Commun Nonlinear Sci Numer Simulat 32 (2016) 262–272
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Commun Nonlinear Sci Numer Simulat
journal homepage: www.elsevier.com/locate/cnsns
Effect of calcium channel noise in astrocytes on neuronal
transmission
Jun Tang
a,∗
, Tong-Bo Liu
a
, Jun Ma
b
, Jin-Ming Luo
a
, Xian-Qing Yang
a
a
College of Science, China University of Mining and Technology, Xuzhou 221116, China
b
Department of Physics, Lanzhou University of Technology, Lanzhou 730050, China
article info
Article history:
Received 15 May 2015
Revised 25 July 2015
Accepted 21 August 2015
Available online 28 August 2015
Keywords:
Astrocyte
Neuron information transmission
Noise
abstract
In this study, a Langevin model is constructed by modifying a neuron–astrocyte coupled model
that comprises a pyramidal neuron, an interneuron, and an astrocyte. This Langevin model
considers random open-close transitions of calcium ion channels in the endoplasmic reticu-
lum membrane of astrocytes. The effect of noise in the astrocytes on neuronal transmission
is investigated numerically based on a random model under both normal and overexpression
conditions of metabotropic glutamate receptors on astrocyte membranes. This study suggests
that noise could change the firing patterns of two neurons during neuronal information trans-
mission. Noise facilitates the occurrence of episodic spikes (ESs) in both neurons. However,
the noise-induced ESs occur irregularly, compared with ESs in a deterministic model, and the
change in regularity with noise exhibits the coherence- resonance phenomenon. Furthermore,
synchronicity between noisy ESs in two neurons depends significantly on various parameters.
ESs completely occur synchronously but irregularly in certain parameter regions, whereas ESs
in other parameter values are antiphase synchronous. This study implies not only that the cal-
cium dynamics in astrocytes could participate in neuronal transmission, but also that noise in
astrocytes may be transferred to neurons and may affect synaptic transmission significantly.
© 2015 Elsevier B.V. All rights reserved.
1. Introduction
As the major subtype of glial cells in the brain, astrocyte cells are traditionally considered as non-excitable support cells of
neuron systems because these cells cannot generate action potentials (APs). Over the past decades, astrocytes have been found
to participate in synaptic transmission by modulating and responding to the release of neurotransmitters [1–3]. Astrocytic pro-
cesses are often opposed to synaptic junctions. These processes allow astrocytes to “listen and communicate” with neurons,
thereby generating the “tripartite synapse” notion that consists of a presynaptic neuron, an astrocyte, and a postsynaptic neuron
[4]. The fire of the presynaptic neuron facilitates the release of neurotransmitters, such as glutamate. Released glutamates then
diffuse and bind to metabotropic glutamate (mGlu) receptors on the membrane of adjacent astrocytes. The activation of mGlu
receptors triggers a complex pathway that augments inositol 1, 4, 5-triphosphate (IP
3
) in astrocytes and increases intra-astrocytic
Ca
2+
concentration. Calcium elevation causes a release of glutamates from an astrocyte to the synaptic cleft. The released glu-
tamates can bind mGlu receptors on the presynaptic membrane and/or NMDA receptors on the postsynaptic side, thus synaptic
transmission is modulated [5–8]. In fact, the calcium elevation can also result in the release of other neurotransmitters, such as
Adenosine Triphosphate (ATP), which enhances the neuronal excitability [9–12].
∗
Corresponding author.
E-mail address: tjuns1979@126.com (J. Tang).
http://dx.doi.org/10.1016/j.cnsns.2015.08.019
1007-5704/© 2015 Elsevier B.V. All rights reserved.