Different time courses of learning-related activity in the prefrontal cortex and striatum

To navigate our complex world, our brains have evolved a sophisticated ability to quickly learn arbitrary rules such as 'stop at red'. Studies in monkeys using a laboratory test of this capacity--conditional association learning--have revealed that frontal lobe structures (including the prefrontal cortex) as well as subcortical nuclei of the basal ganglia are involved in such learning. Neural correlates of associative learning have been observed in both brain regions, but whether or not these regions have unique functions is unclear, as they have typically been studied separately using different tasks. Here we show that during associative learning in monkeys, neural activity in these areas changes at different rates: the striatum (an input structure of the basal ganglia) showed rapid, almost bistable, changes compared with a slower trend in the prefrontal cortex that was more in accordance with slow improvements in behavioural performance. Also, pre-saccadic activity began progressively earlier in the striatum but not in the prefrontal cortex as learning took place. These results support the hypothesis that rewarded associations are first identified by the basal ganglia, the output of which 'trains' slower learning mechanisms in the frontal cortex.     

Modulation of the two promoters of the galactose operon of Escherichia coli.

The gal operon of Escherichia coli is controlled by two independent promotors--one is activated and the other inhibited by cyclic AMP and cyclic AMP receptor protein. The two promotors are modulated, however, by the same operator locus and receptor protein.     

Generation of cytotoxic T-lymphocyte precursor cells in T-cell colonies grown in vitro

The role of the thymus in T-lymphocyte differentiation remains unclear. The demonstration that the thymus can restrict the T-lymphocyte specificity repertoire suggests that T cells acquire specificity within the thymus. However, the demonstrations of immunocompetent helper T cells and cytotoxic T-lymphocyte precursor cells (CLPs) in athymic nude mice suggest that the acquisition of some T-cell reactivity may occur without the thymus. We have been using T-cell colonies grown in vitro as a model system for studying various aspects of T-cell differentiation in both mouse and man. In one study we showed that CLPs can be found in T-cell colonies grown from spleen cells of normal mice, each colony containing CLPs of several different specificities. The colonies containing CLPs are not clonal, appearing to have a colony-forming unit (CFU-T) of two (perhaps three) cells. Here we provide direct evidence that the CLPs are spontaneously produced in the colonies. In addition, the cells of the CFU-T were characterized with antisera directed against the cell-surface marker Thy-1, which is present on all murine T cells, and the cell-surface markers Lyt-1 and Lyt-2, which are differentially distributed on different T-cell subclasses. We found that the CFU-T contains both a Thy-1+ and a Thy-1- cell, neither of which seems to carry either Lyt-1 or Lyt-2 surface markers.     

Potentiation of NMDA receptor currents by arachidonic acid.

Arachidonic acid is released by phospholipase A2 when activation of N-methyl-D-aspartate (NMDA) receptors by neurotransmitter glutamate raises the calcium concentration in neurons, for example during the initiation of long-term potentiation and during brain anoxia. Here we investigate the effect of arachidonic acid on glutamate-gated ion channels by whole-cell clamping isolated cerebellar granule cells. Arachidonic acid potentiates, and makes more transient, the current through NMDA receptor channels, and slightly reduces the current through non-NMDA receptor channels. Potentiation of the NMDA receptor current results from an increase in channel open probability, with no change in open channel current. We observe potentiation even with saturating levels of agonist at the glutamate- and glycine-binding sites on these channels; it does not result from conversion of arachidonic acid to lipoxygenase or cyclooxygenase derivatives, or from activation of protein kinase C. Arachidonic acid may act by binding to a site on the NMDA receptor, or by modifying the receptor's lipid environment. Our results suggest that arachidonic acid released by activation of NMDA (or other) receptors will potentiate NMDA receptor currents, and thus amplify increases in intracellular calcium concentration caused by glutamate. This may explain why inhibition of phospholipase A2 blocks the induction of long-term potentiation.     

A filament of dark matter between two clusters of galaxies

It is a firm prediction of the concordance cold-dark-matter cosmological model that galaxy clusters occur at the intersection of large-scale structure filaments. The thread-like structure of this 'cosmic web' has been traced by galaxy redshift surveys for decades. More recently, the warm–hot intergalactic medium (a sparse plasma with temperatures of 10(5) kelvin to 10(7) kelvin) residing in low-redshift filaments has been observed in emission and absorption. However, a reliable direct detection of the underlying dark-matter skeleton, which should contain more than half of all matter, has remained elusive, because earlier candidates for such detections were either falsified or suffered from low signal-to-noise ratios and unphysical misalignments of dark and luminous matter. Here we report the detection of a dark-matter filament connecting the two main components of the Abell 222/223 supercluster system from its weak gravitational lensing signal, both in a non-parametric mass reconstruction and in parametric model fits. This filament is coincident with an overdensity of galaxies and diffuse, soft-X-ray emission, and contributes a mass comparable to that of an additional galaxy cluster to the total mass of the supercluster. By combining this result with X-ray observations, we can place an upper limit of 0.09 on the hot gas fraction (the mass of X-ray-emitting gas divided by the total mass) in the filament.