Basal Ganglia Flashcards
What is the function of the basal ganglia?
To make sure specific muscles are active and others inactive to allow for movements.
Describe Striatum
Caudate + putamen + accumbens nucleus
Describe Globus Pallidus
External and internal components. Turn on and off certain areas of thalamus. GPi inhibits thalamus. GPe inhibits GPi and subthalamic nucleus.
Describe substantia nigra
SN compact releases dopamine. SN reticular functions similar to GPi (inhibits thalamus).
Describe subthalamic nucleus
Excites GPi -> inhibition of thalamus.
Describe lenticular nucleus
Putamen + globus pallidus
List components of BG circuitry and associated neurotransmitters.
Cortex, striatum, substantia nigra compacta, GPe and GPi, subthalamic nucleus, thalamus, motor cortex (area 4). Excitatory = glutamate. Inhibitory = GABA.
List and describe BG loops.
- Motor loop: learned movements
- Cognitive loop: motor “intention”
- Limbic loop: emotional aspects of movements
Describe direct motor loop pathway
Direct pathway = GO pathway. In presence of excitatory signal from cortex to striatum (or binding of dopamine from substantia nigra compacta to D1 receptor in striatum), striatum sends inhibitory signal to GPi (which normally inhibits thalamus). In presence of this inhibition of an inhibitor, thalamus if free to send excitatory signal to motor cortex resulting in motor movement.
Describe indirect motor loop pathway
Indirect pathway = NO GO pathway. In presence of binding of dopamine from substantia nigra compacta to D2 receptors in striatum, inhibitory signal sent to GPe (which normally inhibits GPi and subthalamic nucleus). In presence of this inhibition, subthalamic nucleus free to excite GPi, resulting in inhibition of thalamus and lack of signal to motor cortex = no movement.
Describe motor loop pathway deficiency in Parkinsons disease.
In parkinsons, dopamine degeneration. This results in decreased inhibition of GPi -> inhibition of thalamus -> lack of movement. Clinical symptoms = slow movements.
Describe motor loop pathway deficiency in Huntingtons disease.
In huntingtons, degeneration of caudate nucleus (degeneration of striatum). This results in loss of inhibition of GPe -> GPe inhibits subthalamic nucleus and GPi -> inability to inhibit thalamus. Clinical manifestation = spastic movements.