Learning-facilitated long-term depression and long-term potentiation at mossy fiber-CA3 synapses requires activation of β-adrenergic receptors.
Learning-facilitated long-term depression and long-term potentiation at mossy fiber-CA3 synapses requires activation of β-adrenergic receptors.
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DOI：
10.3389/fnint.2012.00023
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发表时间：
2012
影响因子：
3.5
通讯作者：
Manahan-Vaughan D
中科院分区：
文献类型：
--
作者：
Hagena H;Manahan-Vaughan D
学习易化可塑性是指新的空间学习事件易化海马突触可塑性。长时程增强（LTP）和长时程抑制（LTD）都是由新的海马区依赖性学习促进的。这对我们理解海马体如何编码记忆有着重要的影响。一个很少在体内研究的结构，但被认为是至关重要的工作和长期记忆处理是海马CA 3区。虽然学习促进可塑性已被描述在这个结构中，这种现象背后的机制还没有被探索。去甲肾上腺素能系统在唤醒和确认新信息为显著信息中起着重要作用。它调节齿状回和CA 1的突触可塑性，但目前尚不清楚去甲肾上腺素能系统对CA 3区域突触可塑性的调节。我们探讨了行为大鼠苔藓纤维（mf）-CA 3突触的β-肾上腺素能受体是否参与学习易化可塑性。我们发现，受体拮抗作用对基础突触传递，短时程增强（STP），短时程抑制，LTP，或LTD没有影响，这些都是由模式化传入刺激电诱导的。然而，我们发现，学习易化的LTP和LTD都被β-肾上腺素能受体的拮抗作用所阻止，而激动剂异丙肾上腺素则促进STP进入LTP。因此，学习促进和电诱导的可塑性可能没有相同的先决条件。这些结果支持mf突触参与空间信息编码的一个独特方面，涉及LTP和LTD。此外，与新学习相关的唤醒变化与海马β-肾上腺素能受体的激活相关，而海马β-肾上腺素能受体反过来又包含CA 3区获取和处理此类信息的关键要素。
Learning-facilitated plasticity refers to hippocampal synaptic plasticity that is facilitated by novel spatial learning events. Both long-term potentiation (LTP) and long-term depression (LTD) are facilitated by novel hippocampus-dependent learning. This has important ramifications for our understanding of how the hippocampus encodes memory. One structure that is rarely studied in vivo, but is believed to be crucially important for working and long-term memory processing is the hippocampal CA3 region. Whereas learning-facilitated plasticity has been described in this structure, the mechanisms underlying this phenomenon have not been explored. The noradrenergic system plays an important role in arousal and qualification of new information as salient. It regulates synaptic plasticity in the dentate gyrus and CA1, but nothing is known about the regulation by the noradrenergic system of synaptic plasticity in the CA3 region. We explored whether β-adrenergic receptors contribute to learning-facilitated plasticity at mossy fiber (mf)-CA3 synapses of behaving rats. We found that receptor antagonism had no effect on basal synaptic transmission, short-term potentiation (STP), short-term depression, LTP, or LTD, that were electrically induced by patterned afferent stimulation. We found, however, that both learning-facilitated LTP and LTD were prevented by antagonism of β-adrenergic receptors, whereas the agonist isoproterenol facilitated STP into LTP. Thus, learning-facilitated and electrically-induced plasticity may not share the same prerequisites. These results support that the mf synapse engages in a distinct aspect of encoding of spatial information that involves both LTP and LTD. Furthermore, changes in arousal that are coupled to new learning are associated with activation of hippocampal β-adrenergic receptors that in turn comprise a key element in this type of information acquisition and processing by the CA3 region.