Vasopressin-induced neurotrophism in cultured hippocampal neurons via V1 receptor activation.
Vasopressin-induced neurotrophism in cultured hippocampal neurons via V1 receptor activation.
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加压素通过 V1 受体激活在培养的海马神经元中诱导神经营养作用。
DOI：
10.1002/neu.480250404
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Fernandez,JG
中科院分区：
文献类型：
--
作者：
Brinton,RD;Monreal,AW;Fernandez,JG
神经细胞形态的结构增强被认为是导致神经系统中信息存储的细胞过程中的一个组成步骤。为了研究这一假设，我们确定是否加压素（AVP），一种神经肽，可以增强记忆功能，将提高培养海马神经元的细胞结构特征。这些研究的结果表明，在存在血清的情况下，加压素（1 μM）在暴露48小时后诱导神经突数量、神经突长度和神经突直径显著增加。血管加压素暴露后，形态复杂性也得到增强，表现为丝状伪足/分支数量、分支长度和分支分叉点数量显著增加。后叶加压素暴露后，装饰神经炎分支的微刺的数量也显着增加。为了确定加压素的神经营养作用是否依赖于血清中存在的因子，将海马神经细胞在无血清培养基中培养并暴露于100-1000 nMAVP。这些研究的结果表明，在不存在血清的情况下，AVP诱导海马神经细胞生长的显著增强，并且最低有效浓度从存在血清时所需的1 μM降低至100 nM。此外，神经细胞生长明显增加所需的时间从48小时减少到24小时。这些结果表明，AVP诱导的神经营养作用不依赖于血清中未鉴定的因子。AVP诱导的神经营养作用是由V1受体激活介导的。暴露于V1受体激动剂（100-1000 nM）后神经细胞生长显著增强，而暴露于V2受体激动剂（100-1000 nM）未增加任何测量的形态学参数。综合考虑，这些数据表明加压素可以对培养的海马神经细胞产生显著的神经营养作用。此外，AVP诱导的神经营养作用是一种直接效应，不依赖于血清中存在的未鉴定因子。海马神经细胞生长的增强发生在特定的V1受体激动剂的存在下，而不是暴露于V2受体激动剂后，这表明通过V1受体激活介导AVP诱导的神经营养作用的磷脂酰肌醇途径的激活。讨论了这些研究的结果对了解加压素参与神经发育以及诱导与记忆形成相关的细胞结构修饰的影响。John Wiley & Sons，Inc.
Structural enhancement of nerve cell morphology has been postulated to be an integral step in the cellular process leading to information storage in the nervous system. To investigate this postulate, we determined whether vasopressin (AVP), a neural peptide that can enhance memory function, would enhance the cytoarchitectural features of hippocampal neurons in culture. Results of these studies demonstrated that in the presence of serum, vasopressin (1 μM), induced a significant in crease in the number of neurites, in neuritic length, and in neurite diameter following 48 h of exposure. Morphological complexity was also enhanced following vasopressin exposure as indicated by a significant increase in the number of filopodia/branches, in the sum of branch lengths, and in the number of branch bifurcation points. The number of microspikes decorating neuritic branches was also significantly increased following vasopressin exposure. To determine whether the neurotrophic effects of vasopressin was dependent upon factors present in serum, hippocampal nerve cells were cultured in serum‐free media and exposed to 100–1000 nMAVP. Results of these studies demonstrated that in the absence of serum, AVP induced significant enhancement of hippocampal nerve cell growth and that the minimally effective concentration was reduced from 1 μM, as required in the presence serum, to 100 nM. In addition, the time required for a significant increase in nerve cell growth to become apparent decreased from 48 to 24 h. These results demonstrate that AVP‐induced neurotrophism is not dependent upon unidentified factors in serum. AVP‐induced neurotrophism was found to be mediated by V1receptor activation. Significant enhancement of nerve cell growth occurred following exposure to V1receptor agonist (100–1000 nM), whereas exposure to V2receptor agonist (100–1000 nM) did not increase any of the morphological parameters measured. Considered together, these data indicate that vasopressin can exert a significant neurotrophic effect upon hippocampal nerve cells in culture. Moreover, AVP‐induced neurotrophism is a direct effect and not dependent upon unidentified factors present in serum. Enhancement of hippocampal nerve cell growth occurred in the presence of a specific V1receptor agonist and not following exposure to a V2agonist, suggesting that activation of the phosphatidyl inositol pathway via V1receptor activation mediates AVP‐induced neurotrophism. Results of these studies are discussed with respect to their implications for understanding vasopressin involvement during neural development and induction of cytoarchitectual modifications associated with memory formation. 1994 John Wiley & Sons, Inc.
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