basal ganglia Flashcards
list the four major subcortical nuclei of the basal ganglia
- striatum
• STR
• caudate nucleus + putamen - globus pallidus
• external (lateral) = GPe
• internal (medial) = GPi - subthalamic nucleus
• STN - substantia nigra
• pars compacta = SNc
• pars reticulata = SNr)
the striatum consists of …?
caudate nucleus + putamen
lenticular nucleus consists of …?
putamen + pallidum
what are the major connection of the basal ganglia?
- major input = striatum
- major output = Gpi and pars reticulata of substantia nigra
• basal ganglia work closely with supplementary cortex (not so much with premotor cortex)
—–> indirectly modulate pyramidal pathways via supplementary cortex
- input into extrapyramidal pathways
- no direct connections to spinal cord
cortico-basal ganglia-cortical loop: direct pathway
diagram
1) cortex sends excitatory input to striatum
2) excited neurons inhibit major output (Gpi + SNr)
3) Gpi and DNr inhibited, cannot inhibit thalamus = DISINHIBITION
4) therefore thalamus excites cerebral cortex
→ activation of the direct pathway disinhibits the thalamocortical tract
→ increases thalamocortical tone tone
→ initiate and promote voluntary movements in accordance to cortical motor command
cortico-basal ganglia-cortical loop: indirect pathway
1) cortex send excitatory input to striatum
2) excited neurons strongly inhibit external pallidum (GPe)
3) Gpe inhibited, cannot inhibit STN = DISINHIBITION
4) strong excitation of GPi and SNr by STN
5) strong inhibition of thalamus
6) thalamus cannot excite cerebral cortex
→ reduces thalamocorticol tone
→ suppressing involuntary movement
what is unique about the projections from the striatum?
projections from the STN is the only excitatory (glutamatergic) intrinsic connection of the basal ganglia.
how does the substantia nigra pars compacta influence the basal ganglia loops?
functions as a modulator of the cortical input into the striatum
dopamine acts on excitatory D1 receptors to stimulate direct pathway
dopamine acts on inhibitory D2 receptors to inhibit indirect pathway
overall, SNc disinhibits thalamocortical neurons and facilitate voluntary movements
how do the basal ganglia connect to the spinal cord?
basal ganglia do not have a direct connection to spinal cord
GPi + SNr → pedunculopontine nucleus (PPN)* → reticulospinal tract → spinal cord
- the pedunculopontine nucleus (PPN) is located in the pontomesencephalic tegmentum
where are the dopamine inputs into the striatum?
dopamine has input to both ventral and dorsal striatum
VTA (ventral tegmental area) has dopamine input into the ventral striatum (Ncl. accumbens) for reward feeling (e.g. food, drinks, drugs, sex)
SNc has dopamine input into the dorsal striatum to initiate movements thxat are predicted to having rewarding effects (reinforcement learning)
cortico-basal ganglia-cortical loop: hyperdirect pathway
1) primary motor cortex sends excitatory signal to subthalamic nuclei
2) subthalamic nuclei send excitatory signal to GPi + SNr
3) GPi + SNr strongly inhibit thalamus (VA, VL)
4) thalamus cannot excite primary motor cortex
results in fast inhibition of all motor programs
list and describe two hyperkinetic disorders of the basal ganglia
HEMIBALLSIM
• higher excitatory control compared to normal
• degeneration of STN = under-activity in indirect pathway
• uncontrollable, rapid ballistic movement of limbs
CHOREA HUNTINGTON
• higher excitatory control to thalamus
• degeneration of putamen = under-activity in indirect pathway
• involuntary and rapid limb and trunk movement
list and describe one hypokinetic disorder of the basal ganglia
PARKINSON’S DISEASE
• degeneration of SNc = reduction in dopamine input = over-activity of indirect pathway + under-activity of direct pathway
• thalamus receives strong inhibitory tone = strong reduction in excitatory input from thalamus to cortex
• reduced voluntary movement = bradykinesia
what are two possible treatments for parkinson’s disease?
1) lesion of subthalamic nucleus
2) lesion of globus pallidus internus
effectively reduce parkinsonian signs and dyskinesias by respectively normalizating or eliminating abnormal and excessive output from the internal pallidal segment