Department of Physiology and Center for Cognition, Learning and Memory, University of Bern, 3012 Bern, Switzerland.
J Neurosci. 2013 Oct 2;33(40):15675-85. doi: 10.1523/JNEUROSCI.0247-13.2013.
The thalamus integrates and transmits sensory information to the neocortex. The activity of thalamocortical relay (TC) cells is modulated by specific inhibitory circuits. Although this inhibition plays a crucial role in regulating thalamic activity, little is known about long-term changes in synaptic strength at these inhibitory synapses. Therefore, we studied long-term plasticity of inhibitory inputs to TC cells in the posterior medial nucleus of the thalamus by combining patch-clamp recordings with two-photon fluorescence microscopy in rat brain slices. We found that specific activity patterns in the postsynaptic TC cell induced inhibitory long-term potentiation (iLTP). This iLTP was non-Hebbian because it did not depend on the timing between presynaptic and postsynaptic activity, but it could be induced by postsynaptic burst activity alone. iLTP required postsynaptic dendritic Ca(2+) influx evoked by low-threshold Ca(2+) spikes. In contrast, tonic postsynaptic spiking from a depolarized membrane potential (-50 mV), which suppressed these low-threshold Ca(2+) spikes, induced no plasticity. The postsynaptic dendritic Ca(2+) increase triggered the synthesis of nitric oxide that retrogradely activated presynaptic guanylyl cyclase, resulting in the presynaptic expression of iLTP. The dependence of iLTP on the membrane potential and therefore on the postsynaptic discharge mode suggests that this form of iLTP might occur during sleep, when TC cells discharge in bursts. Therefore, iLTP might be involved in sleep state-dependent modulation of thalamic information processing and thalamic oscillations.
丘脑整合并将感觉信息传输到新皮层。丘脑皮质中继 (TC) 细胞的活动受特定抑制性回路调节。尽管这种抑制在调节丘脑活动中起着至关重要的作用，但关于这些抑制性突触处突触强度的长期变化知之甚少。因此，我们通过在大鼠脑片上结合膜片钳记录和双光子荧光显微镜，研究了后内侧丘脑核中 TC 细胞的抑制性输入的长期可塑性。我们发现，突触后 TC 细胞中的特定活动模式诱导了抑制性长期增强（iLTP）。这种 iLTP 是非赫布型的，因为它不依赖于突触前和突触后活动之间的时间，但它可以仅由突触后爆发活动诱导。iLTP 需要由低阈值 Ca2+ 峰引起的突触后树突 Ca2+ 内流来引发。相比之下，来自去极化膜电位（-50 mV）的持续突触后尖峰活动抑制了这些低阈值 Ca2+ 峰，不会诱导可塑性。突触后树突 Ca2+ 增加触发了一氧化氮的合成，一氧化氮逆行激活了突触前鸟苷酸环化酶，导致 iLTP 的表达。iLTP 对膜电位的依赖性，因此对突触后放电模式的依赖性表明，这种形式的 iLTP 可能发生在 TC 细胞爆发放电的睡眠期间。因此，iLTP 可能参与了睡眠状态依赖性的丘脑信息处理和丘脑振荡的调制。
