New DWI lesions occur more frequently after CAS than after CEA. However, technical advances mainly in the field of endovascular therapy potentially reduce the incidence of these adverse ischemic events. In this scenario, DWI appears to be an ideal tool to compare and further improve both techniques.

Background and Purpose-Angioplasty and stenting is increasingly being used for the treatment of intracranial stenoses.Based

The superior olivary complex (SOC) is an auditory brainstem region that represents a favourable system to study rapid neurotransmission and the maturation of neuronal circuits. Here we performed serial analysis of gene expression (SAGE) on the SOC in 60-day-old Sprague-Dawley rats to identify genes specifically important for its function and to create a transcriptome reference for the subsequent identification of age-related or disease-related changes. Sequencing of 31 035 tags identified 10 473 different transcripts. Fifty-seven per cent of the unique tags with a count greater than four were statistically more highly represented in the SOC than in the hippocampus. Among them were genes encoding proteins involved in energy supply, the glutamate/glutamine shuttle, and myelination. Approximately 80 plasma membrane transporters, receptors, channels, and vesicular transporters were identified, and 25% of them displayed a significantly higher expression level in the SOC than in the hippocampus. Some of the plasma membrane proteins were not previously characterized in the SOC, e.g. the purinergic receptor subunit P2X(6) and the metabotropic GABA receptor Gpr51. Differential gene expression between SOC and hippocampus was confirmed using RNA in situ hybridization or immunohistochemistry. The extensive gene inventory presented here will alleviate the dissection of the molecular mechanisms underlying specific SOC functions and the comparison with other SAGE libraries from brain will ease the identification of promoters to generate region-specific transgenic animals. The analysis will be part of the publicly available database ID-GRAB.

A recently symptomatic carotid artery stenosis carries a high risk of subsequent ischaemic events and thus requires rapid treatment. We investigated the influence of the time delay between the last symptomatic event of a carotid stenosis and subsequent carotid artery stenting (CAS) with respect to the combined 30-day outcome of stroke and death. In a group of 320 patients undergoing CAS the median delay before the intervention was 19 days (interquartile range 10-36) and the combined 30-day complication rate was 8.4%. Time delay was not significantly associated with peri-procedural complications, regardless of whether this variable was dichotomized (<14 days and > or =14 days), separated into interquartile ranges or analysed as a continuous variable. Our results indicate that early CAS is not associated with an increased complication rate in patients with a recently symptomatic carotid stenosis. Thus, if CAS has been selected as the treatment modality for a patient, it should be performed as soon as possible to maximize the benefit of the intervention in reducing the risk of stroke.

␣CaMKIIT286A mutant mice lack long-term potentiation (LTP) in the hippocampal CA1 region and are impaired in spatial learning. In situ hybridization confirms that the mutant mice show the same developmental expression of ␣CaMKII as their wild-type littermates. A simple hypothesis would suggest that if LTP is a substrate for learning, then enriching the environment should cause learning-dependent changes in wild-type mice that have LTP. Such changes would not be seen in LTP-deficient ␣CaMKII T286A mutants. Excitatory synaptic currents in CA1 neurons, recorded with patch clamp in brain slices, revealed that enrichment induces an increase in glutamate release probability and a decreased miniature current amplitude. Confocal microscopy also showed dendritic spine density to be reduced. However, contrary to the hypothesis above, these enrichment-induced changes occur only in the mutant mice and are not detectable in wild-type littermates. We suggest that enrichment induces ␣CaMKII-independent changes in both wild-type and mutant mice. Such changes may be subsequently reversed in wild-type animals via ␣CaMKII-dependent mechanisms, such as LTP. Reversal of plasticity has long been hypothesized to be essential for the hippocampus to maintain its role in memory processing. The inability to reverse plasticity in ␣CaMKII T286A mutant mice would then result in impairment of spatial learning.