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This article is part of the supplement: Twentieth Annual Computational Neuroscience Meeting: CNS*2011

Open Access Poster presentation

The effect of glutamate-gated chloride current on the excitability of a Purkinje cell: a modeling study

Shiwei Huang1* and Erik De Schutter12

Author Affiliations

1 Computational Neuroscience Unit, Okinawa Institute of Science and Technology, Okinawa 904-0411, Japan

2 Theoretical Neurobiology, University of Antwerp, B-2610 Antwerpen, Belgium

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BMC Neuroscience 2011, 12(Suppl 1):P154  doi:10.1186/1471-2202-12-S1-P154

The electronic version of this article is the complete one and can be found online at:

Published:18 July 2011

© 2011 Huang and De Schutter; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Poster presentation

Purkinje neurons express, in high abundance, a glutamate gated chloride channel commonly known as the Excitatory Amino Acid Transporter subtype 4 (EAAT4). EAAT4 belongs to the family of glutamate transporters, which in mammalian nervous system is responsible for clearing synaptic glutamate [1]. Studies of these transporters in heterogeneous expression systems demonstrated that in addition to glutamate transport, the binding of glutamate to the transporter activates a chloride current through the transporter with properties liken that of a channel and which is functionally independent from the transport process [2].

The role of the chloride channel in glutamate transporters is only known for the EAAT subtype 5 (EAAT5). On rod bipolar cell axon terminals, EAAT5 activation by glutamate results in membrane hyperpolarization, which consequently inhibits terminal glutamate release [3]. Whether the chloride channel of EAAT4 has a physiological role in Purkinje neurons remains unknown. A synaptic model was developed to determine conditions in which the chloride channel of EAAT4 could influence Purkinje neuron function and whether these conditions are physiologically relevant.

The model comprises a single compartment with uniform distribution of AMPA receptors and EAAT4. The EAAT4 model is based on a 16-state kinetic model of EAAT2 [4] using reaction rates of EAAT4 measured in [5]. AMPA receptor conductance and absolute permeability of EAAT4 were parameterized for adjusting their respective current amplitudes. The model reproduced the EPSC and EAAT4 channel currents evoked in a Purkinje neuron by parallel fiber stimulation under conditions similar to those used in [5]. The result serves as a basis for investigating the effects of the EAAT4 chloride current on Purkinje neuron excitability and intracellular chloride concentration.


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