Epilepsy is a group of neurological disorders commonly associated with the neuronal malfunction leading to generation of seizures. Recent reports point to a possible contribution of astrocytes into this pathology. We used the lithium-pilocarpine model of status epilepticus (SE) in rats to monitor changes in astrocytes. Experiments were performed in acute hippocampal slices 2–4 weeks after SE induction. Nissl staining revealed significant neurodegeneration in the pyramidal cell layers of hippocampal CA1, CA3 areas, and the hilus, but not in the granular cell layer of the dentate gyrus. A significant increase in the density of astrocytes stained with an astrocyte-specific marker, sulforhodamine 101, was observed in CA1 stratum (str.) radiatum. Astrocytes in this area were also whole-cell loaded with a morphological tracer, Alexa Fluor 594, for two-photon excitation imaging. Sholl analyses showed no changes in the size of the astrocytic domain or in the number of primary astrocytic branches, but a significant reduction in the number of distal branches that are resolved with diffraction-limited light microscopy (and are thought to contain Ca2+ stores, such as mitochondria and endoplasmic reticulum). The atrophy of astrocytic branches correlated with the reduced size, but not overall frequency of Ca2+ events. The volume tissue fraction of nanoscopic (beyond the diffraction limit) astrocytic leaflets showed no difference between control and SE animals. The results of spatial entropy-complexity spectrum analysis were also consistent with changes in ratio of astrocytic branches vs. leaflets. In addition, we observed uncoupling of astrocytes through the gap-junctions, which was suggested as a mechanism for reduced K+ buffering. However, no significant difference in time-course of synaptically induced K+ currents in patch-clamped astrocytes argued against possible alterations in K+ clearance by astrocytes. The magnitude of long-term-potentiation (LTP) was reduced after SE. Exogenous D-serine, a co-agonist of NMDA receptors, has rescued the initial phase of LTP. This suggests that the reduced Ca2+-dependent release of D-serine by astrocytes impairs initiation of synaptic plasticity. However, it does not explain the failure of LTP maintenance which may be responsible for cognitive decline associated with epilepsy.

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We propose a memristive interface consisting of two FitzHugh–Nagumo electronic neurons connected via a metal–oxide (Au/Zr/ZrO2(Y)/TiN/Ti) memristive synaptic device. We create a hardware–software complex based on a commercial data acquisition system, which records a signal generated by a presynaptic electronic neuron and transmits it to a postsynaptic neuron through the memristive device. We demonstrate, numerically and experimentally, complex dynamics, including chaos and different types of neural synchronization. The main advantages of our system over similar devices are its simplicity and real-time performance. A change in the amplitude of the presynaptic neurogenerator leads to the potentiation of the memristive device due to the self-tuning of its parameters. This provides an adaptive modulation of the postsynaptic neuron output. The developed memristive interface, due to its stochastic nature, simulates a real synaptic connection, which is very promising for neuroprosthetic applications.

We propose an optoelectronic system for stimulation of living neurons. The system consists of an electronic circuit based on the FitzHugh–Nagumo model, an optical fiber, and a photoelectrical converter. We used this system for electrical stimulation of hippocampal living neurons in acute hippocampal brain slices (350-μm thick) obtained from a 20–28 days old C57BL/6 mouse or a Wistar rat. The main advantage of our system over other similar stimulators is that it contains an optical fiber for signal transmission instead of metallic wires. The fiber is placed between the electronic circuit and stimulated neurons and provides galvanic isolation from external electrical and magnetic fields. The use of the optical fiber allows avoiding electromagnetic noise and current flows which could affect metallic wires. Furthermore, it gives us the possibility to simulate “synaptic plasticity” by adaptive signal transfer through optical fiber. The proposed optoelectronic system (hybrid neural circuit) provides a very high efficiency in stimulating hippocampus neurons and can be used for restoring brain activity in particular regions or replacing brain parts (neuroprosthetics) damaged due to a trauma or neurodegenerative diseases.

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