Spehr Marc, Wetzel Christian H, Hatt Hanns, Ache Barry W
Department of Cell Physiology, Ruhr University Bochum, Bochum, Germany.
Neuron. 2002 Feb 28;33(5):731-9. doi: 10.1016/s0896-6273(02)00610-4.
Phosphatidylinositol 3-kinase (PI3K)-dependent phosphoinositide signaling has been implicated in diverse cellular systems coupled to receptors for many different ligands, but the extent to which it functions in sensory transduction is yet to be determined. We now report that blocking PI3K activity increases odorant-evoked, cyclic nucleotide-dependent elevation of Ca(2+) in acutely dissociated rat olfactory receptor neurons and does so in an odorant-specific manner. These findings imply that 3-phosphoinositide signaling acts in vertebrate olfactory transduction to inhibit cyclic nucleotide-dependent excitation of the cells and that the interaction of the two signaling pathways is important in odorant coding, indicating that 3-phosphoinositide signaling can play a role in sensory transduction.
磷脂酰肌醇3激酶(PI3K)依赖性磷酸肌醇信号传导已涉及到与许多不同配体的受体偶联的多种细胞系统中,但它在感觉转导中的作用程度尚待确定。我们现在报告,阻断PI3K活性会增加急性解离的大鼠嗅觉受体神经元中气味剂诱发的、环核苷酸依赖性的[Ca(2+)]i升高,并且是以气味剂特异性的方式增加。这些发现表明,3-磷酸肌醇信号传导在脊椎动物嗅觉转导中起作用,以抑制细胞的环核苷酸依赖性兴奋,并且这两种信号通路的相互作用在气味编码中很重要,表明3-磷酸肌醇信号传导可以在感觉转导中发挥作用。