Theta-burst stimulation induces LTP at excitatory and inhibitory synapses in the spinal trigeminal subnucleus interpolaris

•TBS induces LTP of excitatory transmission from the Vc to Vi under blockade of inhibitory transmission.•TBS-induced LTP was not mediated by NMDA receptors, and its expression was limited by group I mGluRs.•TBS induces LTP of GABAergic transmission from the Vc to Vi.•TBS-induced GABAergic LTP is resistant to postsynaptic Ca2+ chelation, but depends on NMDA receptors and NO signaling. Long-lasting synaptic modifications of excitatory and inhibitory synaptic transmissions induced by theta-burst stimulation (TBS) were examined in the spinal trigeminal subnucleus interpolaris (Vi). We found that conditioning afferents of another subnucleus caudalis (Vc) to the Vi with TBS produced long-term depression (LTD). However, when GABAA and glycine receptors were blocked, the same stimulation paradigm produced long-term potentiation (LTP). The induction of LTP involved neither NMDA receptors nor a presynaptic change. The expression of LTP was obviously suppressed by the activation of group I mGluRs because its magnitude increased in the presence of antagonists for group I mGluRs. Besides the LTP at excitatory synapses, TBS also induced LTP at inhibitory GABAergic synapses, which required the activation of NMDA receptors and NO-cGMP signaling but was not involved in the increase of postsynaptic Ca2+ concentration. Therefore, this study shows, for the first time, an activity-dependent plasticity at excitatory and inhibitory synapses in the Vi by the same conditioning stimulation.