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培养的鉴定椎实螺神经元神经突生长的多巴胺调节。

Dopamine regulation of neurite outgrowth from identified Lymnaea neurons in culture.

作者信息

Spencer G E, Lukowiak K, Syed N I

机构信息

Department of Anatomy and Physiology, Respiratory and Neuroscience Research Group, Faculty of Medicine, Calgary, Alberta, Canada.

出版信息

Cell Mol Neurobiol. 1996 Oct;16(5):577-89. doi: 10.1007/BF02152058.

DOI:10.1007/BF02152058
PMID:8956010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11563096/
Abstract
  1. An identified dopaminergic interneuron (RPeD1) of the snail Lymnaea stagnalis, makes specific synaptic connections with a number of target (VI and VJ) but not non-target (VF and RPB) neurons in vivo. When cultured in vitro with both target and non-target cells, RPeD1 re-establishes synapses with target cells only. 2. To test whether exogenous dopamine exerts effects on the neurite outgrowth of both target and non-target neurons respectively, these cells were cultured in conditioned media (CM) in the presence of dopamine (10(-5) M). The growth of the non-target cells was severely restricted and retarded in the presence of dopamine. These data suggest that dopamine may regulate neurite outgrowth of non-target cells in culture. 3. The growth regulatory effects of dopamine on the non-target cells were blocked in the presence of a dopamine receptor antagonist (R(+) SCH-23390, 10(-4) M). These results indicate that dopamine-induced growth regulation of the non-target cells is mediated via dopamine receptors on these cells. 4. In the absence of conditioned media, dopamine was not sufficient to exert growth promoting effects on either target or non-target cells. 5. Taken together, our data show that dopamine differentially regulates growth of identified Lymnaea neurons in culture. Dopamine alone, however, is not sufficient to initiate and support neurite outgrowth from these cells. Rather, it functions to suppress the neurite outgrowth of the non-target cells, initiated by the conditioned media.
摘要
  1. 已鉴定出的椎实螺(Lymnaea stagnalis)的多巴胺能中间神经元(RPeD1),在体内与许多靶标(VI和VJ)神经元而非非靶标(VF和RPB)神经元形成特定的突触连接。当与靶标和非靶标细胞一起在体外培养时,RPeD1仅与靶标细胞重新建立突触。2. 为了测试外源性多巴胺是否分别对靶标和非靶标神经元的神经突生长产生影响,将这些细胞在多巴胺(10⁻⁵ M)存在的条件培养基(CM)中培养。在多巴胺存在的情况下,非靶标细胞的生长受到严重限制和阻碍。这些数据表明多巴胺可能调节培养中非靶标细胞的神经突生长。3. 在多巴胺受体拮抗剂(R(+) SCH-23390,10⁻⁴ M)存在的情况下,多巴胺对非靶标细胞的生长调节作用被阻断。这些结果表明多巴胺诱导的非靶标细胞生长调节是通过这些细胞上的多巴胺受体介导的。4. 在没有条件培养基的情况下,多巴胺不足以对靶标或非靶标细胞发挥促生长作用。5. 综上所述,我们的数据表明多巴胺在培养中对已鉴定的椎实螺神经元的生长具有差异性调节作用。然而,单独的多巴胺不足以启动和支持这些细胞的神经突生长。相反,它的作用是抑制由条件培养基引发的非靶标细胞的神经突生长。

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