Long-Term Temporal Imprecision of Information Coding in the Anterior Cingulate Cortex of Mice with Peripheral Inflammation or Nerve Injury
Long-Term Temporal Imprecision of Information Coding in the Anterior Cingulate Cortex of Mice with Peripheral Inflammation or Nerve Injury
复制标题
DOI：
10.1523/jneurosci.5166-13.2014
复制
发表时间：
2014-08-06
影响因子：
5.3
通讯作者：
Zhuo, Min
中科院分区：
文献类型：
--
作者：
Li, Xiang-Yao;Wang, Ning;Zhuo, Min
中枢神经系统（CNS）锋电位发放的时间特性对于神经元编码和信息存储的精确性至关重要。据报道，慢性疼痛除了触发感觉突触和行为敏化的长期可塑性之外，还影响认知和情感功能。目前对慢性疼痛条件下皮层神经元时间精度的可能变化知之甚少。在本研究中，我们研究了在前扣带皮层（ACC）的动作电位放电的时间精度通过使用在体内和体外电生理方法。我们发现，由完全弗氏佐剂（CFA）引起的外周炎症增加了体内成年大鼠ACC中51%的记录神经元的尖峰潜伏期（也称为抖动）的标准差（SD）。使用来自外周炎症或神经损伤的成年小鼠的体外脑切片，在ACC神经元中发现了类似的抖动增加。应用谷氨酸受体拮抗剂CNQX和AP 5可消除CFA注射或神经损伤引起的抖动增强，提示抖动增强依赖于谷氨酸能突触传递。腺苷酸环化酶（AC）的激活浴应用毛喉素增加抖动，而AC1的基因缺失废除CFA炎症引起的抖动的变化。我们的研究为周围神经损伤后皮层神经元信息编码时间精度的长期变化提供了有力的证据，并解释了慢性疼痛导致认知和情绪障碍的神经机制。
Temporal properties of spike firing in the central nervous system (CNS) are critical for neuronal coding and the precision of information storage. Chronic pain has been reported to affect cognitive and emotional functions, in addition to trigger long-term plasticity in sensory synapses and behavioral sensitization. Less is known about the possible changes in temporal precision of cortical neurons in chronic pain conditions. In the present study, we investigated the temporal precision of action potential firing in the anterior cingulate cortex (ACC) by using both in vivo and in vitro electrophysiological approaches. We found that peripheral inflammation caused by complete Freund's adjuvant (CFA) increased the standard deviation (SD) of spikes latency (also called jitter) of similar to 51% of recorded neurons in the ACC of adult rats in vivo. Similar increases in jitter were found in ACC neurons using in vitro brain slices from adult mice with peripheral inflammation or nerve injury. Bath application of glutamate receptor antagonists CNQX and AP5 abolished the enhancement of jitter induced by CFA injection or nerve injury, suggesting that the increased jitter depends on the glutamatergic synaptic transmission. Activation of adenylyl cyclases (ACs) by bath application of forskolin increased jitter, whereas genetic deletion of AC1 abolished the change of jitter caused by CFA inflammation. Our study provides strong evidence for long-term changes of temporal precision of information coding in cortical neurons after peripheral injuries and explains neuronal mechanism for chronic pain caused cognitive and emotional impairment.