Hansson Elisabeth, Westerlund Anna, Björklund Ulrika, Rönnbäck Lars
Department of Clinical Neuroscience and Rehabilitation, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Neuroreport. 2009 Jul 1;20(10):957-62. doi: 10.1097/WNR.0b013e32832ca201.
Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective properties and plays an important role in neuroinflammation. PACAP38 interacts with its receptors, PAC1, and VPAC, on astrocytes at 10(-8) M to induce biphasic Ca2+ transients, which were reduced to a single transient by the PAC1-blocking PACAP antagonist PACAP6-38. At 10(-12) M even the single transient, corresponding to PAC1 was blocked. PACAP-induced Ca2+ transients were more pronounced in astrocytes cocultured with brain endothelial cells than in monocultured astrocytes, indicating that astrocytes that receive signals from microvessels develop more sensitive signal transduction systems for Ca. In this sensitive system, PACAP38 attenuated 5-HT, histamine, and ATP-evoked Ca2+ transients, showing the anti-inflammatory properties of PACAP.
垂体腺苷酸环化酶激活多肽（PACAP）具有神经保护特性，在神经炎症中发挥重要作用。PACAP38以10⁻⁸M的浓度与星形胶质细胞上的受体PAC1和VPAC相互作用，诱导双相Ca²⁺瞬变，而PAC1阻断性PACAP拮抗剂PACAP6 - 38可将其减少为单瞬变。在10⁻¹²M时，即使对应于PAC1的单瞬变也被阻断。与单独培养的星形胶质细胞相比，与脑内皮细胞共培养的星形胶质细胞中PACAP诱导的Ca²⁺瞬变更为明显，这表明从微血管接收信号的星形胶质细胞会形成对Ca更敏感的信号转导系统。在这个敏感系统中，PACAP38减弱了5 - 羟色胺、组胺和ATP诱发的Ca²⁺瞬变，显示出PACAP的抗炎特性。
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