Effects of Low Amyloid-β (Aβ) Concentration on Aβ1-42 Oligomers Binding and GluN2B Membrane Expression.

Numerous studies have shown that amyloid-β (Aβ) modulate intracellular metabolic cascades and an intracellular Ca2+ homeostasis and a cell surface NMDA receptor expression alteration in Alzheimer's disease (AD). However most of these findings have been obtained by using non-physiological Aβ concentrations. The present study deals with the effect of low Aβ concentrations on cellular homeostasis.

Deficits of psychomotor and mnesic functions across aging in mouse lemur primates.

Owing to a similar cerebral neuro-anatomy, non-human primates are viewed as the most valid models for understanding cognitive deficits. This study evaluated psychomotor and mnesic functions of 41 young to old mouse lemurs (Microcebus murinus). Psychomotor capacities and anxiety-related behaviors decreased abruptly from middle to late adulthood.

Clostridium perfringens epsilon toxin targets granule cells in the mouse cerebellum and stimulates glutamate release.

Epsilon toxin (ET) produced by C. perfringens types B and D is a highly potent pore-forming toxin. ET-intoxicated animals express severe neurological disorders that are thought to result from the formation of vasogenic brain edemas and indirect neuronal excitotoxicity.

Protein kinase C as a peripheral biomarker for Alzheimer's disease.

Numerous studies have been performed, which assess an important role of protein kinase C (PKC) in the physiopathology of Alzheimer disease (AD). The alteration of PKC activity stimulates amyloid-beta peptides production and protein tau hyperphosphorylation. This recently led to consider PKC as a potential therapeutic target for disease modifying drugs.

Two chromogranin a-derived peptides induce calcium entry in human neutrophils by calmodulin-regulated calcium independent phospholipase A2.

Background: Antimicrobial peptides derived from the natural processing of chromogranin A (CgA) are co-secreted with catecholamines upon stimulation of chromaffin cells. Since PMNs play a central role in innate immunity, we examine responses by PMNs following stimulation by two antimicrobial CgA-derived peptides.

Methodology/principal Findings: PMNs were treated with different concentrations of CgA-derived peptides in presence of several drugs.

ARF6 regulates the synthesis of fusogenic lipids for calcium-regulated exocytosis in neuroendocrine cells.

An important role for specific lipids in membrane fusion has recently emerged, but regulation of their biosynthesis remains poorly understood. Among fusogenic lipids, phosphatidic acid and phosphoinositol 4,5-bisphosphate (PIP(2)) have been proposed to act at various steps of neurotransmitter and hormone exocytosis. Using real time FRET (fluorescence resonance energy transfer) measurements, we show here that the GTPase ARF6, potentially involved in the synthesis of these lipids, is activated at the exocytotic sites in PC12 cells stimulated for secretion.

Panaxadiol glycosides that induce neuronal differentiation in neurosphere stem cells.

Bioassay-guided fractionation, combined with screening based on EGF-responsive neural stem cells (NSCs) differentiation assay, has been used to search for active molecules from Panax notoginseng. Ginsenosides Rg3 (1), Rk1 (2), and Rg5 (3) were identified as potential neurogenic molecules. The degrees of their neurogenic effects were found to be 3 > 2 > 1.

Functional implication of neuronal calcium sensor-1 and phosphoinositol 4-kinase-beta interaction in regulated exocytosis of PC12 cells.

Several studies have shown that the neuronal calcium sensor (NCS-1) and phosphoinositol 4-kinase-beta (PI4K-beta) regulate the exocytotic process of nerve and neuroendocrine cells. The aim of our study was to investigate their possible interaction at rest and during stimulation in living cells and to decipher the role of this interaction in the secretory process. In PC12 cells, we observed a stimulation-induced recruitment of NCS-1 and PI4K-beta from the intracellular compartment toward the plasma membrane.

Alteration of protein kinase C conformation in red blood cells: a potential marker for Alzheimer's disease but not for Parkinson's disease.

There is a growing evidence of early changes of blood cells in Alzheimer's disease (AD). We have developed an original novel method for quantifying the alteration of protein kinase C (PKC) by its fluorescence spectrum: by using Fim-1, a specific fluorescent probe made for protein kinase C that detects the conformational changes of this. We show that the PKC conformation is altered in red blood cells (RBC) from AD patients as compared to RBC from healthy controls.

F-actin does not modulate the initial steps of the protein kinase C activation process in living nerve cells.

Actin is a major substrate for protein kinase C (PKC) and PKC is considered a modulator of the actin network. In addition in vitro studies (Biochemistry 39 (2000) 271) have suggested that all PKC isoforms bind to actin during the process of activation of the enzyme. To test the physiological significance of such a coupling we used living PC12 cells and primary cultures of cerebellar granule cells.

Ca2+ Mobilization in Cultured Rat Cerebellar Cells: Astrocytes are Activated by t-ACPD.

Using primary rat cerebellar cell cultures we observed that trans-1-amino-cyclopentyl-1,3-dicarboxylic acid (t-ACPD) was able to induce an increase in intracellular [Ca2+] in different cell types. This response was not abolished by external Ca2+ withdrawal, indicating that t-ACPD triggered the release of intracellularly stored Ca2+. In neurons the t-ACPD response was monophasic and inhibited by l-2-amino-4-phosphonobutyrate (APB).