Fig. 1.

Electrocorticography (ECoG) of mGluR4^−/− and mGluR4^+/+ mice given either GBL or PTZ. In all ECoG figuresL_FR-PR andR_FR-PR represent the ECoG recording from the left and right frontoparietal electrodes, respectively. A , Baseline ECoG in a mGluR4^−/− mouse. There was no difference between mGluR4^+/+ and mGluR4^−/− mice in baseline recordings.B, ECoG in a mGluR4^+/+ mouse 20 min after 100 mg/kg of GBL. C, ECoG in a mGluR4^−/− mouse 20 min after 100 mg/kg of GBL.D, ECoG in an mGluR4^+/+ mouse 20 min after 30 mg/kg of PTZ. E, ECoG in an mGluR4^−/− mouse 20 min after 30 mg/kg of PTZ. The dose of PTZ was the CD₁₀₀ in the absence seizure dose–response studies. All drugs were given intraperitoneally. Administration of PTZ and GBL to mGluR4^+/+ mice and of GBL to mGluR4^−/− mice resulted in the bilaterally synchronous SWD shown. These paroxysms were associated with absence-like behavior in all of the mGluR4^−/− mice that were tested, namely facial myoclonus, vibrissal twitching, and arrest of motor activity. Administration of (−) baclofen (20 mg/kg, i.p.) produced EEG and behavioral findings similar to those shown for PTZ and GBL in both mGluR4^−/− and mGluR4^+/+ mice. In addition to being refractory to the PTZ-induced absence seizures as shown in E, mGluR4^−/− mice also were resistant to bicuculline- and picrotoxin-induced absence seizures.