Neuro 62: Basal Ganglia Flashcards
1
Q
How do the basal ganglia affect mvmnt?
A
- play a role in starting mvmnt, not active during rest
- enhance cortical motor activity
- FACILITATE mvmnt –> provide a boost, since the UMN activity in the cortical motor areas is not enough to cause mvmnt
- involved in positive feedback loop with cortical motor areas
- use both excitation and inhibition in pathways
2
Q
Extrapyramidal
A
-another term for the corticospinal tract
3
Q
5 components of the basal ganglia & locations
A
- caudate
- cerebral hemisphere - putamen
- cerebral hemisphere - globus pallidus- has 2 parts = internal (GPi) and external (GPe)
- cerebral hemisphere - substantia nigra- has 2 parts = pars compacta and pars reticulata
- midbrain - subthalamic nucleus
- midbrain
4
Q
The 2 different pathways of the BG
A
- Motor
- Association/cognitive loop
- both pthwys have similar organization & utilize parallel circuits
- why parkinsons and huntington pts can have cognitive and emotional deficits
5
Q
Role of subthalamic nucleus (STN)
A
-STN neurons have excitatory (glutamatergic) synapses on the GPi
6
Q
Role of substantia nigra
A
- pars compacta (SNc) = dopaminergic part
- releases dopamine which will bind to D1 and D2 receptors in the putamen
7
Q
Dopamine receptors in the putamen
A
- D1 = excited by dopamine via opening of Na channels –> depolarization and excitation
- D2 = inhibited by dopamine via K+ channels opening
- so dopamine turns the “accelerator” on and the “brakes” off and causes the VL to be active = +cortex
8
Q
Tonic activity in the BG
A
- many components in the pathway are tonically active = activity is normally ON
- the circuit can influence cortical motor areas even when there is no input to the putamen
- so when there is damage to any component of the pathway the system does not turn off, it just gets out of control
9
Q
Excitatory NTs
A
- Ach
- glutamate
- dopamine
10
Q
Inhibitory NTs
A
- GABA
2. dopamine
11
Q
Parkinson’s disease
A
- loss of substantia nigra’s dopamine effects:
1. direct pathway = less activity of D1 receptors –> GP1 more active –> VL less active –> decrease in voluntary mvmnt = bradykinesia/akineasia
2. Indirect pathway = more activity of GPi –> less VL activity –> decrease in voluntary mvmnt = bradykineasia/akineasia - *get abnormal rhythmic activity in basal ganglia neurons = tremor that decreases during voluntary mvmnt and increases with stress
12
Q
Effect of too little dopamine
A
- decrease in accelerator pathway & increase in break pthwy –> decrease mvmnt
13
Q
Effect of too much dopamine
A
- increase in accelerator & decrease in break –> spontaneous mvmnt
- caused by too much meds
14
Q
Role of Ach
A
- Ach and dopamine have antagonistic effects in the BG circuit
- when there is a loss of dopamine the release of Ach increases –> this worsens the effects of the dopamine loss
- balance of Ach and dopamine can be corrected through the use of anticholinergics
15
Q
Huntington disease
A
- D2 receptors degenerate –> decrease in STN activity –> decreases GPi activity –> increase in VL activity –> increase in motor cortex excitability = spontaneous mvmnt
- autosomal dominant
- sx usually appear in adulthood