Microstructural characterization and high-temperature strength of hot-pressed silicon nitride ceramics with Lu2O3 additives

The microstructures of two hot-pressed Si₃N₄ ceramics, with 3.33 and 12.51 wt% Lu₂O₃ additive, have been characterized using transmission electron microscopy. The microstructures of both samples consisted of elongated β-Si₃N₄ grains and a secondary phase, contained in pockets surrounded by the grains, with a crystalline or amorphous form. In the 3.33 wt% Lu₂O₃-containing Si₃N₄ ceramic, all the multiple-grain junctions were completely crystalline while, in the 12.51 wt% Lu₂O₃-containing Si₃N₄ ceramic, approximately half the junctions were devitrified. A thin intergranular amorphous film present between the two-grain boundary was common; however, a film-free grain boundary was observed in the 12.51 wt% Lu₂O₃ sample. The film-free grain boundary was determined to be approximately 35%. Both ceramics fractured in four-point flexure between 1200 and 1600°C. Their high-temperature strength is closely associated with the nature of the grain-boundary phase formed during the sintering process.     

Entorhinal cortical Island cells regulate temporal association learning with long trace period

Temporal association learning (TAL) allows for the linkage of distinct, nonsynchronous events across a period of time. This function is driven by neural interactions in the entorhinal cortical–hippocampal network, especially the neural input from the pyramidal cells in layer III of medial entorhinal cortex (MECIII) to hippocampal CA1 is crucial for TAL. Successful TAL depends on the strength of event stimuli and the duration of the temporal gap between events. Whereas it has been demonstrated that the neural input from pyramidal cells in layer II of MEC, referred to as Island cells, to inhibitory neurons in dorsal hippocampal CA1 controls TAL when the strength of event stimuli is weak, it remains unknown whether Island cells regulate TAL with long trace periods as well. To understand the role of Island cells in regulating the duration of the learnable trace period in TAL, we used Pavlovian trace fear conditioning (TFC) with a 60-sec long trace period (long trace fear conditioning [L-TFC]) coupled with optogenetic and chemogenetic neural activity manipulations as well as cell type-specific neural ablation. We found that ablation of Island cells in MECII partially increases L-TFC performance. Chemogenetic manipulation of Island cells causes differential effectiveness in Island cell activity and leads to a circuit imbalance that disrupts L-TFC. However, optogenetic terminal inhibition of Island cell input to dorsal hippocampal CA1 during the temporal association period allows for long trace intervals to be learned in TFC. These results demonstrate that Island cells have a critical role in regulating the duration of time bridgeable between associated events in TAL.

