lithium-chloride and phorbolol-myristate-acetate

Up to this day, the roles of PEA15 expression and its phosphorylation in seizure-related events have not been still unclear. In the present study, we found that PEA15 was distinctly phosphorylated in reactive astrocytes and apoptotic astrocytes in the rat hippocampus following LiCl-pilocarpine-induced status epilepticus (SE, a prolonged seizure activity). PEA15-serine (S) 104 phosphorylation was up-regulated in reactive astrocytes following SE, although PEA15 expression and its S116 phosphorylation were unaltered. Bisindolylmaleimide (BIM), a protein kinase C (PKC) inhibitor, attenuated SE-induced reactive astrogliosis, but phorbol 12-myristate 13-acetate (PMA, a PKC activator) aggravated it. Unlike reactive astrocytes, PEA15-S116 phosphorylation was reduced in apoptotic astrocytes. However, PEA15 expression and its S104 phosphorylation were unchanged in apoptotic astrocyte. Neither BIM nor PMA affected SE-induced astroglial apoptosis. PEA15 expression and its phosphorylations were not relevant to SE-induced CA1 neuronal death. These findings indicate that PEA15-S104 and S116 phosphorylations may play a role in reactive astrogliosis and prevention of astroglial apoptosis, respectively. Therefore, we suggest that the selective manipulation of PEA15 phosphorylations may regulate apoptotic and/or proliferative signals in astrocytes.

Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Astrocytes; Benzylamines; Fluorescent Antibody Technique; Gliosis; Hippocampus; Indoles; Lithium Chloride; Male; Maleimides; Phosphoproteins; Phosphorylation; Pilocarpine; Protein Kinase C; Rats; Rats, Sprague-Dawley; Signal Transduction; Status Epilepticus; Sulfonamides; Tetradecanoylphorbol Acetate

The effects of the exposure to a static magnetic field (sMF) of 0.3 +/- 0.03 T on the Fusarium culmorum were investigated in vitro. sMF inhibition of mycelia growth was accompanied by morphological and biochemical changes. Fungal conidia germination and cell viability were also reduced. We provide evidence of the influence of sMF on Ca(2+)-dependent signal transduction pathways involved in conidia germination. Perturbation of these pathways by adding different compounds (i.e. CaCl(2), phorbol 12-myristate 13-acetate, neomycin, EGTA, LiCl) to the medium, suggested that exposed conidia are unable to mobilise calcium from intracellular stores and that the hindered mechanism may be IP(3)-dependent.

Topics: Calcium Chloride; Egtazic Acid; Fusarium; Lithium Chloride; Magnetics; Mycelium; Neomycin; Tetradecanoylphorbol Acetate