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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Aquaporin-4 water channels and synaptic plasticity in the hippocampus
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Aquaporin-4 water channels and synaptic plasticity in the hippocampus

机译：海马Aquaporin-4水通道和突触可塑性

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摘要

Aquaporin-4 (AQP4) is the major water channel expressed in the central nervous system (CNS) and is primarily expressed in glial cells. Many studies have shown that AQP4 regulates the response of the CNS to insults or injury, but far less is known about the potential for AQP4 to influence synaptic plasticity or behavior. Recent studies have examined long-term potentiation (LTP), long-term depression (LTD), and behavior in AQP4 knockout (KO) and wild-type mice to gain more insight into its potential role. The results showed a selective effect of AQP4 deletion on LTP of the Schaffer collateral pathway in hippocampus using an LTP induction protocol that simulates pyramidal cell firing during theta oscillations (theta-burst stimulation; TBS). However, LTP produced by a different induction protocol was unaffected. There was also a defect in LTD after low frequency stimulation (LFS) in AQP4 KO mice. Interestingly, some slices from AQP4 KO mice exhibited LTD after TBS instead of LTP, or LTP following LFS instead of LTD. These data suggest that AQP4 and astrocytes influence the polarity of long-term synaptic plasticity (potentiation or depression). These potentially powerful roles expand the influence of AQP4 and astrocytes beyond the original suggestions related to regulation of extracellular potassium and water balance. Remarkably, AQP4 KO mice did not show deficits in basal transmission, suggesting specificity for long-term synaptic plasticity. The mechanism appears to be related to neurotrophins and specifically brain-derived neurotrophic factor (BDNF) because pharmacological blockade of neurotrophin trk receptors or scavenging ligands such as BDNF restored plasticity. The in vitro studies predicted effects in vivo of AQP4 deletion because AQP4 KO mice performed worse using a task that requires memory for the location of objects (object placement). However, performance on other hippocampal-dependent tasks was spared. The results suggest an unanticipated and selective role of AQP4 in synaptic plasticity and spatial memory, and underscore the growing appreciation of the role of glial cells in functions typically attributed to neurons. Implications for epilepsy are discussed because of the previous evidence that AQP4 influences seizures, and the role of synaptic plasticity in epileptogenesis.
机译：Aquaporin-4（AQP4）是在中枢神经系统（CNS）中表达的主要水通道，主要在神经胶质细胞中表达。许多研究表明，AQP4调节中枢神经系统对损伤或损伤的反应，但对AQP4影响突触可塑性或行为的潜力知之甚少。最近的研究检查了长期增强（LTP），长期抑郁（LTD）以及AQP4基因敲除（KO）和野生型小鼠的行为，以进一步了解其潜在作用。结果显示，使用LTP诱导方案模拟ATA振荡（θ-爆发刺激; TBS）期间锥体细胞射击，AQP4缺失对海马Schaffer侧支途径LTP的选择性作用。但是，由另一种诱导方案产生的LTP不受影响。低频刺激（LFS）在AQP4 KO小鼠中的LTD中也存在缺陷。有趣的是，一些来自AQP4 KO小鼠的切片在TBS代替LTP后显示LTD，或者在LFS代替LTD后显示LTP。这些数据表明，AQP4和星形胶质细胞会影响长期突触可塑性（增强或抑制）的极性。这些潜在的强大作用扩大了AQP4和星形胶质细胞的影响，超出了有关调节细胞外钾和水平衡的最初建议。值得注意的是，AQP4 KO小鼠在基础传递方面未显示出缺陷，这表明其对长期突触可塑性具有特异性。该机制似乎与神经营养蛋白有关，特别是与脑源性神经营养因子（BDNF）有关，因为对神经营养蛋白trk受体或清除配体（如BDNF）的药理作用可以恢复可塑性。体外研究预测了AQP4缺失在体内的影响，因为AQP4 KO小鼠在使用需要记忆物体位置（物体放置）的任务时表现较差。但是，在其他海马依赖性任务上的表现却没有被保留。结果表明，AQP4在突触可塑性和空间记忆中具有出乎意料的选择性作用，并强调了对神经胶质细胞在通常归因于神经元的功能中的作用的日益重视。由于先前的证据表明AQP4影响癫痫发作以及突触可塑性在癫痫发生中的作用，因此对癫痫的影响进行了讨论。

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