High frequency stimulation in thalamic reticular nucleus blocks the effect of pentylenetetrazole.

High-frequency stimulation (HFS) is an alternative and promising treatment for intractable epilepsy; however, the optimal targets remain unknown. The thalamic reticular nucleus (TRN) occupies a key position in the modulation of cortico-thalamic and thalamo-cortical pathways. HFS-TRN retarded the generalization of PTZ-induced seizures. To explore the mechanism underlying HFS-TRN, we recorded TRN multiunitary activity (MUA) in response to HFS-TRN and low doses of pentylenetetrazole (PTZ). Male Wistar rats were used. A borosilicate microelectrode for extracellular recording and a bipolar electrode for HFS were introduced into the left TRN. Spontaneous MUA of the TRN under urethane anesthesia exhibited tonic and burst firing. PTZ caused a significant decrease in firing rate at 70% of MUA, 20% no change, and 10% increase. Pre-treatment with HFS-TRN blocked the subsequent PTZ-induced decrease in firing rate (59%), 8% showed an increase. The results suggest that the TRN participates in the maintenance of characteristic spike-wave discharges, while HFS in the TRN can inhibit the synchronization of oscillatory activity. In conclusion, HFS in the TRN may block burst firing in the TRN and may be sufficient to protect against the spread of convulsive seizures.