We have found previously that bath-applied Tat abnormally increased Ca2+ influx through overactivated, voltage-sensitive L-type Ca2+ channels in pyramidal neurons within the rat medial prefrontal cortex (mPFC). However, it is unknown whether the Tat-induced Ca2+ dysregulation

was mediated by increased activity and/or the number of the L-channels. This study tested the hypothesis that transient/early exposure to Tat in vivo promoted enduring L-channel dysregulation in the mPFC without neuron loss. Accordingly, rats were administered a single intracerebroventricular injection of recombinant Tat (80 mu g/20 mu l; diluted by cerebrospinal fluids to pathophysiological concentrations) or vehicle. Rats were killed 14 days after injection for immunohistochemical SAHA ic50 assessments of the mPFC, motor cortex, caudate-putamen, and nucleus accumbens. Stereological estimates for positively stained cells www.selleckchem.com/products/ink128.html indicated a significant increase in the number of cells expressing the pore-forming Ca(v)1.2-alpha 1c subunit of L-channels in the mPFC compared with other regions in Tat-treated or vehicle-treated

rat brains. Optical density measurements showed a Tat-induced increase in glial fibrillary acidic protein expression, indicating astrogliosis in the cortical regions. There was no significant loss of neurons in any brain region investigated. These findings indicate that transient Tat exposure in vivo induced enduring L-channel dysregulation and astrogliosis in the mPFC without neuron loss. Such maladaptations may contribute toward dysregulated Ca2+ homeostasis and neuropathology in the PFC in the early stages of HIV infection. NeuroReport 23:825-829 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Face processing

Protirelin is crucial to social interaction, but is impaired in schizophrenia patients, who experience delays in face recognition, difficulties identifying others, and misperceptions of affective content. The right fusiform face area plays an important role in the early stages of human face processing and thus may be affected in schizophrenia. The aim of the study was therefore to investigate whether face processing deficits are related to dysfunctions of the right fusiform face area in schizophrenia patients compared with controls. In a rapid, event-related functional magnetic resonance imaging (fMRI) design, we investigated the encoding of new faces, as well as the recognition of newly learned, famous, and unfamiliar faces, in 13 schizophrenia patients and 21 healthy controls. We applied region of interest analysis to each individual’s right fusiform face area and tested for group differences. Controls displayed higher blood oxygenation level dependent (BOLD) activation during the memorization of faces that were later successfully recognized.