Short-term synaptic plasticity in the nociceptive thalamic-anterior cingulate pathway.
Short-term synaptic plasticity in the nociceptive thalamic-anterior cingulate pathway.
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DOI：
10.1186/1744-8069-5-51
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发表时间：
2009-09-04
期刊：
影响因子：
3.3
通讯作者：
Vogt BA
中科院分区：
文献类型：
--
作者：
Shyu BC;Vogt BA
尽管在脊髓中，包括中枢致敏在内的伤害性诱发反应的短期和长期增强机制是众所周知的，但关于大脑皮层中此类事件的信息越来越多。鉴于前扣带皮层（ACC）在慢性疼痛疾病中的重要性，本综述认为丘脑扣带通路中的神经元可塑性可能是与此类综合征相关的最早变化。在体内，对坐骨神经进行单一的痛觉性电刺激会在ACC的II/III层产生明显的下沉电流，而高频刺激会增强该电流的反应。电刺激丘脑中线核、中背核和层内核（MITN）的成对脉冲促进提示MITN向ACC的投射介导了伤害性短期可塑性。我们在体外比较了丘脑内侧和对侧胼胝体传入神经的不同输入神经的短期突触可塑性。刺激中背侧传入诱发了更强的短期突触可塑性，并有效地将丘脑的爆发活动转移到扣带皮层，这在对侧刺激中是不存在的。这种突触传递的短期增强是由多突触通路和NMDA受体介导的。ACC的II/III层神经元表达一种短期可塑性，涉及谷氨酸和突触前钙内流，是短期可塑性的重要机制。丘脑破裂引起的ACC神经元活动增强表明，短期突触可塑性使处理来自内侧丘脑的伤害性信息成为可能，这种时间反应变异性在疼痛中尤为重要，因为反应的时间维持支持皮层整合和与有害事件相关的记忆形成。此外，扣带突触的这些修饰似乎调节传入信号，这些信号可能对与持续外周有害刺激相关的急性到慢性疼痛状况的转变很重要。因此，扣带皮层中伤害性活动的增强和维持可能是不利的，了解如何调节丘脑放电模式的变化将是重要的，这些模式在慢性疼痛的早期阶段向ACC传递伤害性信息。
Although the mechanisms of short- and long-term potentiation of nociceptive-evoked responses are well known in the spinal cord, including central sensitization, there has been a growing body of information on such events in the cerebral cortex. In view of the importance of anterior cingulate cortex (ACC) in chronic pain conditions, this review considers neuronal plasticities in the thalamocingulate pathway that may be the earliest changes associated with such syndromes. A single nociceptive electrical stimulus to the sciatic nerve induced a prominent sink current in the layer II/III of the ACC in vivo, while high frequency stimulation potentiated the response of this current. Paired-pulse facilitation by electrical stimulation of midline, mediodorsal and intralaminar thalamic nuclei (MITN) suggesting that the MITN projection to ACC mediates the nociceptive short-term plasticity. The short-term synaptic plasticities were evaluated for different inputs in vitro where the medial thalamic and contralateral corpus callosum afferents were compared. Stimulation of the mediodorsal afferent evoked a stronger short-term synaptic plasticity and effectively transferred the bursting thalamic activity to cingulate cortex that was not true for contralateral stimulation. This short-term enhancement of synaptic transmission was mediated by polysynaptic pathways and NMDA receptors. Layer II/III neurons of the ACC express a short-term plasticity that involves glutamate and presynaptic calcium influx and is an important mechanism of the short-term plasticity. The potentiation of ACC neuronal activity induced by thalamic bursting suggest that short-term synaptic plasticities enable the processing of nociceptive information from the medial thalamus and this temporal response variability is particularly important in pain because temporal maintenance of the response supports cortical integration and memory formation related to noxious events. Moreover, these modifications of cingulate synapses appear to regulate afferent signals that may be important to the transition from acute to chronic pain conditions associated with persistent peripheral noxious stimulation. Enhanced and maintained nociceptive activities in cingulate cortex, therefore, can become adverse and it will be important to learn how to regulate such changes in thalamic firing patterns that transmit nociceptive information to ACC in early stages of chronic pain.
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