Fossil Signatures of Ancient Accretion Events in the Halo

The role that minor mergers have played in the formation and structure of the Milky Way is still an open question, about which there is much debate. We use numerical simulations to explore the evolution of debris from a tidally disrupted satellite, with the aim of developing a method that can be used to identify and quantify signatures of accretion in a survey of halo stars. For a Milky Way with a spherical halo, we find that debris from minor mergers can remain aligned along great circles throughout the lifetime of the Galaxy. We exploit this result to develop the method of Great Circle Cell Counts (GC3), which we test by applying it to artificially constructed halo distributions. Our results suggest that if as few as 1\% of the stars in a halo survey are accreted from the disruption of a single subsystem smaller than the Large Magellanic Cloud, GC3 can recover the great circle associated with this debris. The dispersion in GC3 can also be used to detect the presence of structure characteristic of accretion in distributions containing a much smaller percentage of material accreted from any single satellite.Comment: 26 pages, AAS TeX, including 11 postscript figures. Accepted for publication in the Astrophysical Journal (Vol 466

N -Methyl-D-Aspartate-Mediated Injury Enhances Quisqualic Acid-Stimulated Phosphoinositide Turnover in Perinatal Rats

Previous work in our laboratory demonstrated that ischemic-hypoxic brain injury in postnatal day 7 rats causes a substantial increase in phosphoinositide (PPI) turnover stimulated by the glutamate analogue quisqualic acid (QUIS) in the hippocampus and striatum. To examine this phenomenon in more detail, we performed similar experiments after producing injury by unilateral intracerebral injections of the glutamate analogue N -methyl-D-aspartate (NMDA). The 7-day-old rodent brain is hypersensitive to NMDA neurotoxicity and NMDA injection causes histopathology that closely resembles that produced by ischemia-hypoxia. NMDA, 17 nmol in 0.5 Μl, was injected into the right posterior striatum of 7-day-old rat pups and they were killed 3 days later. Hippocampal or striatal tissue slices were prepared from ipsilateral and contralateral hemispheres from vehicle-injected control and from noninjected control rat pups. Slices were then incubated with myo -[ 3 H]inositol plus glutamate agonists or antagonists in the presence of lithium ions and [ 3 H]inositol monophosphate ([ 3 H]IP 1 ) accumulation was measured. The glutamate agonists, QUIS, L-glutamic acid, and ( RS )-Α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, stimulated greater [ 3 H]IP 1 release in tissue ipsilateral to the NMDA injection compared with that in the contralateral side and in control pups. The glutamate antagonists, D,L-2-amino-7-phosphonoheptanoic acid, 3-[(+)-2-carboxypiperazin-4-yl]-propyl-l-phosphoric acid, kynurenic acid, and 6,7-dinitroquinoxaline-2,3-dione did not inhibit QUIS-stimulated [ 3 H]IP 1 release. The enhanced PPI turnover in the lesioned tissue was specific to glutamate receptors because carbachol (CARB) failed to elicit preferential enhanced stimulation. To investigate the possibility that alterations in the release of endogenous neurotransmitters had a role in potentiating QUIS-stimulated PPI turnover after NMDA injection, we examined the effect of tetrodotoxin. Tetrodotoxin (0.5 Μ M ) did not alter QUIS-or CARB-stimulated PPI hydrolysis in the lesioned or unlesioned tissue. The influence of extracellular calcium concentration on QUIS-stimulated [ 3 H]IP 1 formation was also examined after the NMDA lesion. Moderate reduction of calcium in the buffer (1 Μ M ) enhanced the lesion effect. Low calcium buffer enhanced QUIS-stimulated PPI turnover in the lesioned hippocampal slices, but reduced QUIS stimulation in contralateral slices and controls. In contrast, CARB-stimulated PPI turnover was not enhanced in low Ca 2+ buffer. A similar pattern of Ca 2+ dependency was observed in striatal slices. Calcium-free (<10 n M ) buffer suppressed PPI turnover in all groups. These studies demonstrate that NMDA-induced excitotoxic injury in neonatal rats causes a selective enhancement of QUIS-stimulated PPI turnover that resembles the effects of ischemia-hypoxia. In addition, we found that agonist-stimulated PPI turnover is sensitive to the in vitro Ca 2+ concentration. These changes could reflect altered coupling of non-NMDA receptors to phospholipase C activity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65991/1/j.1471-4159.1992.tb08337.x.pd

High time-resolution observations of the Vela pulsar

We present high time resolution observations of single pulses from the Vela pulsar (PSR B0833-45) made with a baseband recording system at observing frequencies of 660 and 1413 MHz. We have discovered two startling features in the 1413 MHz single pulse data. The first is the presence of giant micro-pulses which are confined to the leading edge of the pulse profile. One of these pulses has a peak flux density in excess of 2500 Jy, more than 40 times the integrated pulse peak. The second new result is the presence of a large amplitude gaussian component on the trailing edge of the pulse profile. This component can exceed the main pulse in intensity but is switched on only relatively rarely. Fluctutation spectra reveal a possible periodicity in this feature of 140 pulse periods. Unlike the rest of the profile, this component has low net polarization and emits predominantly in the orthogonal mode. This feature appears to be unique to the Vela pulsar. We have also detected microstructure in the Vela pulsar for the first time. These same features are present in the 660 MHz data. We suggest that the full width of the Vela pulse profile might be as large as 10 ms but that the conal edges emit only rarely.Comment: 6 pages, 5 figures, In Press with ApJ Letter

