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621.
A theoretical debate in artificial grammar learning (AGL) regards the learnability of hierarchical structures. Recent studies using an AnBn grammar draw conflicting conclusions (Bahlmann and Friederici, 2006 and
[De Vries et al., 2008]
). We argue that 2 conditions crucially affect learning AnBn structures: sufficient exposure to zero-level-of-embedding (0-LoE) exemplars and a staged-input. In 2 AGL experiments, learning was observed only when the training set was staged and contained 0-LoE exemplars. Our results might help understanding how natural complex structures are learned from exemplars. 相似文献
622.
Jun Yokose William D. Marks Naoki Yamamoto Sachie K. Ogawa Takashi Kitamura 《Learning & memory (Cold Spring Harbor, N.Y.)》2021,28(9):319
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. 相似文献
623.
Accumulating evidence suggests that cognitive declines in old (healthy) animals could arise from depression of intracortical inhibition, for which a decreased ability to produce GABA during senescence might be responsible. By simulating a neural network model of a primary visual cortical (V1) area, we investigated whether and how a lack of GABA affects cognitive performance of the network: detection of the orientation of a visual bar-stimulus. The network was composed of pyramidal (P) cells and GABAergic interneurons such as small (S) and large (L) basket cells. Intrasynaptic GABA-release from presynaptic S or L cells contributed to reducing ongoing-spontaneous (background) neuronal activity in a different manner. Namely, the former exerted feedback (S-to-P) inhibition and reduced the frequency (firing rate) of action potentials evoked in P cells. The latter reduced the number of saliently firing P cells through lateral (L-to-P) inhibition. Non-vesicular GABA-release, presumably from glia and/or neurons, into the extracellular space reduced the both, activating extrasynaptic GABAa receptors and providing P cells with tonic inhibitory currents. By this combinatorial, spatiotemporal inhibitory mechanism, the background activity as noise was significantly reduced, compared to the stimulus-evoked activity as signal, thereby improving signal-to-noise (S/N) ratio. Interestingly, GABA-spillover from the intrasynaptic cleft into the extracellular space was effective for improving orientation selectivity (orientation bias), especially when distractors interfered with detecting the bar-stimulus. These simulation results may provide some insight into how the depression of intracortical inhibition due to a reduction in GABA content in the brain leads to age-related cognitive decline. 相似文献
624.
625.
Sato H Takenaka I Kawahara JI 《Quarterly journal of experimental psychology (2006)》2012,65(4):617-623
Selective attention can be improved under conditions in which a high perceptual load is assumed to exhaust cognitive resources, leaving scarce resources for distractor processing. The present study examined whether perceptual load and acute stress share common attentional resources by manipulating perceptual and stress loads. Participants identified a target within an array of nontargets that were flanked by compatible or incompatible distractors. Attentional selectivity was measured by longer reaction times in response to the incompatible than to the compatible distractors. Participants in the stress group participated in a speech test that increased anxiety and threatened self-esteem. The effect of perceptual load interacted with the stress manipulation in that participants in the control group demonstrated an interference effect under the low perceptual load condition, whereas such interference disappeared under the high perceptual load condition. Importantly, the stress group showed virtually no interference under the low perceptual load condition, whereas substantial interference occurred under the high perceptual load condition. These results suggest that perceptual and stress related demands consume the same attentional resources. 相似文献
626.
627.
随着重症医学的发展,我国重症医学科医生临床胜任能力将面临着巨大挑战;他们不仅需要具备精湛的临床技术,同样重要的是还需要具备高超的合作、沟通能力,充沛的精力和体力,丰满的人文和哲学素养,以及终身的知识更新和实践能力提高. 相似文献
628.
The limited capacity of visual working memory (VWM) requires the existence of an efficient information selection mechanism.
While it has been shown that under low VWM load, an irrelevant simple feature can be processed, its fate under high load (e.g.,
six objects) remains unclear. We explored this issue by probing the “irrelevant-change distracting effect,” in which the change
of a stored irrelevant feature affects performance. Simple colored shapes were used as stimuli, with color as the target.
Using a whole-probe method (presenting six objects in both the memory and test arrays), in Experiment 1 we found that a change to one of the six shapes led to a significant distracting effect. Using a partial-probe method (presenting
the probe either at the screen center or at a location selected from the memory array), in Experiment 2 we showed the distracting effect again. These results suggest that irrelevant simple features can be stored into VWM, regardless
of memory load. 相似文献
629.
Katsuki A Yoshimura R Kishi T Hori H Umene-Nakano W Ikenouchi-Sugita A Hayashi K Atake K Iwata N Nakamura J 《CNS spectrums》2012,17(3):155-163
Object We investigated an association between the polymorphism of brain-derived neurotrophic factor (BDNF) gene Val66Met and the response to mirtazapine in Japanese patients with major depressive disorder (MDD). We also examined mirtazapine's effects on the serum BDNF and plasma levels of catecholamine metabolites in these patients. METHODS: Eighty-four patients who met the DSM-IV-TR criteria for MDD were treated with only mirtazapine for 4 weeks. The BDNF Val66Met polymorphism was detected by direct sequencing in the region, and serum BDNF levels and plasma levels of catecholamine metabolites were measured by ELISA and HPLC-ECD, respectively. RESULTS: Mirtazapine treatment for 4 weeks significantly increased serum BDNF levels in the responders, whereas nonresponders showed significant decreases. No association was found between either of the two genotypes (Val/Val vs. Met-carriers) and the response to mirtazapine at T4 or the serum BDNF levels at T0. Mirtazapine did not alter the plasma levels of homovanillic acid (HVA) or 3-methoxy-4-hydroxyphenylglycol (MHPG). Discussion The dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNF Val66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels. Conclusion Serum BDNF levels, but not plasma levels of HVA or MHPG, and BDNF Val66Met polymorphism are related to the mirtazapine response in MDD. 相似文献
630.
对自然的数学化必然导致人类对自然的对象化思维,从而把自然当作可以加以征服和驾驭的对象物;近代以来科学技术的成功运用更是助长了人类对自然的狂妄,误认为以人类有限的智慧能认识自然的无限奥秘。这是造成当代全球性生态危机的认识论根源。因此,为了走出当代生态危机,人类必须深刻认识到自己认识的有限性,找回“有学识的无知”,从而对无限的终极实在保持应有的敬畏之感。 相似文献