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Volga Neuroscience School 2016 Astroglial control of rhythm genesis in the brain Acknowledgements
This study was partially supported by funding from the Skolkovo Foundation (project 1110034) and from the Russian Science Foundation (15-19-20053).
References
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Computational Model of Neural-Glial-Ecm Interactions
S.V. Stasenko1 *, LA. Lazarevich1, V.B. Kazantsev1 and A.E. Dityatev2
1 Lobachevsky State University, Nizhny Novgorod, Russia;
2 German Center for Neurodegenerative Diseases, Magdeburg, Germany. * Presenting e-mail: stasenko@neuro.nnov.ru
Abstract. The study of principles and mechanisms of information processing in the brain is major issue of the modern neuroscience. Recent works have uncovered a participation glial cells (astrocytes) and ECM in information processing [1-4]. Astrocyte influences neural activity by releasing gliatransmitters: glutamate, D-serine and others. It has been discovered that ECM-mediated regulation mechanisms are involved in homeostatic modulation of neuronal activity [1,2]. Besides the well-known interactions, ECM-astrocyte interactions also may exist. Actrocyte acitivity leads to production of ECM molecules [1]. The influence of ECM molecules on astrocytes is associated with the change in the number and the properties of glial cells [5].
We present a model of neuronal activity regulation including ECM-glial-neuronal interactions. The neural network is modeled by a modification of the mean-field Wilson-Cowan-type model. The neural network consist of excitatory and inhibitory populations. The synaptic dynamics and astrocyte dynamics are modeled by using the mean-filed approach. The ECM is described by three activity-dependent variables (ECM molecules, ectoproteases and ECM receptors), which are involved in the following feedback loops: 1) decreasing the neuron excitation threshold due to ECM production; 2) increasing the excitation threshold due to ECM cleavage by ectoproteases; 3) changing effective strength of synaptic inputs due to signaling via the ECM receptors [2]. The ECM provides the regulation of the average firing rate, preventing hypo- or hyper-excitation of neurons due to the ECM-mediated feedbacks.
It was shown that interaction between ECM, astrocytes and the neuronal network leads to spontaneous activity oscillations on extended timescales. The interaction parameters determine the oscillation period (hours to days) and their existence and switching to bistable regimes.
Acknowledgements
The research was supported by the Russian Science Foundation (Agreement 14-11-00693). References
1. A. Dityatev and D. A. Rusakov, Curr. Opin. Neurobiol., 2011, 21, 353.
2. V. Kazantsev, S. Gordleeva, S. Stasenko, and A. Dityatev, PLoS One, 2012, 7, e41646.
3. A. Semyanov and D. M. Kullmann, Nat. Neurosci., 2001, 4, 718.
4. M. Min, Z. Melyan, and D. Kullmann, Proc. Natl. Acad. Sci. U. S. A., 1999, 96, 9932.
5. D. M. Kullmann, Neuron, 2001, 32, 561.
OM&P
108 Opera Med Physiol 2016 Vol. 2 (S1)
