Schaffhausen J H, Fischer T M, Carew T J
Department of Psychology, Yale University, New Haven, Connecticut 06520, USA.
J Neurosci. 2001 Mar 1;21(5):1739-49. doi: 10.1523/JNEUROSCI.21-05-01739.2001.
Recent studies in Aplysia have revealed a novel postsynaptic Ca(2+) component to posttetanic potentiation (PTP) at the siphon sensory to motor neuron (SN-MN) synapse. Here we asked whether the postsynaptic Ca(2+) component of PTP was a special feature of the SN-MN synapse, and if so, whether it reflected a unique property of the SN or the MN. We examined whether postsynaptic injection of BAPTA reduced PTP at SN synapses onto different postsynaptic targets by comparing PTP at SN-MN and SN-interneuron (L29) synapses. We also examined PTP at L29-MN synapses. Postsynaptic BAPTA reduced PTP only at the SN-MN synapse; it did not affect PTP at either the SN-L29 or the L29-MN synapse, indicating that the SN and the MN do not require postsynaptic Ca(2+) for PTP with all other synaptic partners. The postsynaptic Ca(2+) component of PTP is present at other Aplysia SN-MN synapses; tail SN-MN synapses also showed reduced PTP when the MN was injected with BAPTA. Surprisingly, in both tail and siphon SN-MN synapses, there was an inverse relationship between the initial size of the EPSP and the postsynaptic component to PTP; only the initially weak SN-MN synapses showed a BAPTA-sensitive component. Homosynaptic depression of initially strong SN-MN synapses into the size range of initially weak synapses did not confer postsynaptic Ca(2+) sensitivity to PTP. Finally, the postsynaptic Ca(2+) component of PTP could be induced in the presence of APV, indicating that it is not mediated by NMDA receptors. These results suggest a dual model for PTP at the SN-MN synapse, in which a postsynaptic Ca(2+) contribution summates with the conventional presynaptic mechanisms to yield an enhanced form of PTP.
最近对海兔的研究揭示了在虹吸管感觉神经元到运动神经元（SN-MN）突触的强直后增强（PTP）中一种新的突触后Ca(2+)成分。在此，我们探讨PTP的突触后Ca(2+)成分是否是SN-MN突触的一个特殊特征，如果是，它是否反映了SN或MN的独特属性。我们通过比较SN-MN和SN-中间神经元（L29）突触处的PTP，研究了向不同突触后靶点的SN突触中突触后注射BAPTA是否会降低PTP。我们还研究了L29-MN突触处的PTP。突触后注射BAPTA仅在SN-MN突触处降低PTP；它对SN-L29或L29-MN突触处的PTP均无影响，这表明SN和MN与所有其他突触伙伴形成PTP时不需要突触后Ca(2+)。PTP的突触后Ca(2+)成分存在于海兔的其他SN-MN突触中；当向MN注射BAPTA时，尾部SN-MN突触的PTP也降低。令人惊讶的是，在尾部和虹吸管SN-MN突触中，兴奋性突触后电位（EPSP）的初始大小与PTP的突触后成分之间存在反比关系；只有最初较弱的SN-MN突触表现出对BAPTA敏感的成分。最初较强的SN-MN突触向最初较弱突触的大小范围的同突触抑制并未赋予PTP对突触后Ca(2+)的敏感性。最后，在存在APV的情况下可以诱导出PTP的突触后Ca(2+)成分，这表明它不是由N-甲基-D-天冬氨酸（NMDA）受体介导的。这些结果提示了SN-MN突触处PTP的双重模型，其中突触后Ca(2+)的作用与传统的突触前机制相加，产生增强形式的PTP。
