title: A novel form of capsaicin-modified amygdala LTD mediated by TRPM1.
abstract: Recently we have shown that capsaicin attenuates the strength of LTP in the lateral amygdala (LA) and demonstrated that this effect is mediated by the transient receptor potential (TRP) channel TRPV1. Here we further show that capsaicin, which is thought to act primarily through TRPV1, modifies long term depression (LTD) in the LA. Yet the application of various TRPV1 antagonists does not reverse this effect and it remains in TRPV1-deficient mice. In addition, voltage gated calcium channels, nitric oxide and CB1 receptors are not involved. Using pharmacology and TRPM1-/-mice, our electrophysiological data indicate that capsaicin-induced activation of TRPM1 channels contribute to the induction of LA-LTD. Whereas LA-LTD in general depends on the acitvation of NMDA receptors- and group II metabotropic glutamate receptors (mGluR), the modifying effect of capsaicin on LA-LTD via TRPM1 appears to be specifically mediated by group I mGluRs and in interaction with another member of the TRP family, TRPC5. Additionally, intact GABAergic transmission is required for the capsaicin-effect to take place. This is the first documentation that beside their function in the retina TRPM1 proteins are expressed in the brain and have a functional relevance in modifying synaptic plasticity.
authors.affiliation: Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, CCM, CCO, Charitéplatz 1, 10117 Berlin, Germany.
authors.forename: Christine
authors.initials: C
authors.lastname: Gebhardt
authors.affiliation: Institute of Anatomy and Cell Biology, Universitätsmedizin Greifswald, Germany.
authors.forename: Oliver
authors.initials: O
authors.lastname: von Bohlen Und Halbach
authors.affiliation: Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, CCM, CCO, Charitéplatz 1, 10117 Berlin, Germany.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Hadler
authors.affiliation: Department of Pharmacology and Experimental Therapy, Institute of Experimental and Clinical Pharmacology and Toxicology, Eberhard Karls University Hospitals and Clinics, and Interfaculty Center of Pharmacogenomics and Drug Research, University of Tübingen, Tübingen, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Harteneck
authors.affiliation: Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, CCM, CCO, Charitéplatz 1, 10117 Berlin, Germany. Electronic address: doris.albrecht@charite.de.
authors.forename: Doris
authors.initials: D
authors.lastname: Albrecht
mesh_terms: D000818:Animals; D066272:Basolateral Nuclear Complex / Q000187:drug effects*; D002211:Capsaicin / Q000494:pharmacology*; D007150:Immunohistochemistry; D036881:Long-Term Synaptic Depression / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018689:Sensory System Agents / Q000494:pharmacology*; D050052:TRPC Cation Channels / Q000187:drug effects*; D050053:TRPM Cation Channels / Q000172:deficiency / Q000187:drug effects*
chemical_list: D018689:Sensory System Agents; D050052:TRPC Cation Channels; D050053:TRPM Cation Channels; C112021:Trpc5 protein, mouse; C116297:Trpm1 protein, mouse; D002211:Capsaicin
keywords: Capsaicin; Immunohistochemistry; Lateral nucleus of the amygdala; Long-term depression; Mice; TRPC5; TRPM1