model is presented with a single CRMP molecule

There could be similarities in mechanisms of excitotoxic demise between oligodendrocytes and neurons. Mechanisms concerning in neuronal death have already been estab lished, however, these mechanisms for excitotoxic oligo dendrocyte death remain to be elucidated. In neurons, the contribution of to neuronal death is mediated by pecific produced prostanoids. COX catalyzes the initial reactions in the buy GM6001 forming of prostaglandin E2, prostaglandin D2, prostanoids, prostaglandin F2, prostacyclin and thromboxane from arachidonic acid. All these PGs activates specific G-protein coupled receptors that, with regards to the prostanoid, vary in number from to four receptors as is observed for PGE2. These four receptors for PGE2, have distinct patterns of expression in various tissues and dif ferent pharmacological properties and each receptor is coupled to distinct intracellular signaling pathways. In neuronal excitotoxic death, generated PGE2 has been shown to function as the major prostanoid responsible for the contribution of to neuronal death in vitro and in vivo. Three groups have since shown that PGE2 stimulation of the EP1 prostanoid receptor is responsible Ribonucleic acid (RNA) for the contribution of to NMDA stimulated neuronal death in vivo and in vitro, see for review. Peers fur-ther and iadecola shown that EP1 activation impaired the Na Ca2 exchanger which helps neurons remove excessive intracellular Ca2 following NMDA stimulation. The resulting dysregulation of intracellular Ca2 generated overload of Ca2 in neurons and subsequent death. EP1 receptor activation has additionally been linked order 3-Deazaneplanocin A to the AKT sig naling route that could subscribe to neuronal death. But, PGE2 could have opposing effects on neu ronal viability depending on which receptor is stimulated. Activation of EP1 contributes to neuronal excitotoxic death, as opposed to activation of EP2 and EP4 which increase neuroprotection for review. Not as is known about how exactly certain prostanoids and their receptors affect viability of oligodendrocytes, but as are seen with nerves similar roles could be seen for oligodendrocyte demise. One study has linked certain professionals tanoids to possibility of oligodendrocytes. The prostanoid PGD2 and its metabolite 15d PGJ2 have been proven to directly promote death of oligodendrocyte precursors in vitro. In this case, the consequences of the prostanoids were related to oxidative stress and independent of prostanoid receptors. Other prostanoids were tried and had no immediate toxic effects on oligoden drocytes. However, it's important to remember that with neurons, PGE2 was necessary, but not sufficient to induce excitotoxic death. In this instance, the prostanoid wasn't toxic by itself, but could give rise to the influence of the excitotoxin. Further investigations may have to figure out what function particular prostanoids and their recep tors play in the excitotoxic death of oligodendrocytes.