ABSTRACT
Artificial electronic synapses are commonly used to simulate biological synapses to realize various learning functions, regarded as one of the key technologies in the next generation of neurological computation. This work used a simple spin coating technique to fabricate polyimide (PI):graphene quantum dots(GQDs) memristor structure. As a result, the devices exhibit remarkably stable exponentially decaying postsynaptic suppression current over time, as interpreted in the spike-timing-dependent plasticity phenomenon. Furthermore, with the increase of the applied electrical signal over time, the conductance of the electrical synapse gradually changes, and the electronic synapse also shows plasticity dependence on the amplitude and frequency of the pulse applied. In particular, the devices with the structure of Ag/PI:GQDs/ITO prepared in this study can produce a stable response to the stimulation of electrical signals between millivolt to volt, showing not only high sensitivity but also a wide range of "feelings", which makes the electronic synapses take a step forwards to emulate biological synapses. Meanwhile, the electronic conduction mechanisms of the device are also studied and expounded in detail. The findings in this work lay a foundation for developing brain-like neuromorphic modeling in artificial intelligence.
ABSTRACT
BACKGROUND: The pathogenesis of asthma is complex and continues to be considered as a challenging subject. Some studies have shown that nerve growth factor (NGF) participates in the pathogenesis of asthma, but the mechanism of airway contraction caused by NGF is still unclear. OBJECTIVE: Our aim was to discuss the effect of anti-NGF antibody on RhoA expression, and further explore the role of NGF in airway hyperresponsiveness (AHR). METHODS: Thirty female BALB/c mice were divided into three groups randomly: control group (group C, n = 10), asthma group (group A, n = 10) and anti-NGF antibody intervention group (group N, n = 10). The asthmatic mice were stimulated by OVA suspension, the intervention mice were given nasal instillation of anti-NGF antibody before the stimulation. Airway responsiveness, eosinophils, IL-13, IFN-γ were measured. The protein expression and mRNA level of NGF and RhoA were detected by immunohistochemical and Real Time-PCR (RT-PCR) analyses. RESULTS: Airway responsiveness, eosinophils and IL-13 levels in group A were significantly increased compare with the other groups, and significantly decreased in group N than those in group A. IFN-γ level was significantly reduced in group A and increased in group N. Immunohistochemistry and RT-PCR analyses showed that the protein expression and mRNA level of NGF and RhoA were significantly increased in group A and significantly decreased in group N. CONCLUSION: NGF participates in the pathogenesis of asthma in mice. Anti-NGF antibody can inhibit airway inflammation and alleviate AHR by down-regulating the protein expression and mRNA level of RhoA.
