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This paper presents a game-design workshop built around a digital art installation featuring video games displayed over a real-world skyscraper to stimulate students' interest in computer science and a study testing its short-term effects on improving middle school students' computational thinking (CT) skills and attitudes towards computing. Following a STEAM approach, the workshop aimed to engage participants in age-appropriate activities that focus on CT skills through the lens of creating their own game. A web-based game design interface that allows students to code and play games as simulated on a skyscraper was developed to support the workshop's core activities. The web environment also featured step-by-step tutorials and fully functional games to promote the accessibility of the learning materials for a diverse body of students and educators around the globe. The results of the study indicated that the workshop helped students improve their CT skills and differentially influence their attitudes towards computing. In particular, the workshop experience led students from underserved community districts to lower their attitude ratings, whereas the reverse pattern was observed for students from more affluent districts. The workshop reportedly informed students' perception of computing as a profession and their appreciation of the analytical effort required for developing functional games. Qualitative analysis of artifact-based interviews indicated that students could begin to make abstractions and devise algorithms by associating variables through conditional statements while solving problems related to game development. Interview analysis also revealed that students took pride in the effort that they made during the workshop.

People become highly reactive when performing dynamic, real-time tasks like driving a car, playing a video game, or controlling air traffic. However, people also go through more deliberate stages in which they spend time reasoning about constraints and actions. In this paper, we argue that these are the end points on a learning continuum, and we discuss one potential mechanism for bridging these endpoints within the ACT-R (Anderson, 1993) framework.

this paper, we examine the components of dynamic skill acquisition using a data set collected by Ackerman (1988) with the Kanfer-Ackerman Air-Traffic Controller Task©. Our analysis indicates that subjects arc improving in both the strategies they use to solve the task and the speed with which they execute the task. One strategy that subjects develop reduces the number of oven actions required lo land a plane. Another strategy that subjects develop enables them to land more planes simultaneously. A satisfactory model of this task must include both an improved strategic component and an improved speed component. The ACT-R theory (Anderson, 1993) is well suited to model these components as it is able lo separately learn over trials which strategies are better and how to execute each more efficiently.

Decomposed the learning in the Kanfer-Ackerman Air-Traffic Controller Task (P. Ackerman, 1988) down to learning at the keyboard level. Reanalyzed the Ackerman data to show that learning in this complex task reflects learning at the keystroke level. Conducted an eye-tracking experiment with 10 adults that showed that learning at the key stroke level reflects learning at a lower, attentional, level. (SLD)

INTRODUCTION In such diverse environments as air traffic control and nuclear power plant operation, researchers in human factors have accumulated extensive empirical knowledge of human performance in complex and dynamic […], In this article we describe production compilation, a mechanism for modeling skill acquisition. Production compilation has been developed within the ACT-Rational (ACT-R; J. R. Anderson, D. Bothell, M. D. Byrne, & C. Lebiere, 2002) cognitive architecture and consists of combining and specializing task-independent procedures into task-specific procedures. The benefit of production compilation for researchers in human factors is that it enables them to test the strengths and weaknesses of their task analyses and user models by allowing them to model the learning trajectory from the main task level and the unit task level down to the keystroke level. We provide an example of this process by developing and describing a model learning a simulated air traffic controller task. Actual or potential applications of this research include the evaluation of user interfaces, the design of systems that support learning, and the building of user models.

Research has been conducted on the dopamine D1-like receptors. Experimental results demonstrate that these receptors modulate N-methyl-D-aspartate glutamate receptor-mediated functions via direct protein-protein interactions.

This article investigates the processes involved in learning how to perform complex tasks. Findings indicate that complex tasks are made up of several simpler tasks that are learned by acquiring lower-level skills that facilitate the more complex global task when used in conjunction.

Abstract Over-activation of AMPARs (α−amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptors) is implicated in excitotoxic neuronal death associated with acute brain insults, such as ischemic stroke. However, the specific molecular mechanism by which AMPARs, especially the calcium-impermeable AMPARs, induce neuronal death remains poorly understood. Here we report the identification of a previously unrecognized molecular pathway involving a direct protein-protein interaction that underlies GluR2-containing AMPAR-mediated excitotoxicity. Agonist stimulation of AMPARs promotes GluR2/GAPDH (glyceraldehyde-3-phosphate dehydrogenase) complex formation and subsequent internalization. Disruption of GluR2/GAPDH interaction by administration of an interfering peptide prevents AMPAR-mediated excitotoxicity and protects against damage induced by oxygen-glucose deprivation (OGD), an in vitro model of brain ischemia.

