Burrell Brian D, Sahley Christie L
Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, Room 230, Lee Medical Building, 414 Clark Street, Vermillion, SD 570969.
J Neurosci. 2004 Apr 21;24(16):4011-9. doi: 10.1523/JNEUROSCI.0178-04.2004.
Long-term potentiation (LTP) of synaptic transmission was observed in two types of synapses that converge on the same postsynaptic neuron in the leech CNS. These synapses were made by identifiable sensory neurons, the mechanosensory touch (T-) and pressure (P-) cells, onto the S-cell, an interneuron critical for certain forms of learning. Changes in both the T-S and P-S synapses appear to be activity dependent because LTP was restricted to inputs that had undergone tetanization; however, properties of synaptic plasticity at the T-S and P-S connections differ considerably. At the P-S synapse, LTP was induced in the tetanized synapse but not in the nontetanized synapse tested in parallel. P-S LTP was blocked by the NMDA receptor antagonist dl-2-amino-5-phosphono-valeric acid (AP-5) or by lowering the extracellular concentration of glycine, an NMDA receptor (NMDAR) co-agonist. P-S LTP was strongly affected by the initial amplitude of the synaptic potential at the time LTP was induced. Smaller amplitude synapses (<3.5 mV) underwent robust potentiation, whereas the less common, larger amplitude synapse (>3.5 mV) depressed after tetanization. At the T-S synapse, tetanization simultaneously induced homosynaptic LTP in the tetanized input and heterosynaptic long-term depression (LTD) in the input made by a nontetanized T-cell onto the same S-cell. Interestingly, AP-5 failed to block homosynaptic LTP at the T-S synapse but did prevent heterosynaptic LTD. T-S LTP was not affected by the initial EPSP amplitude. Thus, leech neurons exhibit synaptic plasticity with properties similar to LTP and LTD found in the vertebrate nervous system.
在水蛭中枢神经系统中,在汇聚于同一突触后神经元的两种突触中观察到了突触传递的长时程增强(LTP)。这些突触由可识别的感觉神经元,即机械感觉触觉(T-)细胞和压力(P-)细胞,与S细胞形成,S细胞是一种对某些学习形式至关重要的中间神经元。T-S和P-S突触的变化似乎都依赖于活动,因为LTP仅限于经过强直刺激的输入;然而,T-S和P-S连接处的突触可塑性特性有很大差异。在P-S突触处,LTP在强直刺激的突触中被诱导,但在平行测试的未强直刺激的突触中未被诱导。P-S LTP被NMDA受体拮抗剂dl-2-氨基-5-磷酸戊酸(AP-5)或通过降低细胞外甘氨酸浓度(一种NMDA受体(NMDAR)共激动剂)所阻断。P-S LTP在诱导LTP时受到突触电位初始幅度的强烈影响。较小幅度的突触(<3.5 mV)经历了强烈的增强,而较不常见的较大幅度突触(>3.5 mV)在强直刺激后则出现抑制。在T-S突触处,强直刺激同时在强直刺激的输入中诱导同突触LTP,并在未强直刺激的T细胞与同一S细胞形成的输入中诱导异突触长时程抑制(LTD)。有趣的是,AP-5未能阻断T-S突触处的同突触LTP,但确实阻止了异突触LTD。T-S LTP不受初始EPSP幅度的影响。因此,水蛭神经元表现出与脊椎动物神经系统中发现的LTP和LTD类似特性的突触可塑性。