Bias and noise in proportion estimation: A mixture psychophysical model.

The importance of proportional reasoning has long been recognized by psychologists and educators, yet we still do not have a good understanding of how humans mentally represent proportions. In this paper we present a psychophysical model of proportion estimation, extending previous approaches. We assumed that proportion representations are formed by representing each magnitude of a proportion stimuli (the part and its complement) as Gaussian activations in the mind, which are then mentally combined in the form of a proportion. We next derived the internal representation of proportions, including bias and internal noise parameters -capturing respectively how our estimations depart from true values and how variable estimations are. Methodologically, we introduced a mixture of components to account for contaminating behaviors (guessing and reversal of responses) and framed the model in a hierarchical way. We found empirical support for the model by testing a group of 4th grade children in a spatial proportion estimation task. In particular, the internal density reproduced the asymmetries (skewedness) seen in this and in previous reports of estimation tasks, and the model accurately described wide variations between subjects in behavior. Bias estimates were in general smaller than by using previous approaches, due to the model's capacity to absorb contaminating behaviors. This property of the model can be of especial relevance for studies aimed at linking psychophysical measures with broader cognitive abilities. We also recovered higher levels of noise than those reported in discrimination of spatial magnitudes and discuss possible explanations for it. We conclude by illustrating a concrete application of our model to study the effects of scaling in proportional reasoning, highlighting the value of quantitative models in this field of research.

Training nonsymbolic proportional reasoning in children and its effects on their symbolic math abilities.

Our understanding of proportions can be both symbolic, as when doing calculations in school mathematics, or intuitive, as when folding a bed sheet in half. While an understanding of symbolic proportions is crucial for school mathematics, the cognitive foundations of this ability remain unclear. Here we implemented a computerized training game to test a causal link from intuitive (nonsymbolic) to symbolic proportional reasoning and other math abilities in 4th grade children. An experimental group was trained in nonsymbolic proportional reasoning (PR) with continuous extents, and an active control group was trained on a remarkably similar nonsymbolic magnitude comparison. We found that the experimental group improved at nonsymbolic PR across training sessions, showed near transfer to a paper-and-pencil nonsymbolic PR test, transfer to symbolic proportions, and far transfer to geometry. The active control group showed only a predicted far transfer to geometry. In a second experiment, these results were replicated with an independent cohort of children. Overall this study extends previous correlational evidence, suggesting a functional link between nonsymbolic PR on one hand and symbolic PR and geometry on the other.

Cognitive and Neural Effects of a Brief Nonsymbolic Approximate Arithmetic Training in Healthy First Grade Children.

Recent studies with children and adults have shown that the abilities of the Approximate Number System (ANS), which operates from early infancy and allows estimating the number of elements in a set without symbols, are trainable and transferable to symbolic arithmetic abilities. Here we investigated the brain correlates of these training effects, which are currently unknown. We trained two Groups of first grade children, one in performing nonsymbolic additions with dot arrays (Addition-Group) and another one in performing color comparisons of the same arrays (Color-Group). The training program was computerized, throughout seven sessions and had a pretest-posttest design. To evaluate cognitive gains, we measured math skills before and after the training. To measure the brain changes, we used electroencephalogram (EEG) recordings in the first and the last training sessions. We explored the changes in N1 and P2p, which are two electrophysiological components sensitive to nonsymbolic numeric computations. A passive Control-Group receiving no intervention also had their math skills evaluated. We found that the two training Groups had similarly gain in math skills, suggesting no specific transfer of the nonsymbolic addition training to math skills at the behavioral level. In contrast, at the brain level, we found that only in the Addition-Group the P2p amplitude significantly increased across sessions. Notably, the gain in P2p amplitude positively correlated with the gain in math abilities. Together, our results showed that first graders rapidly gained in math skills by different interventions. However, number-related brain networks seem to be particularly sensitive to nonsymbolic arithmetic training.

A Translational Framework of Educational Neuroscience in Learning Disorders.

Neuroimaging has undergone enormous progress during the last two and a half decades. The combination of neuroscientific methods and educational practice has become a focus of interdisciplinary research in order to answer more applied questions. In this realm, conditions that hamper learning success and have deleterious effects in the population - such as learning disorders (LD) - could especially profit from neuroimaging findings. At the moment, however, there is an ongoing debate about how far neuroscientific research can go to inform the practical work in educational settings. Here, we put forward a theoretical translational framework as a method of conducting neuroimaging and bridging it to education, with a main focus on dyscalculia and dyslexia. Our work seeks to represent a theoretical but mainly empirical guide on the benefits of neuroimaging, which can help people working with different aspects of LD, who need to act collaboratively to reach the full potential of neuroimaging. We provide possible ideas regarding how neuroimaging can inform LD at different levels within our multidirectional framework, i.e., mechanisms, diagnosis/prognosis, training/intervention, and community/education. In addition, we discuss methodological, conceptual, and structural limitations that need to be addressed by future research.

On the mechanism of synaptic depression induced by CaMKIIN, an endogenous inhibitor of CaMKII.

Activity-dependent synaptic plasticity underlies, at least in part, learning and memory processes. NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) is a major synaptic plasticity model. During LTP induction, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated, autophosphorylated and persistently translocated to the postsynaptic density, where it binds to the NMDAR. If any of these steps is inhibited, LTP is disrupted. The endogenous CaMKII inhibitor proteins CaMKIINα,ß are rapidly upregulated in specific brain regions after learning. We recently showed that transient application of peptides derived from CaMKIINα (CN peptides) persistently depresses synaptic strength and reverses LTP saturation, as it allows further LTP induction in previously saturated pathways. The treatment disrupts basal CaMKII-NMDAR interaction and decreases bound CaMKII fraction in spines. To unravel CaMKIIN function and to further understand CaMKII role in synaptic strength maintenance, here we more deeply investigated the mechanism of synaptic depression induced by CN peptides (CN-depression) in rat hippocampal slices. We showed that CN-depression does not require glutamatergic synaptic activity or Ca(2+) signaling, thus discarding unspecific triggering of activity-dependent long-term depression (LTD) in slices. Moreover, occlusion experiments revealed that CN-depression and NMDAR-LTD have different expression mechanisms. We showed that CN-depression does not involve complex metabolic pathways including protein synthesis or proteasome-mediated degradation. Remarkably, CN-depression cannot be resolved in neonate rats, for which CaMKII is mostly cytosolic and virtually absent at the postsynaptic densities. Overall, our results support a direct effect of CN peptides on synaptic CaMKII-NMDAR binding and suggest that CaMKIINα,ß could be critical plasticity-related proteins that may operate as cell-wide homeostatic regulators preventing saturation of LTP mechanisms or may selectively erase LTP-induced traces in specific groups of synapses.