Transcript
BASAL GANGLIA
SUBDIVISION OF BG
A. Neostriatum or Striatum
PutamenCaudate nucleus
B. Pallio striatum or Pallidum
Globus pallidus
C. Lentiform nucleusPutamenGlobus Pallidus
D. ArchistiatumAmygdela
E. Substantia nigraF. Subthalamic nucleus
FUNCTIONAL ORGANIZATION OF BG
MOTOR COMPONENT OF BASAL GANGLIA
BASAL NUCLEI
GROSS ANATOMY OF BG
INTERNAL CAPSULE & BG
BASAL FOREBRAIN
STIATUM
SUBTHALAMIC NUCLEUS
GLOBUS PALLIDUS (INTERNAL)
SUBSTANTIA NIGRA PARS RETICULATA
GLOBUS PALLIDUS (EXTERNUS)
SUBSTANTIA NIGRA 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
CONNECTIONS OF THE NEOSTRIATUM WITH THE SUBSTANTIA NIGRA
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
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 -> Contralateral cocontraction 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 sterotactic Gpi 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
No spontaneous discharge, only during limb movement
increased phasic activity
High spontaneous discharge, inhibit tonicaly thalamus
Phasic reduction of activity during movement due to disinhibition by striatum
Phasic activity during movement
Striatum
GPi SNr
Thalamus
1
2
3
4
5
A CONCEPTUAL MODEL OF ACTION SELECTION BY THE BASAL GANGLIA
PROPOSED MECHANISMS FOR SERIAL SELECTION WITHIN THE BASAL GANGLIA
BG AND EYE MOVEMENT
POSSIBLE ROLE OF INTRINSIC CIRCUITS
THE END
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