780 and / or JNJ 16,259,685th JNJ 16259685 inhibited Akt phosphorylation induced by 17E2 and ICI 182,780 was also effective in reducing phosphorylation of Akt induced by quisqualate. Close Of course, we investigated whether the ER and mGlu1 receptors k Can also interact in the stimulation of polyphosphoinositide hydrolysis, which is enabled by the canonical signal transduction of mGlu1 receptors. The stimulation of PI hydrolysis by the ER membrane and mGlu1 receptors has been established, the neuro for the synthesis of progesterone in hypothalamic astrocytes. DHPG increased significantly Ht InsP formation in cultured cortical neurons, w During 17E2 produced a slight stimulation of InsP accumulation, without the stimulation of PI hydrolysis by DHPG. Both ICI 182780 and JNJ 16,259,685 prevents the effect of the 172 and the stimulation of InsP formation 5-HT Receptor of DHPG induced. ER membrane-long discussion proposed to participate in the neuroprotective effect of estrogen against toxicity of t. Although several signaling pathways are involved, the question of how the signal ER membrane are discussed. Receptor transactivation of Were estrogen by mGlu extensively studied anddemonstrated be included in the controlled on sexual behavior in female rats and the regulation of progesterone synthesis by glia. All of these mechanisms seem by the subtype of RE will be taught. We investigated whether an interaction between ER and mGlu1 receptors, the mechanisms of neuroprotection in cortical neurons challenged with peptide amylo k nnte be extended Of. We found that ER and mGlu1 receptors were colocalized in cultured cortical neurons, in line with previous studies showing colocalization of both receptors in the hippocampus and hypothalamus neurons.
Here, only ER, but not mGlu1 receptors are detected in cortical astrocytes. This contrasts with evidence that mGlu1 receptors in hypothalamic astrocyte cultures prepared from adult rats. The differences in regional development or the expression of glial mGlu1 receptors may be explained the discrepancy Ren. Add toxicity t amylo Of 17E2 attenuated Cht in mixed cortical cultures, as expected. The effect of 17E2 was mimicked by the selective ER agonist PPT, w During the pharmacological stimulation of the ER with DPN caused only a small protective effect. Adding the mGlu1 receptor agonists / 5 mixed, DHPG caused neuroprotection in a Ausma observed compared with 17E2. To analyze the specific contribution of mGlu1 and mGlu5 receptors in neuroprotection, we used an approach to the combination of an antagonist JNJ 16,259,865 with DHPG, the mGlu1 flowering bridges ceiling or the MPEP, the mGlu5 flowering. Neuroprotection was abolished by JNJ 16259865 and MPEP only slightly reduced, suggesting that activation of mGlu1 well known action of DHPG. The r The group I mGlu receptor is controversial in the mechanisms of neurodegeneration / neuroprotection. Activation of mGlu1 / 5 receptors k Can in the amplification of Neurotoxizit Lead t or protection depends Ngig of the experimental paradigm of neuronal death, type of abuse, the exposure time to agonists / antagonists and the origin and composition of the cell culture. Baudry and his colleagues found that neurons protect mGlu1 receptors via activation of the DCP.