Perinatal Hypoxic-Ischemic Brain Injury Enhances Quisqualic Acid-Stimulated Phosphoinositide Turnover

In an experimental model of perinatal hypoxic-ischemic brain injury, we examined quisqualic acid (Quis)-stimulated phosphoinositide (PPI) turnover in hippocampus and striatum. To produce a unilateral forebrain lesion in 7-day-old rat pups, the right carotid artery was ligated and animals were then exposed to moderate hypoxia (8% oxygen) for 2.5 h. Pups were killed 24 h later and Quis-stimulated PPI turnover was assayed in tissue slices obtained from hippocampus and striatum, target regions for hypoxic-ischemic injury. The glutamate agonist Quis (10 -4 M ) preferentially stimulated PPI hydrolysis in injured brain. In hippocampal slices of tissue derived from the right cerebral hemisphere, the addition of Quis stimulated accumulation of inositol phosphates by more than ninefold (1,053 ± 237% of basal, mean ± SEM, n = 9). In contrast, the addition of Quis stimulated accumulation of inositol phosphates by about fivefold in the contralateral hemisphere (588 ± 134%) and by about sixfold in controls (631 ± 177%, p < 0.005, comparison of ischemic tissue with control). In striatal tissue, the corresponding values were 801 ± 157%, 474 ± 89%, and 506 ± 115% (p < 0.05). In contrast, stimulation of PPI turnover elicited by the cho-linergic agonist carbamoylcholine, (10 -4 or 10 -2 M ) was unaffected by hypoxia-ischemia. The results suggest that prior exposure to hypoxia-ischemia enhances coupling of excitatory amino acid receptors to phospholipase C activity. This activation may contribute to the pathogenesis of irreversible brain injury and/or to mechanisms of recovery.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66017/1/j.1471-4159.1988.tb01046.x.pd

Wandering Stars: an Origin of Escaped Populations

We demonstrate that stars beyond the virial radii of galaxies may be generated by the gravitational impulse received by a satellite as it passes through the pericenter of its orbit around its parent. These stars may become energetically unbound (escaped stars), or may travel to further than a few virial radii for longer than a few Gyr, but still remain energetically bound to the system (wandering stars). Larger satellites (10-100% the mass of the parent), and satellites on more radial orbits are responsible for the majority of this ejected population. Wandering stars could be observable on Mpc scales via classical novae, and on 100 Mpc scales via SNIa. The existence of such stars would imply a corresponding population of barely-bound, old, high velocity stars orbiting the Milky Way, generated by the same physical mechanism during the Galaxy's formation epoch. Sizes and properties of these combined populations should place some constraints on the orbits and masses of the progenitor objects from which they came, providing insight into the merging histories of galaxies in general and the Milky Way in particular.Comment: 13 pages, 3 encapsulated postscript figure

Transient Hypoxia Alters Striatal Catecholamine Metabolism in Immature Brain: An In Vivo Microdialysis Study

Microdialysis probes were inserted bilaterally into the striatum of 7-day-old rat pups (n = 30) to examine extracellular fluid levels of dopamine, its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). The dialysis samples were assayed by HPLC with electrochemical detection. Baseline levels, measured after a 2-h stabilization period, were as follows: dopamine, not detected; DOPAC, 617 ± 33 fmol/min; HVA, 974 ± 42 fmol/min; and 5-HIAA, 276 ± 15 fmol/min. After a 40-min baseline sampling period, 12 animals were exposed to 8% oxygen for 120 min. Hypoxia produced marked reductions in the striatal extracellular fluid levels of both dopamine metabolites ( p < 0.001 by analysis of variance) and a more gradual and less prominent reduction in 5-HIAA levels ( p < 0.02 by analysis of variance), compared with controls (n = 12) sampled in room air. In the first hour after hypoxia, DOPAC and HVA levels rose quickly, whereas 5-HIAA levels remained suppressed. The magnitude of depolarization-evoked release of dopamine (elicited by infusion of potassium or veratrine through the microdialysis probes for 20 min) was evaluated in control and hypoxic animals. Depolarization-evoked dopamine efflux was considerably higher in hypoxic pups than in controls: hypoxic (n = 7), 257 ± 32 fmol/min; control (n = 12), 75 ± 14 fmol/min ( p < 0.001 by analysis of variance). These data demonstrate that a brief exposure to moderate hypoxia markedly disrupts striatal catecholamine metabolism in the immature rodent brain.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66218/1/j.1471-4159.1990.tb01914.x.pd