susbtantia nigra and corpus striatum.
Nigrostriatal pathway is one of the major dopaminepathways in the brain.
Nigrostriatal pathway is particularly involved in the production of movement, as part of a system called the basal ganglia motor loop.
This is responsible for holding the other neurons (From ST-SN, ST-GPE, ST-GPE)in a position of ready to fire (Tonically active neurons)
So as soon as glutamate comes down from the cortex, they start firing faster. (e.g. a filled cup ready for the 1 drop from the striatum to overflow)
Neurons from ST-SN, ST-GPE, ST-GPE are_______ which means that they’re in a position of ready to fire.
(Tonically active neurons)
Which bundle of fibres are often damaged in Parkinson’s disease? (In the Basal Ganglia)
Why is this bad?
Striatum to SNc (substantia nigra pars compacta) in the nigrostiatal pathway
the nigrostriatal pathway was supposed to have the other neurons (From ST-SN, ST-GPE, ST-GPE)in a position of ready to fire (Tonically active neurons) (the cup is not full and will not easily overflow)
(like you’re trying to get a hold of someone), the cortex then releases more and more and more glutamate (glutamate is toxicin large doses)
Describe
1) Symptoms
2) Pathology and Neurochemistry
3) Treatment
4) Surgical procedures
of
Parkinsons Disease
- *Symptoms:**
1) Mood (emotionally flat)
2) Bradykinesia (HYPOKINESIA)- slow at initiating movement
3) Tremor at rest
4) Rigidity - *Pathology and Neurochemistry:**
1) Loss of dopamine cells in substantia nigra pars compacta (SNc)
2) Depletion of dopamine in striatum - *Treatment:**
1) Dopamine replacement:
2) drugs (L-DOPA)- precurser of dopamine
3) cell transplantation (fetal/stem cells)
4) gene therapy
Surgery:
1) pallidotomy (GPi)- one side
2) thaladotomy (VA-VL thalamus)- one side
3) deep brain stimulation (GPi, thalamus; pacemaker)
Describe
1) Symptoms
2) Pathology and Neurochemistry
3) Treatment
of
Huntington’s Disease
Dominant gene IT15, short arm chromosome 4
Trinucleotide repeat ("CAG"- \>36)
- *Symptoms:**
1) Behavioural/cognitive changes
2) HYPERKINESIA
3) Involuntary movements - *Pathology and Neurochemistry:**
1) Loss of GABAergic projection neurons in striatum
(lose inhibition of inhibition of the Subthalamic nucleus. GPE can fire as much as it wants which results in hypoexciation of the GPI (decrease in excitation). If these don’t fire as much, it stops the inhibitory fibres from GPI to VAVL from firing and consequently increase in the amount of firing from the VAVL/thalamic pathway to the planning area of the cortex. = exccessive movement
Treatment:
Symptomatic
? gene therapy
? neuron transplants
Describe the Pathways which explains why hyperkinesia is observed in Huntington’s Patients
1) lose inhibition of inhibition of the Subthalamic nucleus.
2) GPE can fire as much as it wants which results in hypoexciation of the GPI (decrease in excitation).
3) If these don’t fire as much, it stops the inhibitory fibres from GPI to VAVL from firing
4) consequently increase in the amount of firing from the VAVL/thalamic pathway to the planning area of the cortex.
= exccessive movement as the cortex is hyperexcited.
