Krug M, Koch M, Grecksch G, Schulzeck K
Otto-von-Guericke University Magdeburg, Medical Faculty, Institute of Pharmacology and Toxicology, Germany.
Physiol Behav. 1997 Oct;62(4):721-7. doi: 10.1016/s0031-9384(97)00167-4.
The present study describes changes of response enhancement of hippocampal field potentials in slices of kindled rats using different methods to induce long-lasting potentiation. Eight-week-old male Wistar rats were subjected to pentylenetetrazol (PTZ) kindling induced by intraperitoneal injection of 45 mg/kg once every 48 h until the occurrence of seizure stages 4-5. Eight to 12 days after the last kindling session, transverse hippocampus slices were prepared and maintained in an artificial medium. Evoked-field potentials were recorded in the CA1 region upon stimulation of the Schaffer collaterals. Potentiation was induced: 1. By moderate tetanic stimulation of the Schaffer collaterals, 2. by changing the perfusion medium to 0-magnesium for 30 min, and 3. by changing the medium to 4 mM Ca2+ for 7 min. In slices from kindled rats, long-term potentiation (LTP) after tetanic stimulation and increase of the evoked potential by 0-magnesium were significantly enhanced in comparison to slices from sham-kindled rats. However, Ca(2+)-induced LTP could not be induced in slices from kindled rats. The results support the assumption that PTZ kindling also induces lasting changes in the responsiveness of hippocampal structures, expressed as an enhanced ability to induce potentiation. An alteration of N-methyl-D-aspartate (NMDA) receptor-coupled processes can be assumed. The inability to induce Ca(2+)-induced LTP points to more complex effects of PTZ, perhaps also on nonNMDA coupled ionic channels.
本研究描述了使用不同方法诱导长时程增强时，点燃大鼠脑片中海马场电位反应增强的变化。8周龄雄性Wistar大鼠腹腔注射45mg/kg的戊四氮（PTZ），每48小时一次，直至出现4-5期癫痫发作，从而诱发点燃。在最后一次点燃后8至12天，制备海马横向切片，并保存在人工培养基中。刺激Schaffer侧支时，在CA1区记录诱发场电位。通过以下方式诱导增强：1. 对Schaffer侧支进行适度强直刺激；2. 将灌流培养基更换为无镁培养基30分钟；3. 将培养基更换为4mM Ca2+ 7分钟。与假点燃大鼠的脑片相比，点燃大鼠脑片中强直刺激后的长时程增强（LTP）和无镁诱发的诱发电位增加显著增强。然而，在点燃大鼠的脑片中无法诱导Ca2+ 诱导的LTP。结果支持以下假设：PTZ点燃也会诱导海马结构反应性的持久变化，表现为诱导增强的能力增强。可以推测N-甲基-D-天冬氨酸（NMDA）受体偶联过程发生了改变。无法诱导Ca2+ 诱导的LTP表明PTZ有更复杂的作用，可能也作用于非NMDA偶联离子通道。
