Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury.
Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury.
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DOI：
10.3389/fncir.2014.00100
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发表时间：
2014
影响因子：
3.5
通讯作者：
Garraway SM
中科院分区：
文献类型：
--
作者：
Grau JW;Huie JR;Lee KH;Hoy KC;Huang YJ;Turtle JD;Strain MM;Baumbauer KM;Miranda RM;Hook MA;Ferguson AR;Garraway SM
研究表明，脊髓回路有能力适应训练、伤害性刺激和外周炎症。神经功能的这些变化由生理和神经化学系统介导，这些系统类似于支持海马内可塑性的系统（例如，长时程增强和NMDA受体）。正如在海马体中观察到的那样，参与脊髓回路可以对可塑性潜力产生持久的影响，从而启用或抑制学习能力。这些效应与亚塑性的概念有关。行为范例被描述为诱导脊髓内的化生作用。不可控/不可预测的刺激和外周炎症诱导了一种抑制脊髓学习的适应不良可塑性。相反，暴露于可控或可预测的刺激会产生一种适应性可塑性，这种可塑性可以对抗这些适应不良的影响，并使学习成为可能。适应性可塑性与脑源性神经营养因子（BDNF）的上调有关。适应不良的可塑性与κ阿片样物质、代谢型谷氨酸（mGlu）受体、神经胶质和细胞因子肿瘤坏死因子（TNF）有关。不可控的伤害性刺激也会损害脊髓挫伤后的恢复，并促进疼痛（异常性疼痛）的发展。这些副作用与TNF的上调和BDNF及其受体（TrkB）的下调有关。在没有损伤的情况下，脑系统通过下行的多巴胺能纤维和5-羟色胺1A（5-HT 1A）受体抑制脊髓回路的敏化。这种保护作用被手术麻醉所阻断。与大脑断开连接，细胞内Cl-浓度增加（由于协同转运蛋白KCC 2的下调），这导致GABA具有兴奋作用。这表明BDNF具有恢复作用，因为它上调KCC 2并重新建立GABA介导的抑制。
Research has shown that spinal circuits have the capacity to adapt in response to training, nociceptive stimulation and peripheral inflammation. These changes in neural function are mediated by physiological and neurochemical systems analogous to those that support plasticity within the hippocampus (e.g., long-term potentiation and the NMDA receptor). As observed in the hippocampus, engaging spinal circuits can have a lasting impact on plastic potential, enabling or inhibiting the capacity to learn. These effects are related to the concept of metaplasticity. Behavioral paradigms are described that induce metaplastic effects within the spinal cord. Uncontrollable/unpredictable stimulation, and peripheral inflammation, induce a form of maladaptive plasticity that inhibits spinal learning. Conversely, exposure to controllable or predictable stimulation engages a form of adaptive plasticity that counters these maladaptive effects and enables learning. Adaptive plasticity is tied to an up-regulation of brain derived neurotrophic factor (BDNF). Maladaptive plasticity is linked to processes that involve kappa opioids, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (TNF). Uncontrollable nociceptive stimulation also impairs recovery after a spinal contusion injury and fosters the development of pain (allodynia). These adverse effects are related to an up-regulation of TNF and a down-regulation of BDNF and its receptor (TrkB). In the absence of injury, brain systems quell the sensitization of spinal circuits through descending serotonergic fibers and the serotonin 1A (5HT 1A) receptor. This protective effect is blocked by surgical anesthesia. Disconnected from the brain, intracellular Cl- concentrations increase (due to a down-regulation of the cotransporter KCC2), which causes GABA to have an excitatory effect. It is suggested that BDNF has a restorative effect because it up-regulates KCC2 and re-establishes GABA-mediated inhibition.
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影响因子：
4.2
作者：
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通讯作者：
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3.4
作者：
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