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      Crossbar Nanoscale HfO 2-Based Electronic Synapses

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          Abstract

          Crossbar resistive switching devices down to 40 × 40 nm 2 in size comprising 3-nm-thick HfO 2 layers are forming-free and exhibit up to 10 5 switching cycles. Four-nanometer-thick devices display the ability of gradual switching in both directions, thus emulating long-term potentiation/depression properties akin to biological synapses. Both forming-free and gradual switching properties are modeled in terms of oxygen vacancy generation in an ultrathin HfO 2 layer. By applying the voltage pulses to the opposite electrodes of nanodevices with the shape emulating spikes in biological neurons, spike-timing-dependent plasticity functionality is demonstrated. Thus, the fabricated memristors in crossbar geometry are promising candidates for hardware implementation of hybrid CMOS-neuron/memristor-synapse neural networks.

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          Most cited references26

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          Competitive Hebbian learning through spike-timing-dependent synaptic plasticity.

          Hebbian models of development and learning require both activity-dependent synaptic plasticity and a mechanism that induces competition between different synapses. One form of experimentally observed long-term synaptic plasticity, which we call spike-timing-dependent plasticity (STDP), depends on the relative timing of pre- and postsynaptic action potentials. In modeling studies, we find that this form of synaptic modification can automatically balance synaptic strengths to make postsynaptic firing irregular but more sensitive to presynaptic spike timing. It has been argued that neurons in vivo operate in such a balanced regime. Synapses modifiable by STDP compete for control of the timing of postsynaptic action potentials. Inputs that fire the postsynaptic neuron with short latency or that act in correlated groups are able to compete most successfully and develop strong synapses, while synapses of longer-latency or less-effective inputs are weakened.
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            Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type.

            Q Bi, G Bi, M Poo (1998)
            In cultures of dissociated rat hippocampal neurons, persistent potentiation and depression of glutamatergic synapses were induced by correlated spiking of presynaptic and postsynaptic neurons. The relative timing between the presynaptic and postsynaptic spiking determined the direction and the extent of synaptic changes. Repetitive postsynaptic spiking within a time window of 20 msec after presynaptic activation resulted in long-term potentiation (LTP), whereas postsynaptic spiking within a window of 20 msec before the repetitive presynaptic activation led to long-term depression (LTD). Significant LTP occurred only at synapses with relatively low initial strength, whereas the extent of LTD did not show obvious dependence on the initial synaptic strength. Both LTP and LTD depended on the activation of NMDA receptors and were absent in cases in which the postsynaptic neurons were GABAergic in nature. Blockade of L-type calcium channels with nimodipine abolished the induction of LTD and reduced the extent of LTP. These results underscore the importance of precise spike timing, synaptic strength, and postsynaptic cell type in the activity-induced modification of central synapses and suggest that Hebb's rule may need to incorporate a quantitative consideration of spike timing that reflects the narrow and asymmetric window for the induction of synaptic modification.
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              Synaptic plasticity: multiple forms, functions, and mechanisms.

              Experiences, whether they be learning in a classroom, a stressful event, or ingestion of a psychoactive substance, impact the brain by modifying the activity and organization of specific neural circuitry. A major mechanism by which the neural activity generated by an experience modifies brain function is via modifications of synaptic transmission; that is, synaptic plasticity. Here, we review current understanding of the mechanisms of the major forms of synaptic plasticity at excitatory synapses in the mammalian brain. We also provide examples of the possible developmental and behavioral functions of synaptic plasticity and how maladaptive synaptic plasticity may contribute to neuropsychiatric disorders.
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                Author and article information

                Contributors
                matveyev.ya@mipt.ru
                Journal
                Nanoscale Res Lett
                Nanoscale Res Lett
                Nanoscale Research Letters
                Springer US (New York )
                1931-7573
                1556-276X
                15 March 2016
                15 March 2016
                2016
                : 11
                : 147
                Affiliations
                Moscow Institute of Physics and Technology, Dolgoprudny, 141700 Russia
                Author information
                http://orcid.org/0000-0001-7661-8462
                Article
                1360
                10.1186/s11671-016-1360-6
                4792835
                26979725
                3f6d9040-e239-40f2-8825-68691809069b
                © Matveyev et al. 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 3 December 2015
                : 7 March 2016
                Funding
                Funded by: FundRef http://dx.doi.org/http://dx.doi.org/10.13039/501100006769, Russian Science Foundation Grant;
                Award ID: 14-19-01698
                Categories
                Nano Express
                Custom metadata
                © The Author(s) 2016

                Nanomaterials
                memristor,crossbar,electronic synapse,stdp,resistive switching,hfo2,85.50.-n,81.07.-b,84.35.+i
                Nanomaterials
                memristor, crossbar, electronic synapse, stdp, resistive switching, hfo2, 85.50.-n, 81.07.-b, 84.35.+i

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