Indeed, application of capsaicin caused a decrease in excitatory transmission. However, it's the location of this regulatory process that was so surprising.
Generally, TRPV1 channels are expressed presynaptically in the PNS; however, in the CNS, TRPV1 channels can be expressed postsynaptically. Analysis of mEPSC data demonstrated that capsaicin's effect on neurotransmission was occurring postsynaptically and, at that, was depressing AMPA currents but not NMDA currents. Loading the postsynaptic neuron with BAPTA showed that capsaicin's depressive effects are dependent upon Ca2+
They eventually found that this postsynaptic mechanism involved AMPA receptor internalization in a manner that is dependent upon Ca2+ and dynamin. Additionally, TRPV1 channels were implicated in a postsynaptic form of LTD. If TRPV1 channels are blocked, LTP is facilitated.
Postsynaptic regulation of neurotransmitter release always amazes me. It's reassuring to see such a good example of mutual dependency in the presynaptic-postsynaptic relationship. In addition to receptor internalization or delivery, sometimes it's a retrograde signaling molecule that lies at the heart of neurotransmitter control; for example, 12(S)HPETE at a particular CA3 neuron-interneuron synapse. Nitric oxide is another probable retrograde signal.