Hello, my name is Angela Cenci.
I am a professor of
experimental medical research
at Lund University in Sweden.
This talk is about the mechanisms
of levodopa-induced dyskinesia
in Parkinson's disease.
Parkinson's disease, as
illustrated in slide number two,
is a neurodegenerative disorder
characterized by some typical motor
symptoms such as slow movements,
loss of spontaneous movements,
muscle rigidity, and resting tremor.
These symptoms are due to
the degeneration of neurons
in the substantia nigra that produce
the neurotransmitter dopamine
as illustrated in
drawing to the left.
The dopaminergic neurons
project their axons
to the large, subcortical
is shaded in red in the
drawing to the right.
This nucleus is called the striatum.
And it is the part of the striatum
called the putamen that processes
motor information from
the cortex and requires
a normal dopaminergic input for
its physiological functions.
Dopamine depletion impairs the
processing of motor information
in neural pathways that connect
the cortex and the basal ganglia.
In brief, these neural pathways
are indicated in the drawing
to the right.
The cerebral cortex
sends glutamatergic axons
to the striatum.
The striatum uses the information
coming from the cortex
to elaborate well-coordinated
signals used to select or supress
movements and then
sends these signals
to other parts of the basal
ganglia, to the globus pallidus
in particular from
which messages are then
sent out to the rest of the brain.