E numerous astrocytes in addition to neurons. Half from the neuronastrocyte network models have been so-called generic models. Other individuals, nevertheless, were specified to model neuron-astrocyte interactions inside the cortex (Allegrini et al., 2009; Liu and Li, 2013a; Chan et al., 2017; Tang et al., 2017; Yao et al., 2018), hippocampus (Amiri et al., 2012a, 2013a; Mesiti et al., 2015a; Li et al., 2016c), spinal cord (Yang and Yeo, 2015), or thalamocortical networks (Amiri et al., 2012b,c). The modeling methods for neurons varied based on the author. 3 from the studied publications utilized Hodgkin and Huxley (1952) model (Liu and Li, 2013b; Li et al., 2016c; Yao et al., 2018) and one particular utilized Traub et al. (1991) model’s derivative Pinsky and Rinzel (1994) model (Mesiti et al., 2015a). Simpler phenomenological models used in the studied publications were the FitzHugh-Nagumo (FitzHugh, 1961) model (Postnov et al., 2009; Hayati et al., 2016), LIF (Gerstner and Kistler, 2002) model (Liu and Li, 2013a; Naeem et al., 2015), Izhikevich (2007) model (Allegrini et al., 2009; Haghiri et al., 2016, 2017; Tang et al., 2017), Morris and Lecar (1981) model or its derivatives (Amiri et al., 2012a, 2013a; Chan et al., 2017), and Suffczynski et al. (2004) neuronal population model (Amiri et al., 2012b,c). The released neurotransmitter was modeled explicitly by Amiri et al. (2012a, 2013a), Liu and Li (2013a), Yang and Yeo (2015), Li et al. (2016c), and Yao et al. (2018). Other models utilized phenomenological transfer functions amongst the neurotransmitter and astrocytic IP3 concentration. The information of your neuron-astrocyte network models could be identified in Table five. The neuron-astrocyte network models were developed to explain lots of distinct biological events as is often noticed in Table 5. Examples incorporated Ca2+ dynamics, synchronization, information transfer, plasticity, and hyperexcitability. All of the other models except the model by Allegrini et al. (2009) had elements for all three; CICR, leak from the ER into the cytosol, plus the SERCA pump. Much more than half on the models had influx of Ca2+ from outdoors from the astrocyte and efflux of Ca2+ to outside on the astrocyte. About one third on the models took into account gliotransmitter release by modeling extracellular glutamate, and few had been also modeling extracellular ATP. Other models made use of phenomenological transfer functions to relay the effect of gliotransmission for the target synaptic terminal (Iastro , Isyn , part of Iast , and Gm ). None of the studied models had a detailed astrocytic vesicle release model. The majority of the models had gap junction signaling for IP3 , and some also for Ca2+ . Therefore, these models had a similar core structure with tiny variations. As an A platelet phospholipase Inhibitors Reagents instance, only Yao et al. (2018) modeled buffering also as astrocytic and extracellular K+ . Diffusion was taken into account within the models by Allegrini et al. (2009), Postnov et al. (2009), Mesiti et al. (2015a), Yang and Yeo (2015), Li et al. (2016c), and Yao et al. (2018). Yao et al. (2018) presented on the list of accessible models for cortical spreading depression.Frontiers in Computational Neuroscience | www.frontiersin.orgApril 2018 | Volume 12 | ArticleTABLE 5 | Traits of neuron-astrocyte network models. Variables Ca2+ fluxes Diffusion GJ Output EventManninen et al.ModelNo.InputDe Young and Keizer (1992) and Li and Rinzel (1994) -TYPE MODELS [Ca2+ ], f, h, [IP3 ] CICR, leak from ER into cyt, SERCA Iast = cf Iast = cf Iast = cf Iast,ATP = c[ATP]e.