Wirkungsweise von Capsaicin auf die synaptische Plastizität in der lateralen Amygdala

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The amygdala plays critical roles in certain types of emotional memory. The underlying mechanisms are believed to depend on activity-dependent long-term potentiation (LTP) and depression (LTD) in the lateral nucleus of the amygdala (LA). In preliminary experiments we have shown that in the LA transient receptor potential proteins from subtype vannilloid 1 (TRPV1) are expressed both in glial and neuronal membranes. TRPV1 receptors have classically been defined as heat-sensitive, ligand gated (among others: capsaicin), nonselective cation channels that integrate nociceptive stimuli in sensory neurons. Here we report that TRPV1 channel activation by capsaicin dose-dependently reduced or suppressed high-frequency-induced LA-LTP. In contrast, from the literature it is known that capsaicin enhances LTP in the CA1 region of the hippocampus, whereas TRPV1 gene-deficient mice show a reduced CA1-LTP. Whereas low-frequency stimulation of cortical fibers did not induce reliable LA-LTD, capsaicin was necessary and sufficient to trigger low frequency-induced LA-LTD. The aim of the project is to clarify which mechanisms are involved in the action of capsaicin on amygdaloid plasticity changes. The results will show which involvement may have pre- and/or postsynaptic mechanisms and detect possible signal cascades. The demonstration of possible TRPV1-mediated plasticity changes after stress (social isolation, forced swim test) should document a relevance of the TRPV1 in long-term changes in physiological and pathological circuit behavior during learning.