Asymmetry in the discrimination of quantity: the role of stimulus generalization

In order to evaluate 1 account for the asymmetry that has been found with discriminations based on stimulus magnitude, in 5 autoshaping experiments, 2 groups of pigeons received a discrimination between 5 and 20 squares presented on a TV screen. One group received a 20+/5– discrimination, with food signaled by 20 squares but not 5 squares; the other group received the opposite discrimination, 5+/20–. The 20+/5– discrimination was acquired more readily than 5+/20– in Experiments 1, 3a, 3b, and 4. For Experiment 1, the screen was white for the intertrial interval (ITI) and the stimuli were black squares on a white background; for Experiment 3a, the screen was black for the ITI and the stimuli were black squares on a white background; and for Experiments 3b and 4, the screen was white for the ITI and the stimuli were white squares on a black background. In Experiment 2, the stimuli were black squares on a white background, but they were separated by an ITI in which 288 black squares were presented against a white background. The 20+/5– discrimination was now acquired more slowly than the 5+/20– discrimination. The asymmetry in the acquisition of the magnitude discriminations in each experiment is attributed to inhibition being associated with the stimuli present during the ITI. The generalization of this inhibition, along a dimension related to the number of squares on the screen, is then assumed to disrupt the acquisition of 1 discrimination to a greater extent than the other

Asymmetry in the discrimination of quantity by rats: the role of the intertrial interval

In three experiments, rats were trained to discriminate between 20 and five (Exps. 1 and 2), or between 40 and five (Exp. 3), black squares. The squares were randomly distributed in the center of a white background and displayed on a computer screen. For one group, the patterns containing the higher quantity of squares signaled the delivery of sucrose (+), whilst patterns with the lower quantity of squares did not (–). For the second group, sucrose was signaled by the lower, but not by the higher, quantity of squares. In Experiment 1, the intertrial interval (ITI) was a white screen, and the 20+/5– discrimination was acquired more readily than the 5+/20– discrimination. For Experiment 2, the ITI was made up of 80 black squares on a white background. In this instance, the 5+/20– discrimination was acquired more successfully than the 20+/5– discrimination. In Experiment 3, two groups were trained with a 40+/5– discrimination, and two with a 5+/40– discrimination. For one group from each of these pairs, the training trials were separated by a white ITI, and the 40+/5– discrimination was acquired more readily than the 5+/40– discrimination. For the remaining two groups, the training trials were not separated by an ITI, and the two groups acquired the task at approximately the same rate. The results indicate that the cues present during the ITI play a role in the asymmetrical acquisition of magnitude discriminations based on quantity

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Protein aggregates in Huntington's disease

Huntington’s disease (HD) is an incurable neurodegenerative disease characterized by abnormal motor movements, personality changes, and early death. HD is caused by a mutation in the IT-15 gene that expands abnormally the number of CAG nucleotide repeats. As a result, the translated protein huntingtin contains disease-causing expansions of glutamines (polyQ) that make it prone to misfold and aggregate. While the gene and mutations that cause HD are known, the mechanisms underlying HD pathogenesis are not. Here we will review the state of knowledge of HD, focusing especially on a hallmark pathological feature—intracellular aggregates of mutant Htt called inclusion bodies (IBs). We will describe the role of IBs in the disease. We speculate that IB formation could be just one component of a broader coping response triggered by misfolded Htt whose efficacy may depend on the extent to which it clears toxic forms of mutant Htt. We will describe how IB formation might be regulated and which factors could determine different coping responses in different subsets of neurons. A differential regulation of IB formation as a function of the cellular context could, eventually, explain part of the neuronal vulnerability observed in HD