Praxis Medica (Jan 2016)

Effect of low potassium concentration on cadmium induced epileptiform activity of leech retzius neurons

  • Milićević Nebojša,
  • Stanojević Marija,
  • Spasić Svetolik,
  • Jovanović Zorica,
  • Prostran Milica,
  • Lopičić Srđan

DOI
https://doi.org/10.5937/pramed1604001M
Journal volume & issue
Vol. 45, no. 3-4
pp. 1 – 6

Abstract

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Epilepsies have a large significance and require detailed investigation of cellular mechanisms that lead to this disorder. Environmental, especially industrial, toxins are having increasingly more prominent role in these investigations. The aim of our research was to investigate the significance of Cd2+ in generation of epileptiform electrical activity of neurons, and the role of Na+/K+ pump in mechanisms that lead to cessation of this activity. Experiments were performed on Retzius nerve cells of the leech Haemopis sanguisuga. Intracellularly placed microelectrodes were used to measure membrane potential changes upon administration of Cd2+ (100 µmol/l), and the same concentration of Cd2+ in low K+ (1 mmol/l) solution. In our experiments Cd2+ led to generation of rhythmic repetitive oscillatory activity. This activity closely resembles paroxysmal depolarizing shifts (PDS) which represent the cellular basis of epilepsy. Cd2+ induced epileptiform activity had the following characteristics: frequency of 3.9±0.8 PDS/minute, PDS duration of 4.0±0.3 s, and PDS amplitude of 8.1±0.7 mV. Cd2+ induces effects similar to those of Ni2+ and Co2+, but in 30 times smaller concentration. Application of Cd2+ in low K+ solution led to a significant reduction of PDS frequency (by 2.34±0.55 PDS/minute, p<0.05, Student's t-test), highly significant increase in PDS duration (by 2.84±0.23 s, p<0.01, Student's t-test) and highly significant reduction in PDS amplitude (by 1.91±0.33 mV, p=0.01, Student's t-test). Our results show that Cd2+ is a potent initiator of epileptiform activity, and that Na+/K+ pump significantly affects this activity and has a potentially important role in mechanisms that lead to its cessation.

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