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Keywords:

  • Amygdale;
  • deep brain stimulation;
  • GABA-B receptor;
  • hippocampal stimulation;
  • kindling epileptic models;
  • pharmacoresistant epilepsy

Objective:  To observe the effect of low-frequency hippocampal stimulation on gamma-amino butyric acid type B (GABA-B) receptor expression in hippocampus pharmacoresistant epileptic rats.

Materials and Methods:  Sixteen pharmacoresistant epileptic rats were selected by testing their seizure response to phenytoin and phenobarbital, and they were randomly divided into a pharmacoresistant control group (PRC group, eight rats) and a pharmacoresistant stimulation group (PRS group, eight rats). Another 16 pharmacosensitive epileptic rats were served as control, also divided randomly into a pharmacosensitive control group (PSC group) and a pharmacosensitive stimulation group (PSS group). A stimulation electrode was implanted into the rats' hippocampus in the four groups. Low-frequency hippocampal stimulation was administered twice per day for two weeks. Following these weeks of stimulation, GABA-B receptor-positive neurons were counted and the gray values of GABA-B receptor expression in the rats' hippocampal tissues were measured.

Results:  The amygdale stimulus-induced epileptic seizures were decreased significantly in the PRS group compared with the PRC group. The parameters of the amygdale after discharge also were improved after hippocampal stimulation. Simultaneously, the GABA-B receptor-positive neurons increased and the GABA-B expression gray values decreased markedly in the PRS group compared with the PRC group. The same phenomenon also was observed between the PSS group and the PSC group. However, no significant difference was found in the GABA-B receptor-positive neurons and the gray values of GABA-B between the PRS group and the PSC group.

Conclusions:  The low-frequency hippocampal stimulation may inhibit the amygdale stimulus-induced epileptic seizures and the after discharges. The antiepileptic effects of the hippocampal stimulation may be achieved partly by increasing the expression of the GABA-B receptor.