Suppression of IPSP by Priming Stimulation in Rat Piriform Cortex

Abstract

High frequency burst stimulation repeated at theta (about 5Hz) frequency is optimal for induction of LTP in hippocampus. TBS is effective since fast IPSP is suppressed by priming stimulation maximal at around 200 ms interval, which results in a large voltage summation and hence activation of NMDA receptors in the postsynaptic neuron. LTP is reliably induced by TBS in piriform cortex, suggesting that the same cellular process (IPSP suppression) may operate in piriform cortex. To test this possibility, effects of priming stimulation on IPSP suppression were examined in the rostral piriform cortex. Intracellular recordings were made from layer H pyramidal neurons, and electrical stimulation was delivered to the intrinsic associational fibers. Both heterosynaptic and homosynaptic priming stimulation induced prolongation of subsequent synaptic responses evoked 200 ms later. However, heterosynaptic stimulation did not affect the peak amplitude of the subsequent synaptic responses, indicating that the effect is not due to other forms of synaptic plasticity such as paired-pulse facilitation. When the same experiments were repeated while the postsynaptic neurons were depolarized by current injection, suppression of fast IPSP by priming stimulation was clearly discernable. Burst stimulation resulted in a large temporal summation of EPSPs for primed burst responses, an ideal condition for activation of NMDA receptors. These results indicate that cellular mechanisms for IPSP suppression by priming stimulation indeed exist in piriform cortex as in hippocampus, and this is probably the reason why TBS is effective for induction of LTP in piriform cortex. Unlike hippocampus, however, homosynaptic stimulation was more effective than heterosynaptic stimulation for suppression of fast IPSP, and maximal effect was around 100 ms interval, suggesting that the optimal frequency and operational modes are different in the two structures.