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首页> 外文期刊>Epilepsia: Journal of the International League against Epilepsy >Neural activity in the periaqueductal gray and other specific subcortical structures is enhanced when a selective serotonin reuptake inhibitor selectively prevents seizure-induced sudden death in the DBA/1 mouse model of sudden unexpected death in epilepsy
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Neural activity in the periaqueductal gray and other specific subcortical structures is enhanced when a selective serotonin reuptake inhibitor selectively prevents seizure-induced sudden death in the DBA/1 mouse model of sudden unexpected death in epilepsy

机译：Neural activity in the periaqueductal gray and other specific subcortical structures is enhanced when a selective serotonin reuptake inhibitor selectively prevents seizure-induced sudden death in the DBA/1 mouse model of sudden unexpected death in epilepsy

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Objective Sudden unexpected death in epilepsy (SUDEP) is a critical issue in epilepsy, and DBA/1 mice are a useful animal model of this devastating epilepsy sequela. The serotonin hypothesis for SUDEP proposes that modifying serotonergic function significantly alters susceptibility to seizure-induced respiratory arrest (S-IRA). Agents that enhance serotonergic function, including a selective serotonin reuptake inhibitor, fluoxetine, selectively prevent S-IRA in DBA/1 mice. This study examined fluoxetine-induced changes in brain activity using manganese-enhanced magnetic resonance imaging (MEMRI) to reveal sites in the DBA/1 mouse brain where fluoxetine acts to prevent S-IRA. Methods DBA/1 mice were subjected to audiogenic seizures (Sz) after saline or fluoxetine (45 mg/kg, intraperitoneal) administration. Control DBA/1 mice received fluoxetine or saline, but Sz were not evoked. A previous MEMRI study established the regions of interest (ROIs) for Sz in the DBA/1 mouse brain, and the present study examined MEMRI differences in the ROIs of these mouse groups. Results The neural activity in several ROIs was significantly increased in fluoxetine-treated DBA/1 mice that exhibited Sz but not S-IRA when compared to the saline-treated mice that exhibited both Sz and respiratory arrest. These structures included the periaqueductal gray (PAG), amygdala, reticular formation (sensorimotor-limbic network), Kolliker-Fuse nucleus, facial-parafacial group (respiratory network), and pontine raphe. Of these ROIs, only the PAG showed significantly decreased neural activity with saline pretreatment when seizure-induced respiratory arrest occurred as compared to saline treatment without seizure. Significance The PAG is known to play an important compensatory role for respiratory distress caused by numerous exigent situations in normal animals. The pattern of fluoxetine-induced activity changes in the present study suggests that PAG may be the most critical target for fluoxetine's action to prevent seizure-induced sudden death. These findings have potential clinical importance, because there is evidence of anomalous serotonergic function and PAG imaging abnormalities in human SUDEP.
机译：目标突然意外的癫痫（sudep）死亡是癫痫中的一个关键问题，DBA / 1小鼠是这种毁灭性癫痫遗产的有用动物模型。 sudep的血清素假设提出改性血清奈奈能功能显着改变易癫痫发育呼吸逮捕（S-IRA）的易感性。增强Serotonergic功能的药剂，包括选择性血清素再摄取抑制剂，氟西汀，选择性地预防DBA / 1小鼠中的S-IRA。该研究检测了使用锰增强的磁共振成像（MEMIRI）在DBA / 1小鼠脑中揭示氟西汀的脑脑中脑活动的变化，以防止S-IRA。方法将DBA / 1小鼠进行盐水或氟西汀（45mg / kg，腹膜内）给药后的发电癫痫发作（SZ）。对照DBA / 1小鼠接受氟西汀或盐水，但没有诱发SZ。先前的MEMRI研究在DBA / 1小鼠脑中建立了SZ的感兴趣区域（ROI），目前的研究检查了这些小鼠组的ROI中的MEMRI差异。结果在氟西汀处理的DBA / 1小鼠中，在氟西汀治疗的DBA / 1小鼠中显着增加了几个ROI中的神经活性，但与表现出SZ和呼吸骤停的盐水处理的小鼠相比，表现出SZ但不是S-IRA。这些结构包括Periaqueyuctal灰色（PAG），Amygdala，网状形成（SensorImotor-incebic网络），Kolliker-Fuse核，面部剖宫产组（呼吸网络）和粪便Raphe。在这些ROI中，只有PAG表明，当与没有癫痫发作的盐水处理相比发生癫痫发作呼吸急性时，盐水预处理显着降低了神经活性。众所周知，PAG的意义在普通动物中许多实际情况造成的呼吸窘迫起到重要的补偿性作用。本研究中氟西汀诱导的活性变化的模式表明，PAG可能是氟西汀的作用最关键的目标，以防止癫痫发作诱导的猝死。这些发现具有潜在的临床重要性，因为存在有证据表明人sudep中的异常血清onerogic函数和PAG成像异常。

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