Relief of synaptic depression produces long-term enhancement in thalamocortical networks
Relief of synaptic depression produces long-term enhancement in thalamocortical networks
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DOI：
10.1152/jn.01145.2005
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发表时间：
2006-04-01
影响因子：
2.5
通讯作者：
Castro-Alamancos, MA
中科院分区：
文献类型：
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作者：
Hirata, A;Castro-Alamancos, MA
丘脑皮质突触可能经历活动依赖性的长期疗效变化，如长期增强。事实上，在体内进行的研究已经发现，丘脑的θ -burst刺激（TBS）会诱发成年啮齿动物新皮层的场电位反应的长期增强（LTE）。由于丘脑和新皮层形成了一个复杂的相互联系的网络，在体内高度活跃，因此丘脑兴奋性的变化可能会反映在新皮层中。为了验证这一可能性，我们从桶状新皮层进行了记录，并在体感丘脑被muscimol灭活的同时将TBS应用于丘脑辐射。当丘脑失活时，丘脑皮质的LTE缺失，表明丘脑兴奋性的变化与此有关。丘脑皮质细胞的单单元记录显示，TBS导致丘脑皮质细胞的自发放电率显著降低。减少丘脑皮质细胞的自发放电直接增强了丘脑皮质通路的功效，因为它减轻了丘脑皮质活动引起的丘脑皮质连接的强直性压抑。因为这些丘脑兴奋性的变化是由皮质丘脑活动触发的，这可能是一种有用的自上而下的机制，可以作为经验的功能来调节行为过程中传入新皮层的感觉输入。
Thalamocortical synapses may be able to undergo activity-dependent long-term changes in efficacy, such as long-term potentiation. Indeed, studies conducted in vivo have found that theta-burst stimulation (TBS) of the thalamus induces a long-term enhancement (LTE) of field potential responses evoked in the neocortex of adult rodents. Because the thalamus and neocortex form a complex interconnected network that is highly active in vivo, it is possible that a change in thalamic excitability would be reflected in the neocortex. To test this possibility, we recorded from barrel neocortex and applied TBS to the thalamic radiation while the somatosensory thalamus was inactivated with muscimol. Thalamocortical LTE was absent when the thalamus was inactivated, suggesting that changes in thalamic excitability are involved. Single-unit recordings from thalamocortical cells revealed that TBS causes a significant reduction in the spontaneous firing rate of thalamocortical cells. Reducing the spontaneous firing of thalamocortical cells directly enhances the efficacy of the thalamocortical pathway because it relieves the tonic depression of the thalamocortical connection caused by thalamocortical activity. Because these changes in thalamic excitability are triggered by corticothalamic activity, this may be a useful top-down mechanism to regulate afferent sensory input to the neocortex during behavior as a function of experience.