9. Basal Ganglia Flashcards
basal ganglia: functions
- activity of upper motor neurons
- movement selection by:
- reinforcing intended movements
- suppressing unintended movements
- movement initiation by anticipatory changes
basal ganglia affects which portion of descending systems (upper motor neurons)
motor cortex
(planning, initiating, and directing voluntary movements)
basal ganglia: components
- caudate
- putamen
- globus pallidus
- external segment (GPe)
- internal segment (GPi)
basa ganglia: closely related structures
- diencephalon
- VA/VL nuclei of thalamus
- subthalamic nucleus
- midbrain
- substantia nigra
- pars compacta (SNc)
- pars reticulata (SNr)
- substantia nigra
basal ganglia: inputs
- input region of BG: striatum (= caudate + putamen)
- inputs from:
- cerebral cortex (many regions)
- substantia nigra pars compacta (SNc)
how is the basal ganglia considered part of a corticostriatal pathway?
almost all cerebral cortical areas (EXCEPT PRIMARY AUDITORY AND PRIMARY VISUAL CORTEXES) project to basal ganglia
which 2 cerebral cortical areas do NOT porject into basal ganglia?
- primary auditory cortex
- primary visual cortex
basal ganglia: output regions and respective targets
Region –> Target
- globus pallidus internal (GPi) –> to thalamus (for relay to motor cortex)
- Substantia nigra pars reticulata (SNr) –> to superior colliculus
output of basal ganglia is:
(EXCITATORY/INHIBITORY)
inhibitory
comparison of outputs from SNr and GPi
(substantia nigra reticularis and globus pallidus internus)
- BOTH: have output nuclei; diff’t targets and functions
SNr:
- projects to superior colliculus
- controls saccadic eye movements (quick, simultaneous movement of both eyes between two or more phases of fixation in the same direction)
GPi
- projects to VA/VL (ventral lateral, ventral anterior) complex of thalamus
- controls body movements
disinhibition as it relates to SNr and GPi
both SNr and GPi are inhibitory to superior colliculus and VA/VL respectively
caudate and putamen connections to SNr and GPi are also inhibitory
So release from inhibition/ or disinhibition is inhibition of inhibitory input
Disinhibition of VA/VL by the GPi
- cortex excites striatum
- striatum inhibits GP
- GP stops inhibiting VA/VL
- VA/VL excites motor cortex
direct pathway:
through BG to GPi & VA/VL for body movements
- from Striatum –> to GPi –> to VA/VL
- Releases VA/VL from inhibition (disinhibition)
- Pormotes activation of motor cortex –> produces movement
function of direct pathway
type of dopamine receptors
PRODUCES MOVEMENT
D1 receptors
function of INDIRECT pathway
type of dopamine receptors
inhibit movement, prevent unwanted movement
D2 receptors
INDIRECT pathway:
from BG to VA/VL
- from Striatum to GPe –> to subthalamic nucleus to GPi to VA/VL
- releases subthalamic n. from inhibition (disinhibition)
- promotes inhibition of VA/VL
- prevents activation of motor cortex
- suppresses movement
normal basal ganglia function and mechanism
to promote selective movement
- reinforcing intended movements via DIRECT pathway
- suppressing all other (unintended movements) via INDIRECT pathway
substantia nigra: function and mechanism (receptors)
promotes movement by:
- excitation of direct pathway via D1 receptors
- inhibiting indirect pathway via D2 receptors
functional organization of DIRECT and INDIRECT pathways
- center: surround organization in GPi
- cortical activation of both direct/indirect pathways
- surround region suppresses competing (unwanted) movements
- center region activated intended movements
consequences of loss of direct pathway
and clinical relation
- less DISINHBITION of VA/VL –> less excitation of motor cortex –> less movement
- CC: Hypokinetic disorders - characterized by paucity and slowness of movement (e.g. parkinsons)
CC: hypokinetic disorders
cause and description
caused by loss of direct pathway
characterized by paucity and slowness of movement (e.g. parkinson’s disease)
Parkinson’s disease circuitry
degeneration of cells in the substantia nigra reticularis –>
less disinhibition of VA/VL via DIRECT pathway and
more inhibition of VA/VL via indirect pathway
CC: Parkinsons disease
characterized by
- tremor at rest (pill rolling)
- difficulting initiating movement (akinesia)
- slowness of movement (bradykinesia)
- difficulty making postrual adjustments
- hypertonia of neck and extremities (cog-wheel rigidity)
- minimal facial expressions
- walking difficulty: short steps, stooped posture, paucity of associated movements (arm swinging)
loss of INDIRECT pathway:
consequences
- less inhibition of VA/VL –> more excitation of motor cortex –> more unwanted movement
- CC: causes HYPERKINETIC disorders
CC: hyperkinetic disorders
in general, what are they? name 3 diseases
characterized by uncontrollable movements
- dyskinesia
- huntington’s disease
- hemiballismus
CC: dyskinesia
hyperkinetic disorder in which is characterized by abnormal, uncontrolled movement
CC: Huntington’s disease
hyperkinesia (uncontrollable movements) w/ choreiform (dance-like) movements
(aka huntington’s chorea)
CC: ballismus vs. hemiballismus
hyperkinesia w/ wild, flinging movements of extremities
hemiballismus: ballistic movements on one side; caused by loss of contralateral subthalamic nucleus
CC: athetoid movement
writhing movement
huntington’s disease circuitry
degeneration of cells in striatum to GPe –> less inhibition of VA/VL via indirect pathway
non-motor loops: what else does basal ganglia mediate?
- pre-frontal loop: decision-making and planning
- limbic loop: emotional behavior