The linkage of temporally discontiguous events, called temporal association learning (TAL), is an essential function for episodic memory formation; for animals, when an event took place, and in what order a series of events occurred is directly linked to adaptation to continuous changes in the environment (Eichenbaum 2000; Tulving 2002a,b; Kitamura et al. 2015a; Kitamura 2017; Pilkiw and Takehara-Nishiuchi 2018). The entorhinal cortical–hippocampal (EC-HPC) network in particular is currently considered to bridge the temporal discontinuity between events (Solomon et al. 1986; Moyer et al. 1990; Wallenstein et al. 1998; McEchron et al. 1999; Eichenbaum 2000; Huerta et al. 2000; Ryou et al. 2001; Takehara et al. 2003; Chowdhury et al. 2005; Esclassan et al. 2009; Morrissey et al. 2012; Suter et al. 2013; Sellami et al. 2017; Wilmot et al. 2019).Two major excitatory inputs to HPC arise from the superficial layers of the EC (Fig. 1A), forming the direct (monosynaptic), and indirect (trisynaptic) pathways (Amaral and Witter 1989; Amaral and Lavenex 2007; Kitamura 2017; Kitamura et al. 2017). While pyramidal cells in EC layer III (ECIII cells) project directly to CA1 (Kohara et al. 2014; Kitamura et al. 2015b), the trisynaptic pathway originates from excitatory Reelin⁺ stellate cells in EC layer II (ECII) projecting directly to DG, CA3, and CA2 (Fig. 1B; Tamamaki and Nojyo 1993; Varga et al. 2010). CalbindinD-28K⁺/Wolfram syndrome 1 (Wfs1)⁺ pyramidal cells, another excitatory neural population in EC layer II called “Island cells,” form cell clusters along the ECII/ECI border (Alonso and Klink 1993; Fujimaru and Kosaka 1996; Klink and Alonso 1997; Kawano et al. 2009; Varga et al. 2010; Kitamura et al. 2014; Ray et al. 2014) and directly project to the GABAergic interneurons of stratum lacunosum (SL-INs) in HPC CA1 and drive feedforward inhibition to HPC CA1 pyramidal cells (Fig. 1B; Kitamura et al. 2014; Surmeli et al. 2016; Kitamura 2017; Ohara et al. 2018; Yang et al. 2018; Zutshi et al. 2018).Open in a separate windowFigure 1.Circuit schematic diagram of the medial entorhinal cortex (MEC)–hippocampal (HPC) circuit. (A) Major projections in the entorhinal cortical (EC)-HPC network. ECIII neurons (green) project directly to CA1. ECII Ocean cells (ECIIo, purple) project to the dentate gyrus (DG) (light blue)/CA3 (pink) initiating the trisynaptic pathway. ECII Island cells (ECIIi, blue) project directly into CA1. (B) ECIII projections (green) excite the distal portions of CA1 pyramidal cell (yellow) dendrites in the stratum moleculare. Island cells (ECIIi, blue) excite the interneurons of stratum lacunosum (SL-INs, red), which in turn inhibit the distal dendrites of CA1 pyramidal cells in SL.Trace fear conditioning (TFC) has been established as one suitable animal model for TAL (Fendt and Fanselow 1999; Maren 2001; Kim and Jung 2006) that can be also used as a translational bridge between animal and human learning (Clark and Squire 1998; Buchel and Dolan 2000; Delgado et al. 2006). Lesion, pharmacological, molecular, and optogenetic manipulation, as well as disease models in medial entorhinal cortex (MEC), demonstrate that MEC is crucial for TFC and temporal learning (Ryou et al. 2001; Woodruff-Pak 2001; Runyan et al. 2004; Esclassan et al. 2009; Gilmartin and Helmstetter 2010; Suh et al. 2011; Morrissey et al. 2012; Shu et al. 2016; Hales et al. 2018; Yang et al. 2018; Heys et al. 2020). Specifically, MECIII inputs into the HPC CA1 pyramidal cells are essential for the formation of TFC (Yoshida et al. 2008; Suh et al. 2011; Kitamura et al. 2014; Kitamura 2017). However, the temporal association function driven by MECIII neurons must be regulated for optimal adaptive memory formation, as too strong an association of a particular pair of events may interfere with associations of other useful pairs, whereas too weak an association for a given pair of events, in terms of weaker impact of events or longer duration of temporal gap between events, would not result in an effective memory (Kitamura et al. 2015a; Marks et al. 2020). In a naturalistic context, this would mean that more distant/quieter sounds, less intense somatic sensations (e.g., pain), or increased temporal distance between any two events would signal that the events are less likely to be causally associated, therefore less relevant, and less likely to be stored and recalled. In fact, successful TFC depends on the strength of event stimuli and duration of temporal gap between events (Stiedl and Spiess 1997; Misane et al. 2005; Kitamura et al. 2014; Kitamura 2017). However, the underlying regulatory mechanism for TAL remains hidden. Previously we demonstrated that feedforward inhibition by Island cells acts as a gating controller for the MECIII inputs to the distal dendrites of HPC CA1 pyramidal cells in stratum moleculare (SM) (Kitamura et al. 2014) to control TFC when weaker (in this case diminished footshock intensity) unconditioned stimuli were delivered for TFC, indicating that Island cell activity controls the temporal association when the strength of two discontinuous events are relatively weaker. However, the way in which the EC-HPC network regulates TFC with a longer trace period still remains unknown. Because the activation of Island cells would result in a net inhibitory effect on the local network in CA1, imposing a tight and specific regulation on associations of events across the temporal gap in TAL (Crestani et al. 2002; Moore et al. 2010; Kitamura et al. 2014, 2015b), we hypothesized that the length of the temporal gap between events would also be modulated by this mechanism. In this study, we examined the role of the regulatory input to this circuit arising specifically from the Island cells in the MECII using apoptotic elimination of Island cells, chemogenetic neural inhibition, and optogenetic terminal inhibition methods within an L-TFC protocol to give a thorough and complete assessment of the circuit involvement while considering each technique''s unique features.     

Effects of hemispace on tactile bisection by young children

The validity of Bowers and Heilman's (1983) hypothesis that both hemisphere-hemispace and hemisphere-hand connections contribute to the laterality effects for tactile bisection task was examined with 24 children 6.7 yr. old. Stimulus spatial location did not influence laterality.     

The Vulnerability of Young Japanese Women and Suicide

ABSTRACT: Young Japanese females had the highest suicide rate in the world until the end of the 1960s, and it is still extremely high. This paper attempts to explain this phenomenon primarily in terms of vulnerability—in their personalities, social conditions, and role conflicts. Concomitant psychological traits and social conditions are discussed. The cultural conflict of young Japanese women is explicated in terms of psychological and historical information. In addition, the reasons for the differences between the suicide rates among females in the Tokyo area and the Kyoto-Osaka area are explored largely in terms of concepts relating to authoritarianism and its correlates.     

The Chrysanthemum versus the Sword in Suicide: Yasunari Kawabata and Yukio Mishima

ABSTRACT: Within the last few years, two world-famous Japanese writers have committed suicide. Kawabata represents the chrysanthemum aspect of Japanese culture and resignation-despair. Mishima symbolizes the sword aspect and aggression. Kawabata described loneliness-helplessness and Mishima an ecstasy under the threat of imminent death. Their different childhood experiences produced an “orphan” complex in Kawabata and the problem of sexual identity with an inferiority complex in Mishima. The former sublimated his complex in literature, the latter overreacted to it. For both, an immediate cause of suicide was the conflict between their ideal and the postwar reality. For Mishima, there were also occasions that gave vital blows to his extremely narcissistic temperament.