Basal Ganglia Circuit

Hello everyone!  Confusing loop has now simplified look! 👀 

First of all, Basal ganglia receives cortical input, provides negative feedback to cortex to modulate movement.

3 things must be remembered. 

• SNc (Substantia nigra) input to the striatum via the nigrostriatal dopaminergic pathway releases GABA.
• Dopamine binds to D1 , stimulating the excitatory pathway, and to D2 , inhibiting the inhibitory pathway. 
• Pathways from Thalamus to Motor cortex & from Motor cortex to Basal ganglia - “Stimulatory” 

That’s why this circuit is important in voluntary movements and adjusting posture. 

Here is my attempt to simplify this circuit through a drawing. By understanding that you’ll never forget it! 

• I-N-hibitory pathway goes through Gp-I & N-ucleus(Subthalamic)!
• If BG output = +, then increased motor activity
• If BG output = -, then decreased motor activity 

In PARKINSON’S DISEASE, SNc degenerates = lose dopaminergic input to BG

Less stimulation of direct pathway (⬇️gas) and less Inhibition of Indirect pathway (⬆️ brake) = overall indirect wins =less motor activity. This explains bradykinesia and rigidity of PD but not tremor. 

STN and GPi are targets of Deep Brain Stimulation in PD. 

Deep brain Stimulation INHIBITS activity in these structures—inhibiting either would lead to decreased inhibitory output of BG = increased motor activity-> improve PD symptoms. 

Lesion of STN -HEMIBALLISMUS= uncontrolled erratic large amplitude movements on one side.  Why INCREASED movement with STN lesion? 

By decreasing STN excitation of GPi we essentially ‘remove’ indirect pathway from equation, and direct pathway becomes unchecked -> ⬆️ movement      

Thank you! 🩺