Activity of thalamic neurons has been shown to be modulated via type-1 metabotropic glutamate receptor (mGluR1) activation, which initiates an intracellular Ca signaling cascade involving phospholipase Cbeta4 (PLCbeta4) and leading to the activation of conventional protein kinase C (cPKC). In the present study, we investigated the role of PLCbeta4 in thalamic neuron. PLCbeta4-deficient mutant mice were found to exhibit three phenotypic characteristics: (1) a 2-Hz increase in the peak frequency of electroencephalogram (EEG) of rapid eye movement (REM) sleep, (2) an increase in the frequency of miniature excitatory postsynaptic currents (mEPSCs) recorded in thalamus, and (3) waveform distortion of EEG. We postulate here that changes in protein phosphorylation due to reduced cPKC activity by PLCbeta4 deletion in thalamic neurons may give rise to these phenotypic characteristics. Taken together, these results indicate that reduced PLCbeta4 activity in thalamic neurons may underlie high-cortical oscillation frequency.