perhaps by regulating the localized formation of a signaling complex

There may be similarities in mechanisms of excitotoxic death between oligodendrocytes and neurons. Mechanisms involving in neuronal death have been estab lished, nevertheless, these mechanisms for excitotoxic oligo dendrocyte death stay to be elucidated. In neurons, the factor of to neuronal death is mediated by pecific produced prostanoids. Imatinib 152459-95-5 COX catalyzes the initial reactions in the synthesis of prostanoids, prostaglandin D2, prostaglandin E2, prostaglandin F2, prostacyclin and thromboxane from arachidonic acid. Each of these PGs activates specific G-protein coupled receptors that, depending on the prostanoid, vary in number from one to four receptors as sometimes appears for PGE2. These four receptors for PGE2, have distinct styles of expression in numerous tissues and dif ferent pharmacological properties and each receptor is coupled to distinct intracellular signaling pathways. In neuronal excitotoxic death, produced PGE2 has been shown to be the major prostanoid accountable for the contribution of to neuronal death in vitro and in vivo. Three groups have since found that PGE2 stimulation Skin infection of the EP1 prostanoid receptor is responsible for the factor of to NMDA activated neuronal death in vitro and in vivo, see for review. Colleagues fur ther and iadecola shown that EP1 activation impaired the Na Ca2 exchanger which helps neurons remove extra intracellular Ca2 following NMDA stimulation. The resulting dysregulation of intracellular Ca2 generated excess of Ca2 in neurons and subsequent death. EP1 receptor activation has also been linked to the AKT sig naling pathway that may donate to neuronal death. Nevertheless, PGE2 might have opposing effects on neu ronal viability depending on which receptor is stimulated. Activation of EP1 plays a role in neuronal excitotoxic death, order ApoG2 contrary to activation of EP4 and EP2 which encourage neuroprotection for evaluation. Not as is known about how specific prostanoids and their receptors affect viability of oligodendrocytes, but similar roles may be seen for oligodendrocyte death as are seen with nerves. One study has linked specific professionals tanoids to possibility of oligodendrocytes. The prostanoid PGD2 and its metabolite 15d PGJ2 have already been shown to directly stimulate death of oligodendrocyte precursors in vitro. In this case, the effects of those prostanoids were associated with oxidative stress and independent of prostanoid receptors. Other prostanoids were tested and had no immediate toxic effects on oligoden drocytes. However, it is important to remember that with neurons, PGE2 was necessary, although not sufficient to induce excitotoxic death. In this case, the prostanoid was not toxic by itself, but could contribute to the effect of the excitotoxin. Further investigations may be asked to know what function certain prostanoids and their recep tors play within the death of oligodendrocytes.