Glutamate receptor GluA1 subunit is implicated in capsaicin induced modulation of amygdala LTP but not LTD.

Capsaicin has been shown to modulate synaptic plasticity in various brain regions including the amygdala. Whereas in the lateral amygdala the modulatory effect of capsaicin on long-term potentiation (LA-LTP) is mediated by TRPV1 channels, we have recently shown that capsaicin-induced enhancement of long term depression (LA-LTD) is mediated by TRPM1 receptors. However, the underlying mechanism by which capsaicin modulates synaptic plasticity is poorly understood. In the present study, we investigate the modulatory effect of capsaicin on synaptic plasticity in mice lacking the AMPAR subunit GluA1. Capsaicin reduced the magnitude of LA-LTP in slices derived from wild-type mice as previously described, whereas this capsaicin-induced suppression was absent in GluA1-deficient mice. In contrast, neither LA-LTD nor the capsaicin-mediated enhancement of LA-LTD was changed in GluA1 knockout mice. Our data indicate that capsaicin-induced modulation of LA-LTP via TRPV1 involves GluA1-containing AMPARs whereas capsaicin-induced modulation of LA-LTD via TRPM1 is independent of the expression of the AMPAR GluA1 subunit.