1. Basal Ganglia

2. Subdivision of BG A. Neostriatum or Striatum Putamen Caudate nucleus B. Pallio striatum or Pallidum Globuspallidus C. Lentiform nucleus Putamen GlobusPallidus D. Archistiatum Amygdela E. Substantianigra F. Subthalamic nucleus

3. Functional organization of BG

4. Motor Component of Basal Ganglia

5. BG Input Output in Mamals

6. Basal nuclei

7. Gross anatomy of BG

8. Internal capsule & BG

9. Basal Forebrain

10. Stiatum

11. Subthalamic Nucleus

12. Globuspallidus (internal)

13. Substantianigra pars reticulata

14. Globuspallidus (Externus)

15. Substantianigra pars compacta

16. Striatal Parallel Pathway

17. Efferent of BG

18. Output of the Basal Ganglia

19. Outputs of the basal ganglia and their trajectories

20. BG Effernts

21. Neruons and Circuits of BG

22. Dysinhibition

23. Connections of the Neostriatum with the SubstantiaNigra

24. Cortical Loop Cortex: 4,6,temporo, parietal and occipital glutamate Striatum spiky GABA Pallidum medial GABA Thalamus VL, VA

25. BG: Subcortical loops In the case of all sub-cortical loops the position of the thalamic relay is on the input side of the loop Red – Excitatory Blue - Inhibitory

26. Internal Connections of the Basal Ganglia: Direct Pathway

27. Indirect Pathways

28. Projections from the Basal Ganglia to Other Brain Regions

29. BG Circuits

31. Function of BG Voluntary movement Initiation of movement Control of ramp movement Change from one pattern to other Programming and correcting movement while in progress (thalamocortical circuts) Postural control Righting reflex Automatic associated movement (walking) Control of muscle tone Reticulospinal Vestibulospinal

32. Ablation Study Unilateral lesion minimal effect Denny Brown – Bilateral lesion -> Akinesia + Flexion dystonia Brook – Cooling of GP -> Contralateralcocontraction of antagoniastic muscle -> Flexion, alternate and amplitude of movement Bilateral striatal ablation -> Overactive, does not respond to visual cue – walk to wall Bilateral pallidal ablation -> Hypoactive akinetic Human sterotacticGpi lesion -> tremor >rigidity Subthalamic Nucleus ablation -> Hemibalismus Bilateral CN ablation -> immobile animal VL thalamic cooling -> Ia discharge to stretch reflex -> rigidity by y tone

33. Stimulation studies CN stimulation -> head and body turn to opposite site, circling movement, or mild hypertonia, late tremor, changes tonic to clonic phase of epilepsy Neostriatal stimulation -> arrest of motion in progress

34. Microelectrode recording Activity seen during initiation of internally generated movement but not to stimulus triggered movement Activity seen during co-contraction of agonist (stimulus triggered thus control amplitude and velocity of movement Preparation of motor act or programming as MC and SMA React Spontaneous movement of individual body part Alternating movement Visually and kinesthetically triggered movement Postural adjustment to body tilt Rapid ballistic movement Slow ramp movement Isometric muscle contraction SNc – tonic discharge -> postural control SNr - phasic discharge change with limb movement

35. Cortex Discharge of motor circuit 5 Phasic activity during movement 1 No spontaneous discharge, only during limb movement increased phasic activity Striatum 2 High spontaneous discharge, inhibit tonicaly thalamus GPiSNr 3 4 Phasic reduction of activity during movement due to disinhibition by striatum Thalamus

36. A conceptual model of action selection by the basal ganglia

37. Proposed mechanisms for serial selection within the basal ganglia

38. BG and Eye movement

39. Reinforcement learning

41. Possible Role of Intrinsic Circuits

44. The End