Center for Brain Science, Harvard University, 52 Oxford St. NWL 202, Cambridge, MA 02138, USA.
Brain Res. 2012 Dec 3;1487:140-9. doi: 10.1016/j.brainres.2012.05.061. Epub 2012 Jul 5.
Changes in synaptic strength resulting from neuronal activity have been described in great detail for chemical synapses, but the relationship between natural forms of activity and the strength of electrical synapses had previously not been investigated. The thalamic reticular nucleus (TRN), a brain area rich in gap junctional (electrical) synapses, regulates cortical attention, initiates sleep spindles, and participates in shifts between states of arousal. Plasticity of electrical synapses in the TRN may be a key mechanism underlying these processes. Recently, we demonstrated a novel activity-dependent form of long-term depression of electrical synapses in the TRN (Haas et al., 2011). Here we provide an overview of those findings and discuss them in broader context. Because gap junctional proteins are widely expressed in the mammalian brain, modification of synaptic strength is likely to be a widespread and powerful mechanism at electrical synapses throughout the brain.
神经元活动导致的突触强度变化在化学突触中已有详细描述,但自然活动形式与电突触强度之间的关系此前尚未得到研究。丘脑网状核(TRN)是一个富含缝隙连接(电)突触的脑区,调节皮质注意力、引发睡眠纺锤波,并参与觉醒状态之间的转换。TRN 中电突触的可塑性可能是这些过程的关键机制。最近,我们在 TRN 中证明了一种新型的电突触活动依赖性长时程压抑(Haas 等人,2011)。本文提供了这些发现的概述,并在更广泛的背景下进行了讨论。由于缝隙连接蛋白在哺乳动物大脑中广泛表达,因此突触强度的改变很可能是大脑中电突触的一种广泛而强大的机制。