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.