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Gabriel et al. [45], including an empirical parametric model that fits well to the
experimental data.
A more practical model for describing the dielectric properties at the neuroelec-
trode interface was developed by Johnson et al. [79]. In that study, an equivalent
circuit model is used for explaining voltage-biasing effects of the recorded signal.
13.4 Parkinson's Disease
Parkinson's disease is due to the death or alteration of cells that produce the neu-
rotransmitter dopamine in a region of the brain called
substantia nigra pars com-
pacta
(SNc). In turn, the lack of dopamine weakens synaptic pathways between the
SNc and the region called the striatum resulting in a general imbalance of activity
within a group of brain nuclei collectively known as the basal ganglia [31]. As a
result, the spike patterns of neurons in the
external globus pallidus
(GPe) become
sparse, while the neurons in the
subthalamic nucleus
(STN) and
internal globus
pallidus
(GPi) exhibit pronounced activity that is often in the form of synchro-
nized oscillatory bursting [16, 92, 156, 71, 126]. Figures 13.2 and 13.3 show neural
pathways of the basal ganglia as well as activity of key nuclei under normal phys-
iological conditions and Parkinsonism, respectively. Moreover, dark arrows repre-
sent inhibitory synaptic pathways, gray arrows excitatory, and perforated arrows are
pathways associated with dopamine. Externally, these processes are manifested as
the Parkinsonian symptoms of essential tremor, muscle rigidity, bradykinesia (slow-
ness of movement), and postural imbalance.
Fig. 13.2: Basal ganglia under normal conditions. This figure shows the nuclei in the
basal ganglia and their synaptic paths including excitatory (
gray line
), inhibitory
(
dark line
), and dopaminergic paths (
gray perforated line, dark perforated line
).
A feedback loop between the STN and the GPe can be seen. This figure is mod-
ified from the figures reported by Gurney et al. [56] to emphasize changes due to
dopamine depletion as described by Delong [31].
