Basal Ganglia Flashcards
What 3 structures make up the basal ganglia
Subthalamus
Substantia nigra
Striatum
What 3 structures make up the striatum
Caudate nucleus
Putamen
Globus Pallidus
Describe the structure/ path of the head of the caudate
Fits into concave recess
Forms a long tapering rod on side of ventricle entering the temporal lobe
Where is the putamen located
Lateral to caudate
Linked to the caudate by spokes of the grey matter
Where is the accumbens located
Lies at anterior inferior junction of caudate and putamen
What makes up the dorsal striatum
Caudate and putamen
What makes up the ventral striatum
Nucleus accumbens
Where does input to basal ganglia come from
The whole body via the substantia nigra pars compacta
Where does output to basal ganglia come from
Thalamus, cortex and globus pallidus interna/ externa
4 functions of basal ganglia
Motor programme switch
Regulates intensity of slow/ stereotyped movements
Inhibit antagonistic and unecessary movements
Regulates attention and cognition
What are medium spiny neurons
Special type of GABAergic inhibitory neurones
95% of neurones with the human body
What is meant by convergence
Large dendritic trees of striatal output neurons
Is the direct pathway excitatory or inhibitory
Excitatory
At rest is the thalamus excited or inhibited
Inhibited
What is the aim of the direct pathway
To remove inhibition of the thalamus
Describe the steps of the direct motor cortex (not including the ‘extra bits’)
1) Excitatory (glutamate) output from the motor cortex synapses with an inhibitory neurone on striatum
2) Inhibition (GABA) of the GPi from striaum
3) Normally the GPi inhibits the thalamus, so when the GPi is inhibited, can’t inhibit thalamus anymore. Thalamus excitatory
4) Thalamus excitatory to the motor cortex
5) Excitation of muscles
Why does excitation of striuatum lead to inhibition of GPi
Striatum is inhibitory to GPi, so more excitation of inhibitory effect- more inhibition
Which 2 structures are involved in the fine tuning of the direct pathway
Substantia nigra and subthalamic nucleus
How does substantia nigra fine tune the direct pathway
Inhibitory neurones to striatum
Synapse with inhibitory neurones from striatum to GPi
Increased activity so increased dopamine to inhibit neurones in striatum
Further excites inhibitory neurones so more inhibition
Describe the steps of the indirect pathway
Motor cortex releases glutamate, excitatory to striatum
Excitation of striatum means more inhibition to GPe
GPe normally inhibits subthalamic nucleus, no more inhibition to Gpe means excitation of STN
STN excites GPI
GPi inhibitory to thalamus- excited GPi= more inhibition to thalamus
In repetitive movement, which pathway is active and which is inactive
Indirect=active
Direct= inactive
In changes of movement which pathway is active and which is inactive
Indirect= inactive Direct= active
Which type of dopamine receptor is involved in which pathway
D1= direct D2= indirect
What happens when dopamine binds to D1 receptor
Increased synthesis of cAMP
Increases sensitivity of striatal cells to glutamate
Projects to GPi directly
What is the overall function of dopamine
Allows motor programme to stop and start at will
How do the subthalamic nucleus and substantia nucleus work in the background for the indirect pathway
STN excites SN
DOpamine neurones from SN go to striatum
Dopamine binds to D2 receptors reducing activity in excitatory neurones
Where in the brain is there a loss of dopaminergic input in PD
Caudate and putamen
Where are cells lost from in PD
Substantia Nigra
What % of cells in the substantia nigra have to be dead before clinical signs of PD show themselves
80
What are the 4 cardinal motor signs of PD
Tremor at rest
Rigidity
Bradykinesia
Loss of postural reflexes
How do you treat early PD with cardinal symptoms but no other complications
Levodopa
Dopamine agonists
MAO-B inhibitors
How do you treat motor and non motor complications, medications and side effects
Levodopa
Dopamine agonists
MAO-B inhibitors
COMT inhibitors
How do you treat life limiting PD with significant disability
Deep brain stimulation
Signs and symptoms of Huntingtons
Hyperkinesis
Extra involuntary movements
Dementia
What changes in the brain change in Huntingtons
loss of GABA-ergic neurones in the striatum
Define ballismus
Involuntary sudden jerky movement
Define athetosis
Involuntary smooth sinuous movement
How can Huntingtons be managed
Neuroleptics (dopamine antagonists)
Atypical antipsychotics
SSRI for depression
Define disinhibition
When there are 2 inhibitory neurones in sequence- inhibition of inhibition= overall excitation
Inputs from where to where are degenerated in parkinsons
From substantia nigra to caudate/ putamen
Is there more of less tonic inhibition of the thalamus in parkinsons
More
Is there increased or decreased excitation of the frontal cortex in PD
Decreased
Input from where to where is degenerated in Huntingtons disease
Caudate to GPe
Is there more or less tonic inhibition of thalamus in huntingtons
Less
Is there increased or decreased excitation of frontal cortex
Increased
