Tancredi V, Avoli M, Hwa G G
Department of Experimental Medicine (Physiology), Universita' di Roma Tor Vergata, Roma, Italy.
Neurosci Lett. 1988 Jul 8;89(3):293-8. doi: 10.1016/0304-3940(88)90542-3.
Spontaneous, synchronous epileptiform discharges were recorded in both CA3 and CA1 subfields of rat hippocampal slices perfused with Mg2+-free medium. Surgical separation of the two areas abolished the spontaneous discharges only in the CA1 subfield. However, epileptiform responses in the isolated CA1 subfield could still be evoked by orthodromic stimulation. Intracellularly these stimulus-induced responses were characterized by a depolarization associated with a burst of action potentials. Stimulation of the alveus still evoked a hyperpolarizing potential, presumably a recurrent inhibitory postsynaptic potential (IPSP) in CA1 pyramidal cells. Both spontaneous and stimulus-induced epileptiform discharges were blocked by the selective antagonist of N-methyl-D-aspartate (NMDA) receptors DL-2-amino-phosphonovalerate (APV). APV also reduced the amplitude and duration of the IPSP induced by alveus stimulation. Thus, epileptiform discharges evoked by lowering Mg2+ in the CA1 subfield are associated with a preservation of inhibitory mechanisms. Furthermore the effects exerted by APV upon the IPSP implicate that NMDA receptors might be involved in the neuronal circuit responsible for the hyperpolarizing IPSP generated by CA1 pyramidal neurons.
在灌注无镁离子培养基的大鼠海马切片的CA3和CA1亚区记录到了自发性同步癫痫样放电。对这两个区域进行手术分离后，仅CA1亚区的自发放电消失。然而，通过顺向刺激仍可在分离出的CA1亚区诱发癫痫样反应。在细胞内，这些刺激诱发的反应表现为与动作电位爆发相关的去极化。刺激海马槽仍可诱发超极化电位，推测这是CA1锥体细胞中的一种回返性抑制性突触后电位（IPSP）。自发性和刺激诱发的癫痫样放电均被N-甲基-D-天冬氨酸（NMDA）受体的选择性拮抗剂DL-2-氨基-膦酰基戊酸（APV）阻断。APV还降低了海马槽刺激诱发的IPSP的幅度和持续时间。因此，CA1亚区因降低镁离子而诱发的癫痫样放电与抑制机制的保留有关。此外，APV对IPSP的作用表明，NMDA受体可能参与了负责CA1锥体细胞产生超极化IPSP的神经回路。
