Short-Term Plasticity Shapes the Response to Simulated Normal and Parkinsonian Input Patterns in the Globus Pallidus

• Type of Material: Article
• Authors: Jesse E. Hanson, Emory University; Dieter Jaeger, Emory University
• Language: English
• Date: 2002-06-15
• Publisher: Society for Neuroscience
• Publication Version: Final Published Version
• Copyright Statement: © 2002 Society for Neuroscience
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): https://doi.org/10.1523/JNEUROSCI.22-12-05164.2002
• Title of Journal or Parent Work: The Journal of Neuroscience
• Volume: 22
• Issue: 12
• Start Page: 5164
• End Page: 5172
• Grant/Funding Agency: National Institutes of Health
• Grant/Funding Information: This work was supported by National Institutes of Health Grants NS39852 and MH12999.
• Keywords: dynamic clamp; basal ganglia; synaptic depression; temporal coding; subthalamic nucleus; synaptic facilitation
• Subject - Topics: Neurosciences; Neurophysiology

Abstract

Basal ganglia structures show strong activity modulation during movement and synchronous bursting in Parkinson's disease. Recent work has shown that short-term synaptic plasticity (STP) can play an important role in the effect of temporal activity patterns on postsynaptic targets. To determine the role of STP in the subthalamic nucleus (STN) to globus pallidus (GP) connection, which has been suggested to underlie rhythmical bursting in Parkinson's disease, we first measured STP using trains of electrical input stimulationin vitro. We found that STN inputs to GP typically show both facilitation and depression with input frequencies of 10–100 Hz and that facilitation is dominant for the first few inputs in a train but that depression takes over subsequently. We quantified the strength and time course of facilitation and depression using a computational model of STP. Using the STP model, we constructed synaptic conductance patterns of normal and Parkinsonian STN activity and applied these conductances to GP neurons in vitro using the technique of dynamic clamping. We show that STP controls the slope and shape of the function describing the steady-state level of GP neuron firing in response to different levels of STN input. In addition, we show that STP modulates responses of GP neurons to bursts and pauses in the input pattern. These findings indicate that STP plays an important role in modulating both spike rates and temporal patterns of GP activity in the normal state, as well as in Parkinson's disease.