Moreover, unbiased microarray expression analysis showed that Cxcl10 was among 112 transcripts in the neocortex upregulated at least threefold in both TBI and ageing TgSwe

mice, many of them involved in inflammation. The identity of the Cxcl10+ cells remains unclear but flow cytometry showed increased numbers of activated microglia/macrophages as well as myeloid dendritic cells in the TBI and experimental autoimmune encephalomyelitis models. It is concluded that the Cxcl10+ cells appear in the inflamed central nervous system and may represent a novel population of cells that it may be possible to target pharmacologically in a broad range of neurodegenerative conditions. “
“We combined computational modeling and experimental measurements to determine the influence of dendritic structure on the diffusion of Docetaxel intracellular chemical signals in mouse cerebellar Purkinje cells and hippocamal CA1 pyramidal cells. Modeling predicts

that molecular trapping by dendritic spines causes diffusion along spiny dendrites to be anomalous and that the value of the anomalous exponent (dw) is proportional to spine density in both cell types. To test these predictions we combined the local photorelease of an inert dye, rhodamine dextran, with two-photon fluorescence Baf-A1 imaging to track diffusion along dendrites. Our results show that anomalous diffusion is present in spiny dendrites of both cell types. Further, the anomalous exponent is linearly related to the density of spines in pyramidal cells and dw in Purkinje cells is consistent with such a relationship. We conclude that anomalous diffusion occurs in the dendrites of multiple types of neurons. Because spine density is dynamic and depends on neuronal activity, the degree of anomalous diffusion induced by spines can dynamically regulate

the movement of molecules along dendrites. “
“Preconditioning rat hippocampal–entorhinocortical (HEC) slice or cerebellar cell cultures with moderate concentrations of ethanol (20–30 mm) neuroprotects against pro-inflammatory proteins such as HIV-1 glycoprotein 120 (gp120) or amyloid-β. The neuroprotective mechanism of ethanol is unclear, but it conceivably involves sensorstransducerseffectors, analogous Urease to other preconditioning modalities. We initially found that the preconditioning augmented two likely heat shock protein (HSP) ‘effectors’, HSP70 and HSP27, and that precluding HSP upregulation abolished neuroprotection. Here we examined whether pro-survival kinases are transducers potentially leading to HSP effectors. In cerebellar cultures, protein kinase C (PKC) activity increased modestly after 2 days of 30 mm ethanol and was significantly induced after 6 days, when neuroprotection against gp120 becomes manifest.