The caudate nucleus is a curved or C-shaped structure in its complete form. The head of the caudate can be identified in the inferolateral walls of the frontal horns of the lateral ventricles. The caudate nucleus and putamen together make up the striatum, which is critical for movement control and coordination along with behavioral regulation.
Clinical significance: Molecular changes in Huntington disease lead to neuronal loss in the striatum
The purpose is to regulate the activity of motor cortex, using thalamus.
Direct pathway: Starts with cortical excitation of D1-receptor-expressing Medium Spiny Neurons (MSNs) in the Striatum.
D1 Receptor: Dopamine binds to and activates the D1 receptor. The consequence of this activation is typically excitatory for the neuron (e.g., increased cAMP, making it more likely to fire).
Like an air conditioner that cools the room (inhibits GPi). Dopamine makes the AC run stronger. Removing dopamine makes the AC weaker.
Indirect pathway: Starts with cortical excitation of D2-receptor-expressing Medium Spiny Neurons (MSNs) in the Striatum.
D2 Receptor: Dopamine binds to and activates the D2 receptor. The consequence of this activation is typically inhibitory for the neuron (e.g., decreased cAMP, making it less likely to fire).
Like a heater that warms the room (excites GPi). Dopamine turns the heater down. Removing dopamine lets the heater run hotter.
Either way, dopamine stimulates the activity of cortex.
Parkinson disease: no dopamine → no stimulation
Huntington disease:
Early: D2-MSNs in striatum is affected → can't inhibit indirect pathway → too much activation
Later: all striatum damaged → no activation at all
Mnemonic
The direct pathway Comes Straight Into the Thalamus:
Cortex → Striatum → Internal GP → Thalamus.
The indirect pathway Comes Straight, Exits, then Sidesteps Into the Thalamus:
Cortex → Striatum → External GP → STN → Internal GP → Thalamus.
