Endogenous cannabinoids trigger the depolarization-induced suppression of excitation in the lateral amygdala
Author(s) -
Sodikdjon A. Kodirov,
Julia Jasiewicz,
Parisa Amirmahani,
Dimitrios Psyrakis,
Kathrin Bonni,
Michael Wehrmeister,
Beat Lutz
Publication year - 2009
Publication title -
learning and memory
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 136
eISSN - 1549-5485
pISSN - 1072-0502
DOI - 10.1101/lm.1663410
Subject(s) - neuroscience , amygdala , long term potentiation , glutamatergic , synaptic plasticity , excitatory postsynaptic potential , neurotransmission , retrograde signaling , depolarization , metaplasticity , psychology , endocannabinoid system , chemistry , biology , inhibitory postsynaptic potential , receptor , glutamate receptor , signal transduction , biophysics , biochemistry
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.
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