Ferreira A, Li L, Chin L S, Greengard P, Kosik K S
Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Mol Cell Neurosci. 1996;8(4):286-99. doi: 10.1006/mcne.1996.0064.
In a previous study, we reported a retardation in process outgrowth and synapse formation in cultured hippocampal neurons from synapsin I-deficient mice. Here we investigated whether this delay in synaptogenesis was attributable to pre- or postsynaptic elements. The experimental paradigm used in this study involved the establishment of heterochronic cocultures of neurons from wild-type and synapsin I-deficient neurons established synapses with mature wild-type postsynaptic elements after 24 and 72 h, respectively. In contrast, synapsin I-deficient postsynaptic elements were able to receive synapses only after 9 days in culture, representing a 5-day delay compared to controls. The results suggest a broad role of synapsin I in the structural development of the synapse, participating directly or indirectly in the maturation of both presynaptic and postsynaptic sites.
在之前的一项研究中,我们报道了来自突触素I缺陷小鼠的培养海马神经元在轴突生长和突触形成方面存在延迟。在此,我们研究了这种突触发生延迟是归因于突触前还是突触后元件。本研究中使用的实验范式包括建立野生型和突触素I缺陷神经元的异时共培养,分别在24小时和72小时后,野生型神经元与成熟的野生型突触后元件建立突触。相比之下,突触素I缺陷的突触后元件只有在培养9天后才能接受突触,与对照组相比延迟了5天。结果表明突触素I在突触的结构发育中具有广泛作用,直接或间接参与突触前和突触后位点的成熟。