Objectives: 

The transient receptor potential vanilloid subfamily member 1 (TRPV1) is a polymodal nociceptor and abundantly exist in the hippocampus. Recent studies show that TRPV1 is involved in synaptic plasticity at CA1 synapses which underlie the mechanism of learning and memory. However, although TRPV1 is also located at mossy fiber-CA3 synapses, the role of TRPV1 still remains unclear. In this study, we examined the TRPV1 modification on short-term and long-term synaptic plasticity at hippocampal mossy fiber-CA3 synapses.

Materials: 

We recorded field excitatory postsynaptic potentials (fEPSPs) from striatum lucidum of hippocampal CA3 area of postnatal day 13 to 22 C57BL/6J mice. To evaluate the short-term and long-term plasticity, we determined the paired-pulse ratio and long-term potentiation (LTP), respectively. Furthermore, we addressed the possibility that GABAergic interneurons mediate this modification. The Student's unpaired t test was used for statistics.

Results: 

Application of capsaicin, a TRPV1 receptor agonist, did not influence to the basal synaptic transmission or paired-pulse ratio of fEPSPs. On the other hand, LTP was attenuated in the presence of capsaicin in a dose dependent manner. This attenuation was recovered by the pretreatment of capsazepine, a competitive antagonist of TRPV1. Moreover, the attenuation of LTP by capsaicin application was not observed in the presence of antagonists of GABAA receptors.

Conclusions: 

These results suggest that TRPV1 is not involved in the basic synaptic transmissions but in the induction of LTP via GABAergic interneurons at mossy fiber-CA3 synapses. This study indicates that TRPV1 may modulate learning and memory.