Synaptic plasticity is fundamental to many neurobiological functions, including memory and pain. Long-term potentiation (LTP) - a long lasting signal enhancement in synaptic strength - is a cellular substrate for memory and chronic pain. Rostral Agranular Insular Cortex (RAIC) is one of the few cortical areas consistently activated by painful stimuli.

Whole-cell patch recordings were made from neurons in RAIC hold at -70mV. By tetanus stimulation at 100Hz at RAIC layer II/III , showing a marked long-term potentiation (LTP) of EPSPs on RAIC within layer V pyramidal cells. Here we show that the LTP on RAIC is "train number-dependent" and "NMDA receptor-dependent".

The train number indicates the repeated high frequency stimulation (HFS, 100Hz, interval=20 secs). As train number is 7, the level of LTP is 208.92 ± 29.12 %. As train number is 5, the level of LTP is 162.36 ± 35.21 %. As train number is 3, the long-term ratio is 110.56 ± 25.29 % and showing no significant LTP after high frequency stimulus, which might suggest a threshold for inducing LTP in RAIC. The NMDA receptor antagonist, AP5, significantly blocks the LTP in RAIC as train number is 7.

Since RAIC plays an important role in pain, enhanced synaptic function might partially account for the mechanism underlying chronic pain.