Burtscher Johannes, Schwarzer Christoph
Department of Pharmacology, Medical University of InnsbruckInnsbruck, Austria.
Front Mol Neurosci. 2017 Aug 7;10:245. doi: 10.3389/fnmol.2017.00245. eCollection 2017.
Temporal lobe epilepsy is considered to be one of the most common and severe forms of focal epilepsies. Patients often develop cognitive deficits and emotional blunting along the progression of the disease. The high incidence of resistance to antiepileptic drugs and a frequent lack of admissibility to surgery poses an unmet medical challenge. In the urgent quest of novel treatment strategies, neuropeptides are interesting candidates, however, their therapeutic potential has not yet been exploited. This review focuses on the functional role of the endogenous opioid system with respect to temporal lobe epilepsy, specifically in the hippocampus. The role of dynorphins and kappa opioid receptors (KOPr) as modulators of neuronal excitability is well understood: both the reduced release of glutamate as well of postsynaptic hyperpolarization were shown in glutamatergic neurons. In line with this, low levels of dynorphin in humans and mice increase the risk of epilepsy development. The role of enkephalins is not understood so well. On one hand, some agonists of the delta opioid receptors (DOPr) display pro-convulsant properties probably through inhibition of GABAergic interneurons. On the other hand, enkephalins play a neuro-protective role under hypoxic or anoxic conditions, most probably through positive effects on mitochondrial function. Despite the supposed absence of endorphins in the hippocampus, exogenous activation of the mu opioid receptors (MOPr) induces pro-convulsant effects. Recently-expanded knowledge of the complex ways opioid receptors ligands elicit their effects (including biased agonism, mixed binding, and opioid receptor heteromers), opens up exciting new therapeutic potentials with regards to seizures and epilepsy. Potential adverse side effects of KOPr agonists may be minimized through functional selectivity. Preclinical data suggest a high potential of such compounds to control seizures, with a strong predictive validity toward human patients. The discovery of DOPr-agonists without proconvulsant potential stimulates the research on the therapeutic use of neuroprotective potential of the enkephalin/DOPr system.
颞叶癫痫被认为是局灶性癫痫最常见且最严重的形式之一。随着疾病进展,患者常出现认知缺陷和情感迟钝。对抗癫痫药物耐药的高发生率以及手术的频繁不可行构成了未满足的医学挑战。在急切寻求新治疗策略的过程中,神经肽是有吸引力的候选者,然而,它们的治疗潜力尚未得到开发。本综述聚焦内源性阿片系统在颞叶癫痫方面的功能作用,特别是在海马体中的作用。强啡肽和κ阿片受体(KOPr)作为神经元兴奋性调节剂的作用已得到充分理解:在谷氨酸能神经元中,已显示出谷氨酸释放减少以及突触后超极化。与此一致,人类和小鼠体内低水平的强啡肽会增加癫痫发生的风险。脑啡肽的作用尚未得到很好的理解。一方面,一些δ阿片受体(DOPr)激动剂可能通过抑制GABA能中间神经元而表现出促惊厥特性。另一方面,脑啡肽在缺氧或无氧条件下起神经保护作用,很可能是通过对线粒体功能产生积极影响。尽管推测海马体中不存在内啡肽,但μ阿片受体(MOPr)的外源性激活会诱导促惊厥作用。最近关于阿片受体配体引发其效应的复杂方式(包括偏向激动、混合结合和阿片受体异聚体)的知识扩展,为癫痫发作和癫痫带来了令人兴奋的新治疗潜力。通过功能选择性可将KOPr激动剂的潜在不良副作用降至最低。临床前数据表明此类化合物具有控制癫痫发作的高潜力,对人类患者具有很强的预测效度。无促惊厥潜力的DOPr激动剂的发现刺激了对脑啡肽/DOPr系统神经保护潜力治疗用途的研究。