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Basal Ganglia
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
Functional organization of BG
Motor Component of Basal Ganglia
BG Input Output in Mamals
Basal nuclei
Gross anatomy of BG
Internal capsule & BG
Basal Forebrain
Stiatum
Subthalamic Nucleus
Globuspallidus (internal)
Substantianigra pars reticulata
Globuspallidus (Externus)
Substantianigra pars compacta
Striatal Parallel Pathway
Efferent of BG
Output of the Basal Ganglia
Outputs of the basal ganglia and their trajectories
BG Effernts
Neruons and Circuits of BG
Dysinhibition
Connections of the Neostriatum with the SubstantiaNigra
Cortical Loop Cortex: 4,6,temporo, parietal and occipital glutamate Striatum spiky GABA Pallidum medial GABA Thalamus VL, VA
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
Internal Connections of the Basal Ganglia: Direct Pathway
Indirect Pathways
Projections from the Basal Ganglia to Other Brain Regions
BG Circuits
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
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
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
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
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
A conceptual model of action selection by the basal ganglia
Proposed mechanisms for serial selection within the basal ganglia
BG and Eye movement
Reinforcement learning
Possible Role of Intrinsic Circuits
The End

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Basal ganglia 2010