Department of Oral Physiology, School of Dentistry and BK21, Kyungpook National University, 2177 Dalgubeol Blvd, Jung-gu, Daegu 41940, Republic of Korea.
Department of Oral Physiology, School of Dentistry and BK21, Kyungpook National University, 2177 Dalgubeol Blvd, Jung-gu, Daegu 41940, Republic of Korea.
Life Sci. 2016 Jan 1;144:54-60. doi: 10.1016/j.lfs.2015.11.024. Epub 2015 Nov 24.
Patterns of synaptic activity determine synaptic strengthening or weakening that is typically represented as long-term potentiation (LTP) and long-term depression (LTD), respectively. In the present study, we aim to test whether a conditioning stimulation of the spinal trigeminal subnucleus caudalis (Vc) induces LTP at excitatory synapses in the subnucleus interpolaris (Vi) and to characterize the LTP.
Generally, a presynaptic high-frequency stimulation (HFS) protocol can induce LTP at excitatory synapses in the brain, including the spinal cord. Therefore, LTP in the Vi was induced by the HFS (3 tetani at 100 Hz) of Vc in the horizontal brainstem slices. By pretreating slices with antagonists for NMDA receptors, metabotropic glutamate receptor subtype 1 or 5 (mGluR1 or 5), GABAA receptors, glycine receptors and Ca(2+) chelator, the LTP was characterized.
The HFS reliably but slowly induced LTP of excitatory synaptic transmission in the Vi. This LTP was not dependent on NMDA receptor activation; however, it did require the activation of mGluR1, but not mGluR5, and an intracellular Ca(2+) rise. Interestingly, this LTP induction required inhibitory synaptic transmission mediated by GABAA and glycine receptors, and coincided with the slow development of LTD at GABAergic synapses. The GABAergic LTD was mediated by mGluR1 and the intracellular Ca(2+) rise.
These data suggest that the modulation of GABAergic synaptic transmission by conditioning synaptic activity contributes to the induction and expression of LTP at excitatory synapses in the Vi.
突触活动模式决定了突触的强化或削弱，分别表现为长时程增强（LTP）和长时程抑制（LTD）。在本研究中，我们旨在测试刺激三叉神经脊束核尾侧亚核（Vc）是否能在中间亚核（Vi）的兴奋性突触上诱导 LTP，并对其特征进行描述。
一般来说，在大脑中，包括脊髓在内，高频率刺激（HFS）方案可以诱导兴奋性突触的 LTP。因此，在水平脑切片中通过 HFS（100Hz 下的 3 个串）刺激 Vc 来诱导 Vi 中的 LTP。通过用 NMDA 受体、代谢型谷氨酸受体亚型 1 或 5（mGluR1 或 5）、GABAA 受体、甘氨酸受体和 Ca2+螯合剂预处理切片，对 LTP 进行了特征描述。
HFS 可靠但缓慢地诱导了 Vi 中兴奋性突触传递的 LTP。这种 LTP 不依赖于 NMDA 受体的激活；然而，它确实需要 mGluR1 的激活，但不需要 mGluR5 的激活，并且需要细胞内 Ca2+的上升。有趣的是，这种 LTP 的诱导需要由 GABAA 和甘氨酸受体介导的抑制性突触传递，并且与 GABA 能突触的 LTD 缓慢发展相吻合。GABA 能 LTD 由 mGluR1 和细胞内 Ca2+的上升介导。
这些数据表明，通过条件性突触活动对 GABA 能突触传递的调制有助于诱导和表达 Vi 中兴奋性突触的 LTP。
