Neuropeptide Y and Epilepsy.
Neuropeptide Y and Epilepsy.
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DOI：
10.1046/j.1535-7597.2003.03208.x
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发表时间：
2003-03-01
影响因子：
3.6
通讯作者：
El Bahh, Bouchaib
中科院分区：
文献类型：
--
作者：
Colmers, William F.;El Bahh, Bouchaib
癫痫领域的一个核心原则是，癫痫发作是由兴奋超过抑制的不平衡引起的(1)。大部分兴奋是由神经递质谷氨酸介导的，而抑制主要是由γ -氨基丁酸（GABA）的作用引起的。在新皮层和海马体中，GABA的内在来源是中间神经元，最近受到了密切的关注。很明显，大量不同类型的中间神经元可以部分地通过它们共同表达的神经肽阵列来区分（cf.(2)）。越来越多的证据表明，中间神经元的神经肽补体在中间神经元调节兴奋性的方式中起着重要作用。在这里，我们讨论了一种已知的神经肽，神经肽Y (NPY)，在实验动物和人类中与癫痫的关系，并提出了受体作为控制癫痫过度兴奋的目标的可能作用。
It is a central tenet of the epilepsy field that seizures result from the imbalance of excitation over inhibition (1). The bulk of excitation is mediated by the neurotransmitter glutamate, whereas inhibition results mainly from the actions of gamma-aminobutyric acid (GABA). In the neocortex and hippocampus, the intrinsic sources of GABA are the interneurons, which lately have come under intense scrutiny. It has become clear that a large number of distinct types of interneurons can be differentiated in part by the array of neuropeptides they coexpress (cf. (2)). Evidence is emerging that the neuropeptide complement of interneurons plays important roles in the way that interneurons regulate excitability. Here we discuss what is known about the relation of one well-characterized neuropeptide, neuropeptide Y (NPY), and epilepsy in experimental animals and humans, and suggest possible roles for the receptors as targets for the control of excessive excitation in epilepsy.