Giocomo Lisa M, Hasselmo Michael E
Program in Neuroscience, Center for Memory and Brain, Boston University, Boston, MA 02214, USA.
Hippocampus. 2006;16(11):1004-16. doi: 10.1002/hipo.20231.
We investigated the time course of modulation of synaptic transmission by group II and group III metabotropic glutamate receptors in region CA1 of the hippocampus. In the presence of 50 microM picrotoxin, pressure pulse application of 1 mM glutamate resulted in a fast onset of suppression of synaptic transmission in stratum lacunosum moleculare and a slower onset of suppression in stratum radiatum, with both effects returning to baseline over the course of several minutes. Application of 50 microM of the group II agonist (2R,4R)-APDC in stratum lacunosum moleculare resulted in the same fast onset of suppression while having no effect in stratum radiatum. Pressure pulse application of 100 microM DL-AP4 in stratum lacunosum moleculare and stratum radiatum resulted in a much slower onset of suppression of synaptic transmission than (2R,4R)-APDC. Suppression by (2R,4R)-APDC was accompanied by a rapid enhancement of paired pulse facilitation, indicative of a presynaptic mechanism. This demonstrates that activation of group II mGluRs in the hippocampus causes a fast onset of suppression in stratum lacunosum moleculare, while activation of group III mGluRs causes a slower onset of suppression. The difference in time course for group II vs. group III mGluRs suggests a different functional role, with group II playing a potential role in making synapses act as low pass filters.
我们研究了海马体CA1区中II组和III组代谢型谷氨酸受体对突触传递调节的时间进程。在存在50微摩尔苦味毒的情况下,压力脉冲施加1毫摩尔谷氨酸会导致分子层中突触传递的抑制快速开始,而辐射层中的抑制开始较慢,两种效应在几分钟内都恢复到基线。在分子层中施加50微摩尔的II组激动剂(2R,4R)-APDC会导致相同的快速抑制开始,而在辐射层中没有影响。在分子层和辐射层中压力脉冲施加100微摩尔DL-AP4导致突触传递抑制的开始比(2R,4R)-APDC慢得多。(2R,4R)-APDC引起的抑制伴随着双脉冲易化的快速增强,表明是一种突触前机制。这表明海马体中II组代谢型谷氨酸受体的激活会导致分子层中快速开始抑制,而III组代谢型谷氨酸受体的激活会导致较慢的抑制开始。II组和III组代谢型谷氨酸受体在时间进程上的差异表明了不同的功能作用,II组在使突触充当低通滤波器方面可能发挥作用。