Hippocampal spreading depression bilaterally activates the caudal trigeminal nucleus in rodents
Hippocampal spreading depression bilaterally activates the caudal trigeminal nucleus in rodents
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DOI：
10.1002/hipo.10139
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发表时间：
2003-01-01
期刊：
影响因子：
3.5
通讯作者：
Kraig, RP
中科院分区：
文献类型：
--
作者：
Kunkler, PE;Kraig, RP
扩散性抑郁（SD）和偏头痛先兆涉及短暂改变（即，增加，然后减少）电生理活动，以毫米/分钟（mm/min）的独特速率传播，导致暗示它们（以及可能来自偏头痛的疼痛）通过相同大脑结构的变化而因果相关。新皮质被认为是与偏头痛先兆相关的解剖区域，并且是已知在啮齿动物中诱导SD的三叉神经尾侧核（TNC）激活的唯一区域。然而，在人类新皮层中的SD的经典证据仅在严重的脑部疾病中报道，而偏头痛是一种常见的且相对良性的疾病。由于SID发生在人的海马，而偏头痛患者的记忆功能障碍与海马有关，因此我们确定了局限于大鼠海马的反复SID是否能诱导TNC激活。我们的工作表明，与假手术对照组相比，复发性海马SD引起双侧TNC浅层c-fos免疫染色显著增加（P < 0.05-0.001）。此外，海马SD的发生与同侧新皮质的自发活动和血流的相关和短暂的变化，而没有SD扩散到该区域。因此，海马SD可能是一个以前未认识的，潜在的触发伤害性激活TNC可能与偏头痛。(C)2003 Wiley-Liss，Inc.
Spreading depression (SD) and migraine aura involve transiently altered (i.e., increased followed by decreased) electrophysiological activity that propagates at the distinctive rate of millimeters per minute (mm/min), leading to the suggestion that they (and perhaps pain from migraine) are causally related via changes in the same brain structure. Neocortex is considered the anatomical zone associated with migraine aura and is the sole area known to induce caudal trigeminal nucleus (TNC) activation from SD in rodents. However, classical evidence of SD in human neocortex is reported only with severe brain disease, while migraine is a common and comparatively benign disorder. Because SID occurs in human hippocampus, and memory dysfunction referable to hippocampus is seen in migraineurs, we determined whether recurrent SID confined to hippocampus in rat could induce TNC activation. Our work shows that recurrent hippocampal SD evoked a significant (P < 0.05-0.001) increase in bilateral c-fos immunostaining within TNC superficial laminae compared with sham controls. Furthermore, hippocampal SD occurred with a correlated and transient change in spontaneous activity and blood flow in the ipsilateral neocortex without spread of SD to that area. Thus, hippocampal SD may be a previously unrecognized, potential trigger for nociceptive activation of TNC perhaps associated with migraine. (C) 2003 Wiley-Liss, Inc.