Irradiation-induced grain boundary facet motion: In situ observations and atomic-scale mechanisms.

Metals subjected to irradiation environments undergo microstructural evolution and concomitant degradation, yet the nanoscale mechanisms for such evolution remain elusive. Here, we combine in situ heavy ion irradiation, atomic resolution microscopy, and atomistic simulation to elucidate how radiation damage and interfacial defects interplay to control grain boundary (GB) motion. While classical notions of boundary evolution under irradiation rest on simple ideas of curvature-driven motion, the reality is far more complex. Focusing on an ion-irradiated Pt Σ3 GB, we show how this boundary evolves by the motion of 120° facet junctions separating nanoscale {112} facets. Our analysis considers the short- and mid-range ion interactions, which roughen the facets and induce local motion, and longer-range interactions associated with interfacial disconnections, which accommodate the intergranular misorientation. We suggest how climb of these disconnections could drive coordinated facet junction motion. These findings emphasize that both local and longer-range, collective interactions are important to understanding irradiation-induced interfacial evolution.

Origins of the change in mechanical strength of silicon/gold nanocomposites during irradiation.

Silicon-based layered nanocomposites, comprised of covalent-metal interfaces, have demonstrated elevated resistance to radiation. The amorphization of the crystalline silicon sublayer during irradiation and/or heating can provide an additional mechanism for accommodating irradiation-induced defects. In this study, we investigated the mechanical strength of irradiated Si-based nanocomposites using atomistic modeling. We first examined dose effects on the defect evolution mechanisms near silicon-gold crystalline and amorphous interfaces. Our simulations reveal the growth of an emergent amorphous interfacial layer with increasing dose, a dominant factor mitigating radiation damage. We then examined the effect of radiation on the mechanical strength of silicon-gold multilayers by constructing yield surfaces. These results demonstrate a rapid onset strength loss with dose. Nearly identical behavior is observed in bulk gold, a phenomenon that can be rooted to the formation of radiation-induced stacking fault tetrahedra which dominate the dislocation emission mechanism during mechanical loading. Taken together, these results advance our understanding of the interaction between radiation-induced point defects and metal-covalent interfaces.

Pressure-Induced Formation and Mechanical Properties of 2D Diamond Boron Nitride.

Understanding phase transformations in 2D materials can unlock unprecedented developments in nanotechnology, since their unique properties can be dramatically modified by external fields that control the phase change. Here, experiments and simulations are used to investigate the mechanical properties of a 2D diamond boron nitride (BN) phase induced by applying local pressure on atomically thin h-BN on a SiO2 substrate, at room temperature, and without chemical functionalization. Molecular dynamics (MD) simulations show a metastable local rearrangement of the h-BN atoms into diamond crystal clusters when increasing the indentation pressure. Raman spectroscopy experiments confirm the presence of a pressure-induced cubic BN phase, and its metastability upon release of pressure. Å-indentation experiments and simulations show that at pressures of 2-4 GPa, the indentation stiffness of monolayer h-BN on SiO2 is the same of bare SiO2, whereas for two- and three-layer-thick h-BN on SiO2 the stiffness increases of up to 50% compared to bare SiO2, and then it decreases when increasing the number of layers. Up to 4 GPa, the reduced strain in the layers closer to the substrate decreases the probability of the sp2-to-sp3 phase transition, explaining the lower stiffness observed in thicker h-BN.

Reduced-order atomistic cascade method for simulating radiation damage in metals.

Atomistic modeling of radiation damage through displacement cascades is deceptively non-trivial. Due to the high energy and stochastic nature of atomic collisions, individual primary knock-on atom (PKA) cascade simulations are computationally expensive and ill-suited for length and dose upscaling. Here, we propose a reduced-order atomistic cascade model capable of predicting and replicating radiation events in metals across a wide range of recoil energies. Our methodology approximates cascade and displacement damage production by modeling the cascade as a core-shell atomic structure composed of two damage production estimators, namely an athermal recombination corrected displacements per atom (arc-dpa) in the shell and a replacements per atom (rpa) representing atomic mixing in the core. These estimators are calibrated from explicit PKA simulations and a standard displacement damage model that incorporates cascade defect production efficiency and mixing effects. We illustrate the predictability and accuracy of our reduced-order atomistic cascade method for the cases of copper and niobium by comparing its results with those from full PKA simulations in terms of defect production as well as the resulting cascade evolution and structure. We provide examples for simulating high energy cascade fragmentation and large dose ion-bombardment to demonstrate its possible applicability. Finally, we discuss the various practical considerations and challenges associated with this methodology especially when simulating subcascade formation and dose effects.

Integrated regulation of AMPA glutamate receptor phosphorylation in the striatum by dopamine and acetylcholine.

Dopamine (DA) and acetylcholine (ACh) signals converge onto protein kinase A (PKA) in medium spiny neurons of the striatum to control cellular and synaptic activities of these neurons, although underlying molecular mechanisms are less clear. Here we measured phosphorylation of the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) at a PKA site (S845) as an indicator of AMPAR responses in adult rat brains in vivo to explore how DA and ACh interact to modulate AMPARs. We found that subtype-selective activation of DA D1 receptors (D1Rs), D2 receptors (D2Rs), or muscarinic M4 receptors (M4Rs) induced specific patterns of GluA1 S845 responses in the striatum. These defined patterns support a local multitransmitter interaction model in which D2Rs inhibited an intrinsic inhibitory element mediated by M4Rs to enhance the D1R efficacy in modulating AMPARs. Consistent with this, selective enhancement of M4R activity by a positive allosteric modulator resumed the cholinergic inhibition of D1Rs. In addition, D1R and D2R coactivation recruited GluA1 and PKA preferentially to extrasynaptic sites. In sum, our in vivo data support an existence of a dynamic DA-ACh balance in the striatum which actively modulates GluA1 AMPAR phosphorylation and trafficking. This article is part of the Special Issue entitled 'Ionotropic glutamate receptors'.