title: Endogenous cannabinoids trigger the depolarization-induced suppression of excitation in the lateral amygdala.
abstract: The amygdala is a key area of the brain where the emotional memories are stored throughout the lifespan. It is well established that synapses in the lateral nucleus of amygdala (LA) can undergo long-term potentiation, a putative cellular correlate of learning and memory. However, a type of short-term synaptic plasticity, known as depolarization-induced suppression of excitation (DSE), has not been studied previously in the amygdala in general and in the LA in particular. In this study we aimed to prove either the absence or the presence of this phenomenon in the LA. Our data demonstrate for the first time that DSE is present in the LA and that it modulates the cortical excitatory synaptic input into this region. The existence of this type of retrograde neurotransmission in glutamatergic pyramidal neurons of the LA suggests that the axonal terminals of cortical inputs do possess functional type 1 cannabinoid receptors, and provides a novel insight regarding inputs into the LA. Further experiments indeed revealed endocannabinoids as the messenger for this retrograde signaling in the LA. In conclusion, the DSE may play a functional role in synaptic plasticity and related emotional memory processing in the LA.
authors.affiliation: Institute of Physiological Chemistry and Pathobiochemistry, University Medical Center Mainz, Germany. Sodikdjon.Kodirov@utb.edu
authors.forename: Sodikdjon A
authors.initials: SA
authors.lastname: Kodirov
authors.forename: Julia
authors.initials: J
authors.lastname: Jasiewicz
authors.forename: Parisa
authors.initials: P
authors.lastname: Amirmahani
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Psyrakis
authors.forename: Kathrin
authors.initials: K
authors.lastname: Bonni
authors.forename: Michael
authors.initials: M
authors.lastname: Wehrmeister
authors.forename: Beat
authors.initials: B
authors.lastname: Lutz
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D063385:Cannabinoid Receptor Modulators / Q000502:physiology*; D004594:Electrophysiology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D055369:Miniature Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D010880:Piperidines / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D043884:Receptor, Cannabinoid, CB1 / Q000037:antagonists & inhibitors / Q000502:physiology; D012815:Signal Processing, Computer-Assisted; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D063385:Cannabinoid Receptor Modulators; D010880:Piperidines; D011720:Pyrazoles; D043884:Receptor, Cannabinoid, CB1; C103505:AM 251; D002118:Calcium