Hirasawa T, Nakamura T, Morita M, Ezawa I, Miyakawa H, Kudo Y
Graduate School of Human Life Science, Japan Women's University, Tokyo, Japan.
Neurosci Lett. 1998 Nov 13;256(3):139-42. doi: 10.1016/s0304-3940(98)00782-4.
We examined the effects of parathyroid hormone (PTH) on rat hippocampal neurons in culture to determine whether it caused a similar intracellular calcium concentration ([Ca2+]i) increase in these cells to that seen with renal epithelial cells and found that PTH induced the effect in about 30% of the neurons. The effects appeared gradually during continuous administration of full-length PTH(1-84) or its active fragment, PTH(1-34), but not of an inactive fragment, PTH(39-84). However, the active fragment of the PTH-related peptide (PTHrP(1-34)) had little effect on [Ca2+]i during 60 min of administration. The PTH effect was inhibited by nifedipine, an L-type Ca2+ channel antagonist, and facilitated by S-(-)-BAY K 8644, an L-type Ca2+ channel agonist. Our findings suggest that PTH is one of the causal factors for the age-related increase in the density of voltage gated Ca2+ channels in hippocampal neurons.
我们研究了甲状旁腺激素(PTH)对培养的大鼠海马神经元的影响,以确定它是否会使这些细胞内的钙浓度([Ca2+]i)升高,其升高程度与肾上皮细胞中的情况类似,结果发现PTH在约30%的神经元中诱导了这种效应。在持续给予全长PTH(1 - 84)或其活性片段PTH(1 - 34)的过程中,效应逐渐显现,但给予无活性片段PTH(39 - 84)时则没有这种效应。然而,在给药60分钟期间,甲状旁腺激素相关肽的活性片段(PTHrP(1 - 34))对[Ca2+]i几乎没有影响。PTH的效应被L型钙通道拮抗剂硝苯地平抑制,并被L型钙通道激动剂S-(-)-BAY K 8644增强。我们的研究结果表明,PTH是导致海马神经元中电压门控钙通道密度随年龄增长而增加的原因之一。