There is considerable evidence that dopamine D2 receptors can modulate AMPA receptor-mediated neurotoxicity. However, the molecular mechanism underlying this process remains essentially unclear. Here we report that D2 receptors inhibit AMPA-mediated neurotoxicity through two pathways: the activation of phosphoinositide-3 kinase (PI-3K) and downregulation of AMPA receptor plasma membrane expression, both involving a series of protein-protein coupling/uncoupling events. Agonist stimulation of D2 receptors promotes the formation of the direct protein-protein interaction between the third intracellular loop of the D2 receptor and the ATPase N-ethylmaleimide-sensitive factor (NSF) while uncoupling the NSF interaction with the carboxyl tail (CT) of the glutamate receptor GluR2 subunit of AMPA receptors. Previous studies have shown that full-length NSF directly couples to the GluR2CT and facilitates AMPA receptor plasma membrane expression. Furthermore, the CT region of GluR2 subunit is also responsible for several other intracellular protein couplings, including p85 subunit of PI-3K. Therefore, the direct coupling of D2-NSF and concomitant decrease in the NSF-GluR2 interaction results in a decrease of AMPA receptor membrane expression and an increase in the interaction between GluR2 and the p85 and subsequent activation of PI-3K. Disruption of the D2-NSF interaction abolished the ability of D2 receptor to attenuate AMPA-mediated neurotoxicity by blocking the D2 activation-induced changes in PI-3K activity and AMPA receptor plasma membrane expression. Furthermore, the D2-NSF-GluR2-p85 interactions are also responsible for the D2 inhibition of ischemia-induced cell death. These data may provide a new avenue to identify specific targets for therapeutics to modulate glutamate receptor-governed diseases, such as stroke. [ABSTRACT FROM AUTHOR]

Functional interactions between dopamine D1-like receptors and NMDA subtype glutamate receptors have been implicated in the maintenance of normal brain activity and neurological dysfunction. Although modulation of NMDA receptor functions by D1 receptor activation has been the subject of extensive investigation, little is known as to how the activation of NMDA receptors alters D1 function. Here we report that NMDA receptors regulate D1 receptor function via a direct protein-protein interaction mediated by the carboxyl tail regions of both receptors. In both cotransfected cells and cultured hippocampal neurons the activation of NMDA receptors increases the number of D1 receptors on the plasma membrane surface and enhances D1 receptor-mediated cAMP accumulation via a SNARE-dependent mechanism. Furthermore, overexpression of mini-genes encoding either NR1 or D1 carboxyl tail fragments disrupts the D1-NR1 direct protein-protein interaction and abolishes NMDA-induced changes in both D1 cell surface expression and D1-mediated cAMP accumulation. Our results demonstrate that the D1-NR1 physical interaction enables NMDA receptors to increase plasma membrane insertion of D1 receptors and provides a novel mechanism by which the activation of NMDA receptors upregulates D1 receptor function. Understanding the molecular mechanisms by which D1 and NMDA receptors functionally interact may provide insight toward elucidating the molecular neurobiological mechanisms involved in many neuropsychiatric illnesses, such as schizophronia. [ABSTRACT FROM AUTHOR]

The retromer complex is an evolutionarily conserved protein complex involved in the endosomal recycling of various cargo proteins. It is ubiquitously expressed in all tissue and is found in both invertebrate as well as mammalian nervous systems, where it recycles various synaptic membrane proteins including the dopamine transporter and dopamine D1 receptor, two proteins implicated in dopamine homeostasis and neurotransmission. The involvement of the retromer complex in dopamine neurobiology is further underscored by its links to Parkinson's disease, a neurodegenerative disorder of the dopamine system. In this article, the existing literature linking the retromer complex to synaptic function and dopamine homeostasis is reviewed. Additional possible links are highlighted by exploring the retromer and other Parkinson's disease-associated proteins and possible relationships to synaptic function and dopamine transmission., (© 2022 Wiley Periodicals LLC.)