Levenson Jonathan M, Weeber Edwin J, Sweatt J David, Eskin Arnold
Baylor College of Medicine, Division of Neuroscience, Houston, TX 77030, USA.
Curr Mol Med. 2002 Nov;2(7):593-603. doi: 10.2174/1566524023362069.
A great deal of research has been directed toward understanding the cellular mechanisms underlying synaptic plasticity and memory formation. To this point, most research has focused on the more "active" components of synaptic transmission: presynaptic transmitter release and postsynaptic transmitter receptors. Little work has been done characterizing the role neurotransmitter transporters might play during changes in synaptic efficacy. We review several new experiments that demonstrate glutamate transporters are regulated during changes in the efficacy of glutamatergic synapses. This regulation occurred during long-term facilitation of the sensorimotor synapse of Aplysia and long-term potentiation of the Schaffer-collateral synapse of the rat. We propose that glutamate transporters are "co-regulated" with other molecules/processes involved in synaptic plasticity, and that this process is phylogenetically conserved. These new findings indicate that glutamate transporters most likely play a more active role in neurotransmission than previously believed.
大量研究致力于理解突触可塑性和记忆形成背后的细胞机制。至此，大多数研究聚焦于突触传递中更“活跃”的成分：突触前递质释放和突触后递质受体。关于神经递质转运体在突触效能变化过程中可能发挥的作用，相关研究甚少。我们回顾了几项新实验，这些实验表明谷氨酸转运体在谷氨酸能突触效能变化过程中受到调节。这种调节发生在海兔感觉运动突触的长期易化以及大鼠海马体Schaffer侧支突触的长期增强过程中。我们提出，谷氨酸转运体与参与突触可塑性的其他分子/过程“共同调节”，并且这一过程在系统发育上是保守的。这些新发现表明，谷氨酸转运体在神经传递中很可能发挥着比之前认为的更积极的作用。
