Basal Ganglia Flashcards
Function of Basal Ganglia
The Supervisor - regulates UMN activity
Structures that make up the Subcortical Loop
Caudate, Putamen, Globus Pallidus.
Substantia Nigra Pars Compacta & Pars Reticulata.
Subthalamic Nuclei.
Direct pathway function
Green light - releases UMNs from tonic inhibition
Indirect pathway function
Brakes - increases tonic inhibition
Input zone
Corpus Striatum (Caudate + Putamen)
Corpus Striatum receives projections from
- Cortex (Corticostriatal Pathway).
2. SNpc (Nigrostriatal Fibers).
Medium Spiny N (from the Striatum) project to
Globus Pallidus
SNpr
Output zones
Globus Pallidus
SNpr
Striatum releases
GABA (inhibitory)
Direct pathway: which Dopamine receptor? Excitatory or inhbitory?
D1 excitatory
Indirect pathway: which Dopamine receptor? Excitatory or inhbitory?
D2 inhibitory
Hemiballismus
Violent uncontrolled movements (unilateral).
Damage to contralateral Subthalamic Nuclei - UMNs receive less tonic inhibition.
4 Cardinal Signs of Parkinsons
- Tremor
- Rigidity
- Akinesia
- Posture changes
Parkinsons: posture & gait
Stooped over, arms flexed.
No arm swing, shuffles, unable to stop.
Parkinsons: Cogwheel Rigidity
segmental, jerky motions
How does Parkinson’s affect the direct pathway?
Decreased inputs from SNpc to Caudate/Putamen.
Less inhibition to GPI (so GPI more active).
More inhibition to Thalamus.
Decreased excitatory output from Thalamus to Cortex.
How does Parkinsons affect the indirect pathway?
Decreased inputs from SNpc to Caudate/Putamen.
More inhibition to GPE (so GPE less active).
GPE no longer sending inhibitory signals to Subthalamic Nuclei (so Subthal more active).
Subthalamic Nuclei sends more excitatory to GPI (so GPI more active).
Huntington’s Disease
Inappropriate motor activity - “choreiform” movements.
Genetic disease, gradual onset, atrophy of C+P.
Bilateral s/s.
How does Huntington’s affect the pathway?
C+P send less inhibitory to GPE (so GPE more active).
GPE sends more inhibitory to Subthalmic & GPI (both less active).
Subthalamic sends less excitatory to GPI (continues making it inactive).
GPI no longer inhibiting Thalamus (so Thalamus hyperactive).
Thalamus increases excitatory output to Cortex.
