Authors
Shigeru Kubota, Jonathan E. Rubin
Corresponding Author
Shigeru Kubota
Available Online 30 June 2014.
DOI
https://doi.org/10.2991/jrnal.2014.1.1.10
Keywords
subthalamic nucleus, cortex, globus pallidus, Parkinson’s disease, burst
oscillations
Abstract
Burst firing in subthalamic nucleus (STN) has been suggested to be highly
associated with the motor symptoms in Parkinson’s disease, which result
from a loss of dopamine. Although it is clinically very important to clarify
the mechanism underlying the bursting dynamics, complex interactions between
STN and other brain areas make it difficult to understand. In anesthetized
rats, STN neurons exhibit low-frequency (1 Hz) bursts, which are synchronous
with cortical slow oscillations and are significantly strengthened by dopamine
depletion. To reproduce these low-frequency bursts, we examine a conductance-based
model of an STN neuron that includes NMDA-type glutamatergic inputs reflecting
cortical oscillations. In addition, the neuron model contains GABAergic
inhibitory inputs, which are assumed to result from the activities of globus
pallidus (GP). We show that the STN neuron model can reproduce low-frequency
bursts synchronized with cortical activity, in the presence of GABAergic
inhibition. In addition, we demonstrate that increased GABA activity leads
to enhanced burstiness whereas increased NMDA conductances mainly augment
STN firing rate. The induction of burst firing additionally decreases the
coherence between STN and cortical activities. These results may give insights
into how the complicated interactions between the STN, cortex, and GP can
modulate the dynamics of bursting oscillations in the basal ganglia.
Copyright
© 2013, the Authors. Published by y ALife Robotics Corp. Ltd.
Open Access
This is an open access article distributed under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/).