Epileptiform activity induction with electrolyte imbalance in brain slices: Mechanisms involved in control

Saybasili H., Arslan R. B.

23rd Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society, İstanbul, Türkiye, 25 - 28 Ekim 2001, cilt.23, ss.947-950 identifier identifier

  • Yayın Türü: Bildiri / Tam Metin Bildiri
  • Cilt numarası: 23
  • Basıldığı Şehir: İstanbul
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.947-950
  • Anahtar Kelimeler: hippocampal slices, patch clamp recording, epileptiform activity, CA1 pyramidal neuron, NMDA receptor, LOW EXTRACELLULAR MAGNESIUM, HIPPOCAMPAL SLICES, BINDING-SITES, GLUTAMATE, ASPARTATE, NEURONS, NEUROTOXICITY, DEPRESSION, MEMBRANES, RECEPTORS
  • Galatasaray Üniversitesi Adresli: Evet

Özet

Epilepsy is a disorder of recurrent seizure activity caused by rhythmic firing of neurons. Epileptiform activity can be generated by incubating brain slices in magnesium-free artificial cerebrospinal fluid (ACSF). In the present study, epileptiform discharges induced by the omission of magnesium ions from ACSF has been studied in hippocampal slices obtained from young rats using patch clamp tight-seal whole cell recording technique. Effects of AP5 to block NMDA receptor activation and acidic pH shift of ACSF on the epileptiform current was studied. It was found that magnesium-free ACSF induced epileptiform activity frequency was attenuated with AP5 application more than 50%. The pH shift of the magnesium-free ACSF from 7.3 to 7.1. depressed the epileptiform activity. Both effects were shown to be reversible. According to the results of this study, epileptiform activity and mild extracellular acidic shifts do not interact to aggravate excitotoxicity conditions in CA1 pyramidal neurons.