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Lecture

Physiology 3120 Lecture Notes - Pars Compacta, Basal Ganglia, Supplementary Motor Area


Department
Physiology
Course Code
PHYSIO 3120
Professor
Tom Stavraky

Page:
of 2
Human Physiology
Wednesday, November 18, 2009
“Neuro XII”
Basal Ganglia
function of supplementary motor cortex (SMA) first deduced using PET screens; measured blood flow,
which is indicative of metabolic activity in neurons
metabolic activity mostly due to EPSPs and IPSPs, not APs
simple finger flexion
increased blood flow in somatosensory & motor cortex
sequential finger flexions
increased blood flow in somatosensory & motor cortex, and supplementary motor cortex
think about sequential finger flexions
increased blood flow in supplementary motor area ONLY
conclusion: supplementary motor area programs motor cortex when performing complex,
sequential movements
basal ganglia
composed of several different nuclei
4 different loops; separate pathways through basal ganglia that end up back in the cortex
1. motor
classically associated with motor functions
but there are other loops that are not motor areas
2. oculomotor
3. limbic
4. cognitive (prefrontal)
two inputs to the caudate/putamen
1. from the cerebral cortex
2. from the substantia nigra pars compacta
the major neurotransmitters in the caudate/putamen are dopamine (excitatory or inhibitory), ACh
(for interneurons in the neostriatum), and glutamate
there are direct & indirect pathways from the neostriatum to the internal globus pallidus
GABA is a major inhibitory neurotransmitter
one major output is from the internal globus pallidus to the thalamus
diseases of the basal ganglia
Parkinson’s disease
loss of dopaminergic neurons in substantia nigra pars compacta; can have a lot of
degeneration before symptoms appear; progressive degeneration over lifespan
symptoms
rigidity at joints (not spasticity); happens in flexors & extensors
resting tremor (not intention tremor); usually prominent in fingers (i.e. “pill-
rolling”)
akinesia (poverty of movement)
oincreased frequency of discharge causes decreased discharge in thalamus,
which then causes decreased discharge in motor cortex
bradykinesia (slowed movement)
shuffling gait
dementia (note that there are cognitive loops through the basal ganglia
treatment
lesion internal globus pallidus; produces less decreased activity in the thalamus
high frequency electrical stimulation of the subthalamic nucleus, the interal
globus pallidus or thalamic nucleus; disrupts information transmission
enhanced dopamine activity using L-dopa; only relieves symptoms; must
maintain a balance because too much dopamine can cause chorea
injecting fetal dopamine cells into the neostriatum
Huntington’s chorea
degeneration of neurons in caudate & putamen; associated with abnormal repeats of
Huntingtin gene; increase glutamine causes abnormal protein folding & cell death
features
heritability
chorea (decreased output from globus pallidus); involuntary dance-like
movements
other movement disorders (i.e. slurred speech)
dementia
death
no treatment
hemiballismus
uncontrolled ballistic (fastest you can go) movement of one side of the movement
lesion in subthalamic nucleus
Tourette’s syndrome
inappropriate utterances & tics (brief, repetitive involuntary movements)
excessive activity in cognitive basal ganglia
MPTP
depletes brain dopamine levels
story of drug abusers
heroin addicts took what they thought was synthetic heroin, but which was MPTP instead
caused overnight development of Parkinson’s disease
positive outcomes
MPTP produces animal model of Parkinson’s
proposed that Parkinson’s may have an environmental cause (twin studies); chronic
exposure to rotenone produced the features of Parkinson’s
function of basal ganglia
no generally agreed upon function
suppresses unwanted movement?