Motion onset really does capture attention

Several properties of visual stimuli have been shown to capture attention, one of which is the onset of motion. However, whether motion onset truly captures attention has been debated. It has been argued that motion onset only captured attention in previous studies because properties of the animated motion used in those experiments caused it to be “jerky” (i.e., there were gaps between successive images during animated motion). The present study sought to determine whether natural motion onset captures attention. Additionally, the present study further examined the circumstances under which animated motion onset, the only type of motion onset that can be produced on a computer display, does and does not capture attention. In Experiment 1, participants identified target letters in search arrays containing distinct animated motion types, either accompanied or unaccompanied by a new object. Animated motion onset captured attention, but not when the motion onset was accompanied by a new object, indicating that prior failures to replicate capture by animated motion onset were limited because a new object had always been included in the display. Experiment 2 employed natural motion rather than animated motion and found that participants were fastest at identifying motion-onset targets compared to other target types. These results provide further support for the claim that motion onset captures attention.     

Newborns of depressed mothers

Eighty-three newborns (M GA = 37 weeks) were assigned to depressed (N = 47) and nondepressed mother (N = 36) groups based on Beck Depression Inventory (BDI) scores. The Brazelton Neonatal Assessment Scale was administered to the infants within 24 hours after birth. Infants of depressed mothers demonstrated poorer performance on the orientation cluster. Further analysis of the orientation cluster items revealed inferior orientation to the inanimate stimuli. Infants of depressed mothers also showed less motor tone and activity and more irritability and less robustness and endurance (unavailability, lethargy, and stress behaviors) during the examination.     

Recommendations from Multi-disciplinary Focus Groups on Cascade Testing and Genetic Counseling for Fragile X-associated Disorders

The purpose of this paper is to report the outcome of a collaborative project between the Fragile X Research and Treatment Center at the Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute at the University of California at Davis, the National Fragile X Foundation (NFXF), and the Centers for Disease Control and Prevention (CDC). The objective of this collaboration was to develop and disseminate protocols for genetic counseling and cascade testing for the multiple disorders associated with the fragile X mental retardation 1 (FMR1) mutation. Over the last several years, there has been increasing insight into the phenotypic range associated with both the premutation and the full mutation of the FMR1 gene. To help develop recommendations related to screening for fragile X-associated disorders, four, two day advisory focus group meetings were conducted, each with a different theme. The four themes were: (1) fragile X-associated tremor/ataxia syndrome (FXTAS); (2) premature ovarian failure (POF) and reproductive endocrinology; (3) psychiatric, behavioral and psychological issues; and (4) population screening and related ethical issues.     

New objects can capture attention without a unique luminance transient

Recent evidence has suggested that new objects capture attention solely because they are typically accompanied by a unique luminance transient. In the present study, we presented a stationary pattern mask after an array of placeholders but before a subsequent search display. This allowed all of the search elements to be presented simultaneously, thereby eliminating the unique luminance transient associated with the appearance of any new objects. Under these circumstances, new objects still captured attention. In another experiment, we jiggled the mask. This caused new objects to lose their advantage. We discuss implications for the importance of new objects, and the attentional consequences of motion.     

What determines biological fitness? The problem of the reference environment

Organisms’ environments are thought to play a fundamental role in determining their fitness and hence in natural selection. Existing intuitive conceptions of environment are sufficient for biological practice. I argue, however, that attempts to produce a general characterization of fitness and natural selection are incomplete without the help of general conceptions of what conditions are included in the environment. Thus there is a “problem of the reference environment”—more particularly, problems of specifying principles which pick out those environmental conditions which determine fitness. I distinguish various reference environment problems and propose solutions to some of them. While there has been a limited amount of work on problems concerning what I call “subenvironments”, there appears to be no earlier work on problems of what I call the “whole environment”. The first solution I propose for a whole environment problem specifies the overall environment for natural selection on a set of biological types present in a population over a specified period of time. The second specifies an environment relevant to extinction of types in a population; this kind of environment is especially relevant to certain kinds of long-term evolution.     

Insights into a molecular switch that gates sensory neuron synapses during habituation in Aplysia

This review focuses on synaptic depression at sensory neuron-to-motor neuron synapses in the defensive withdrawal circuit of Aplysia as a model system for analysis of molecular mechanisms of sensory gating and habituation. We address the following topics:1. Of various possible mechanisms that might underlie depression at these sensory neuron-to-motor neuron synapses in Aplysia, historically the most widely-accepted explanation has been depletion of the readily releasable pool of vesicles. Depletion is also believed to account for synaptic depression at long interstimulus intervals in a variety of other systems.2. Multiple lines of evidence now indicate that vesicle depletion is not an important contributing mechanism to synaptic depression at Aplysia sensory neuron-to-motor neuron synapses. More generally, it appears that vesicle depletion does not contribute substantially to depression that occurs with those stimulus patterns that are typically used in studying behavioral habituation.3. Recent evidence suggests that at these sensory neuron-to-motor neuron synapses in Aplysia, synaptic depression is mediated by an activity-dependent, but release-independent, switching of individual release sites to a silent state. This switching off of release sites is initiated by Ca²⁺ influx during individual action potentials. We discuss signaling proteins that may be regulated by Ca²⁺ during the silencing of release sites that underlies synaptic depression.4. Bursts of 2–4 action potentials in presynaptic sensory neurons in Aplysia prevent the switching off of release sites via a mechanism called “burst-dependent protection” from synaptic depression.5. This molecular switch may explain the sensory gating that allows animals to discriminate which stimuli are innocuous and appropriate to ignore and which stimuli are more important and should continue to elicit responses.