Despite the great progress has been made on device parameters and working mechanism of perovskite‐based memristors, thermal instability under extreme conditions limits their performance, and thermal effect on their resistive switching (RS) characteristics remains unclear. Herein, from the viewpoint of organic/inorganic interfacial interaction in a novel 2D <100>‐oriented perovskite [(TZ‐H)2(PbBr4)]n (TZ = 1H‐1,2,4‐triazole), thermal effect on the RS performance of perovskite‐based memristor is investigated. This FTO/[(TZ‐H)2(PbBr4)]n/Ag memristor can exhibit high thermal tolerance with a working temperature of 170 °C, and the best RS characteristics can be achieved at 140 °C. Mechanistic studies are executed based on X‐ray single structural analysis, powder X‐ray diffraction, UV–Vis, and fluorescence. Before the occurrence of phase change below 140 °C (α‐phase), anisotropic lattice expansion illustrated by the weaker inter‐layer NH···Br hydrogen bond, longer layer–layer distances, more distorted PbBr6 octrahedra, larger optical gap, and quenched fluorescence can be beneficial for the trap‐filled limited process. After phase transformation into β‐phase, the breakage of layer–layer interaction and looser layer–layer packing will inhibit the halogen migration, resulting in more space charge limited conduction characters. The unique thermal enhanced RS performance with status monitored by fluorescent chromism can provide a new paradigm for the development of new memristors with highly environmental tolerance.
Intratympanic injection of gentamicin has proven to be an effective therapy for intractable vestibular dysfunction. However, most studies to date have focused on the cochlea, so little is known about the distribution and uptake of gentamicin by the counterpart of the auditory system, specifically vestibular hair cells (HCs). Here, with a combination of in vivo and in vitro approaches, we used a gentamicin‐Texas Red (GTTR) conjugate to investigate the mechanisms of gentamicin vestibulotoxicity in the developing mammalian utricular HCs. In vivo, GTTR fluorescence was concentrated in the apical cytoplasm and the cellular membrane of neonatal utricular HCs, but scarce in the nucleus of HCs and supporting cells. Quantitative analysis showed the GTTR uptake by striolar HCs was significantly higher than that in the extrastriola. In addition, the GTTR fluorescence intensity in the striola was increased gradually from 1 to 8 days, peaking at 8–9 days postnatally. In vitro, utricle explants were incubated with GTTR and candidate uptake conduits, including mechanotransduction (MET) channels and endocytosis in the HC, were inhibited separately. GTTR uptake by HCs could be inhibited by quinine, a blocker of MET channels, under both normal and stressed conditions. Meanwhile, endocytic inhibition only reduced GTTR uptake in the CoCl2 hypoxia model. In sum, the maturation of MET channels mediated uptake of GTTR into vestibular HCs. Under stressed conditions, MET channels play a pronounced role, manifested by channel‐dependent stress enhanced GTTR permeation, while endocytosis participates in GTTR entry in a more selective manner.
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