Attentional shift (or shift of attention) occurs when directing attention to a point to increase the efficiency of processing that point and includes inhibition to decrease attentional resources to unwanted or irrelevant inputs. Shifting of attention is needed to allocate attentional resources to more efficiently process information from a stimulus. Research has shown that when an object or area is attended, processing operates more efficiently. Task switching costs occur when performance on a task suffers due to the increased effort added in shifting attention. There are competing theories that attempt to explain why and how attention is shifted as well as how attention is moved through space.
Here, we update our 1990 Annual Review of Neuroscience article, “The Attention System of the Human Brain.” The framework presented in the original article has helped to integrate behavioral, systems, cellular, and molecular approaches to common problems in attention research. Our framework has been both elaborated and expanded in subsequent years. Research on orienting and executive functions has supported the addition of new networks of brain regions. Developmental studies have shown important changes in control systems between infancy and childhood. In some cases, evidence has supported the role of specific genetic variations, often in conjunction with experience, that account for some of the individual differences in the efficiency of attentional networks. The findings have led to increased understanding of aspects of pathology and to some new interventions.
Published on May 16, 2013
The possibility that our personal memory can play strange tricks on us has been the focus of Giuliana’s research for many years. Her work, based at the University of Hull, has also examined the cognitive and behavioural consequences of suggestion. Giuliana is a recognised memory expert and has recently been part of Channel 4’s documentary The Boy Who Can’t Forget where she examined Aurelien, a boy who claims he can remember every day of his life. This condition is considered impossible by current models of memory.
In psychology, the Stroop effect is a demonstration of interference in thereaction time of a task. When the name of a color (e.g., “blue”, “green”, or “red”) is printed in a color not denoted by the name (e.g., the word “red” printed in blue ink instead of red ink), naming the color of the word takes longer and is more prone to errors than when the color of the ink matches the name of the color. The effect is named after John Ridley Stroop, who first published the effect in English in 1935. The effect had previously been published in Germany in 1929.The original paper has been one of the most cited papers in the history ofexperimental psychology, leading to more than 701 replications. The effect has been used to create a psychological test (Stroop test) that is widely used in clinical practice and investigation.
Brain imaging techniques including magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), and positron emission tomography (PET) have shown that there are two main areas in the brain that are involved in the processing of the Stroop task. They are the anterior cingulate cortex, and the dorsolateral prefrontal cortex.More specifically, while both are activated when resolving conflicts and catching errors, the dorsolateral prefrontal cortex assists in memory and other executive functions, while the anterior cingulate cortex is used to select an appropriate response and allocate attentional resources.
The posterior dorsolateral prefrontal cortex creates the appropriate rules for the brain to accomplish the current goal. For the Stroop effect, this involves activating the areas of the brain involved in color perception, but not those involved in word encoding. It counteracts biases and irrelevant information, for instance, the fact that the semantic perception of the word is more striking than the color in which it is printed. Next, the mid-dorsolateral prefrontal cortex selects the representation that will fulfil the goal. The relevant information must be separated from irrelevant information in the task; thus, the focus is placed on the ink color and not the word. Furthermore, research has suggested that left dorsolateral prefrontal cortex activation during a Stroop task is related to an individual’s’ expectation regarding the conflicting nature of the upcoming trial, and not so much on the conflict itself. Conversely, the right dorsolateral prefrontal cortex aims to reduce the attentional conflict and is activated after the conflict is over.
Moreoever, the posterior dorsal anterior cingulate cortex is responsible for what decision is made (i.e. whether you will say the incorrect answer [written word] or the correct answer [ink color]). Following the response, the anterior dorsal anterior cingulate cortex is involved in response evaluation—deciding whether the answer is correct or incorrect. Activity in this region increases when the probability of an error is higher.
In the neo-Piagetian theories of cognitive development, several variations of the Stroop task have been used to study the relations between speed of processing and executive functions with working memory and cognitive development in various domains. This research shows that reaction time to Stroop tasks decreases systematically from early childhood through early adulthood. These changes suggest that speed of processing increases with age and that cognitive control becomes increasingly efficient. Moreover, this research strongly suggests that changes in these processes with age are very closely associated with development in working memory and various aspects of thought.
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Imagine the brain could reboot, updating its damaged cells with new, improved units. That may sound like science fiction — but it’s a potential reality scientists are investigating right now. Ralitsa Petrova details the science behind neurogenesis and explains how we might harness it to reverse diseases like Alzheimer’s and Parkinson’s.
The ability to communicate through spoken language may be the trait that best sets humans apart from other animals. Last year researchers identified the first gene implicated in the ability to speak. This week, a team shows that the human version of this gene appears to date back no more than 200,000 years–about the time that anatomically modern humans emerged. The authors argue that their findings are consistent with previous speculations that the worldwide expansion of modern humans was driven by the emergence of full-blown language abilities.
The researchers who identified the gene, called FOXP2, showed that FOXP2 mutations cause a wide range of speech and language disabilities (ScienceNOW, 3 October 2002). In collaboration with part of this team, geneticist Svante Pääbo’s group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, set about tracing the gene’s evolutionary history.
As a uniquely human trait, language has long baffled evolutionary biologists. Not until FOXP2was linked to a genetic disorder that caused problems in forming words could they even begin to study language’s roots in our genes. Soon after that discovery, a team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, discovered that just two bases, the letters that make up DNA, distinguished the human and chimp versions ofFOXP2. To try to determine how those changes influenced the gene’s function, that group put the human version of the gene in mice. In 2009, they observed that these “humanized” mice produced more frequent and complex alarm calls, suggesting the human mutations may have been involved in the evolution of more complex speech.
When humanized mice and wild mice were put in mazes that engaged both types of learning,the humanized mice mastered the route to the reward faster than their wild counterparts, report Schreiweis, Graybiel, and their colleagues
The results suggest the human version of the FOXP2 gene may enable a quick switch to repetitive learning—an ability that could have helped infants 200,000 years ago better communicate with their parents. Better communication might have increased their odds of survival and enabled the new version of FOXP2 to spread throughout the entire human population, suggests Björn Brembs, a neurobiologist at the University of Regensburg in Germany, who was not involved with the work.
“The findings fit well with what we already knew about FOXP2 but, importantly, bridge the gap between behavioral, genetic, and evolutionary knowledge,” says Dianne Newbury, a geneticist at the Wellcome Trust Centre for Human Genetics in Oxford, U.K., who was not involved with the new research. “They help us to understand how the FOXP2 gene might have been important in the evolution of the human brain and direct us towards neural mechanisms that play a role in speech and language acquisition.”
Chomsky critiqued the field of AI for adopting an approach reminiscent of behaviorism, except in more modern, computationally sophisticated form. Chomsky argued that the field’s heavy use of statistical techniques to pick regularities in masses of data is unlikely to yield the explanatory insight that science ought to offer. For Chomsky, the “new AI” — focused on using statistical learning techniques to better mine and predict data — is unlikely to yield general principles about the nature of intelligent beings or about cognition.
Published on Oct 6, 2012
Steven Pinker – Psychologist, Cognitive Scientist, and Linguist at Harvard University
How did humans acquire language? In this lecture, best-selling author Steven Pinker introduces you to linguistics, the evolution of spoken language, and the debate over the existence of an innate universal grammar. He also explores why language is such a fundamental part of social relationships, human biology, and human evolution. Finally, Pinker touches on the wide variety of applications for linguistics, from improving how we teach reading and writing to how we interpret law, politics, and literature.
The Floating University