Hatada Y, Wu F, Sun Z Y, Schacher S, Goldberg D J
Department of Pharmacology and Center for Neurobiology and Behavior, Columbia University and New York State Psychiatric Institute, New York, New York 10032, USA.
J Neurosci. 2000 Jul 1;20(13):RC82. doi: 10.1523/JNEUROSCI.20-13-j0001.2000.
Morphological changes are thought to contribute to the expression of long-term synaptic plasticity, a cellular basis for learning and memory. The mechanisms mediating the initiation and maintenance of the morphological changes are poorly understood. We repeatedly imaged the axonal arbors of mechanosensory neurons of Aplysia as they formed new synaptic varicosities and axonal branches after applications of serotonin that cause long-term synaptic facilitation. New varicosities formed exclusively from preexisting varicosities, by splitting or branch outgrowth. These changes were prevented by cytochalasin D, which blocks actin polymerization and the turnover of actin filaments. The suppression of the morphological changes by cytochalasin D did not impair their expression when cytochalasin D was removed 24 hr after exposure to serotonin. These results imply that serotonin induces persistent effects at preexisting presynaptic varicosities, which enhance actin polymerization, and that this is essential for presynaptic morphological changes of long-term facilitation.
形态学变化被认为有助于长期突触可塑性的表达，而长期突触可塑性是学习和记忆的细胞基础。介导形态学变化起始和维持的机制目前还知之甚少。我们反复成像了海兔机械感觉神经元的轴突分支，这些神经元在应用5-羟色胺后形成了新的突触膨体和轴突分支，5-羟色胺会引起长期突触易化。新的膨体仅由预先存在的膨体通过分裂或分支生长形成。细胞松弛素D可阻止这些变化，它能阻断肌动蛋白聚合以及肌动蛋白丝的周转。当在接触5-羟色胺24小时后去除细胞松弛素D时，其对形态学变化的抑制作用并未损害这些变化的表达。这些结果表明，5-羟色胺在预先存在的突触前膨体处诱导持续性效应，增强肌动蛋白聚合，而这对于长期易化的突触前形态学变化至关重要。
