Cherubini E, Neuman R, Rovira C, Ben Ari Y
I.N.S.E.R.M. U.029, Hôpital de Port Royal, Paris, France.
Brain Res. 1988 Mar 29;445(1):91-100. doi: 10.1016/0006-8993(88)91077-3.
The epileptogenic properties of the mast cell degranulating peptide (MCD) have been investigated in the CA3 region of the hippocampal slice preparation. Brief (3-5 min) bath application of MCD (0.5-2 microM) to CA3 hippocampal neurones produced an enhancement of the spontaneous synaptic activity and the appearance of spontaneous bursts that persisted for several hours. These bursts were network driven and the underlying paroxysmal depolarizing shift met the criteria for a giant excitatory postsynaptic potential (EPSP), with a reversal potential close to 0 mV. Furthermore following the application of MCD, stimulation of the mossy fibres, commissural or temporo-ammonic pathway evoked an EPSP followed by an evoked network burst. The bursts which could be elicited for several hours were reversibly blocked by a brief application of tetrodotoxin (TTX; 1 microM) or cobalt (2 mM). In contrast, prior and concomitant treatment with TTX or cobalt prevented the occurrence of the bursts induced by MCD. The effects of MCD were not due to a blockade of GABAergic inhibition since the toxin did not reduce the fast and slow IPSP. Furthermore, the N-methyl-D-aspartate (NMDA) antagonists D-2-amino-phosphonovalerate (D-APV; 30 microM) or DL-amino-phosphoheptanoic acid (AP-7, 30 microM) did not block the action of MCD, suggesting that the activation of NMDA receptors are neither necessary nor sufficient for MCD-induced bursts. It is concluded that MCD induces in the CA3 region long-lasting changes in the synaptic responses which may be mediated through a presynaptic mechanism.
已在海马脑片制备的CA3区研究了肥大细胞脱颗粒肽(MCD)的致痫特性。将MCD(0.5 - 2微摩尔)短暂(3 - 5分钟)浴用于CA3海马神经元,可增强自发突触活动,并出现持续数小时的自发爆发。这些爆发由网络驱动,潜在的阵发性去极化偏移符合巨大兴奋性突触后电位(EPSP)标准,反转电位接近0 mV。此外,应用MCD后,刺激苔藓纤维、连合或颞叶 - 海马通路可诱发一个EPSP,随后是诱发的网络爆发。可诱发数小时的爆发可被短暂应用河豚毒素(TTX;1微摩尔)或钴(2毫摩尔)可逆性阻断。相反,预先和同时用TTX或钴处理可防止MCD诱导的爆发发生。MCD的作用并非由于对GABA能抑制的阻断,因为该毒素并未降低快速和慢速抑制性突触后电位(IPSP)。此外,N - 甲基 - D - 天冬氨酸(NMDA)拮抗剂D - 2 - 氨基 - 磷酸戊酸(D - APV;30微摩尔)或DL - 氨基 - 磷酸庚酸(AP - 7, 30微摩尔)并未阻断MCD的作用,这表明NMDA受体的激活对于MCD诱导的爆发既非必要也不充分。结论是,MCD在CA3区诱导突触反应的长期变化,这可能通过突触前机制介导。