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Register a new userMACHOs in M31? Absence of evidence but not evidence of absence
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We present results of a microlensing survey toward the Andromeda Galaxy (M31) carried out during four observing seasons at the Isaac Newton Telescope (INT). This survey is part of the larger microlensing survey toward M31 performed by the Microlensing Exploration of the Galaxy and Andromeda (MEGA) collaboration. Using a fully automated search algorithm, we indentify 14 candidate microlensing events, three of which are reported here for the first time. Observations obtained at the Mayall telescope are combined with the INT data to produce composite lightcurves for these candidates. The results from the survey are compared with theoretical predictions for the number and distribution of events. These predictions are based on a Monte Carlo calculation of the detection efficiency and disk-bulge-halo models for M31. The models provide the full phase-space distribution functions for the lens and source populations and are motivated by dynamical and observational considerations. They include differential extinction and span a wide range of parameter space characterised primarily by the mass-to-light ratios for the disk and bulge. For most models, the observed event rate is consistent with the rate predicted for self-lensing -- a MACHO halo fraction of 30% or higher can be ruled at the 95% confidence level. The event distribution does show a large near-far asymmetry hinting at a halo contribution to the microlensing signal. Two candidate events are located at particularly large projected radii on the far side of the disk. These events are difficult to explain by self lensing and only somewhat easier to explain by MACHO lensing. A possibility is that one of these is due to a lens in a giant stellar stream.
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Absence epilepsy is believed to be associated with the abnormal interactions between the cerebral cortex and thalamus. Besides the direct coupling, anatomical evidence indicates that the cerebral cortex and thalamus also communicate indirectly through an important intermediate bridge--basal ganglia. It has been thus postulated that the basal ganglia might play key roles in the modulation of absence seizures, but the relevant biophysical mechanisms are still not completely established. Using a biophysically based model, we demonstrate here that the typical absence seizure activities can be controlled and modulated by the direct GABAergic projections from the substantia nigra pars reticulata (SNr) to either the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of thalamus, through different biophysical mechanisms. Under certain conditions, these two types of seizure control are observed to coexist in the same network. More importantly, due to the competition between the inhibitory SNr-TRN and SNr-SRN pathways, we find that both decreasing and increasing the activation of SNr neurons from the normal level may considerably suppress the generation of SWDs in the coexistence region. Overall, these results highlight the bidirectional functional roles of basal ganglia in controlling and modulating absence seizures, and might provide novel insights into the therapeutic treatments of this brain disorder.
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