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Heterosynaptic long‐term potentiation at interneuron–principal neuron synapses in the amygdala requires nitric oxide signalling
Author(s) -
Lange M. D.,
Doengi M.,
Lesting J.,
Pape H. C.,
Jüngling K.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.221317
Subject(s) - long term potentiation , interneuron , neuroscience , signalling , nitric oxide , chemistry , neuron , amygdala , term (time) , biology , microbiology and biotechnology , inhibitory postsynaptic potential , receptor , biochemistry , physics , organic chemistry , quantum mechanics
Non‐technical summary Long‐lasting changes in efficacy of cell–cell communication (long‐term potentiation; LTP) at specialized sites (synapses) between neurons in the brain are thought to underlie forms of learning and memory. These forms of LTP can occur at excitatory synapses and inhibitory synapses, thus in‐ or decreasing the activity of neurons. We provide evidence for a novel form of LTP at inhibitory synapses (LTP i ) on a subset of neurons in the amygdala of mice, a brain region involved in fear and anxiety. This LTP i enhances the release of the inhibitory neurotransmitter GABA at synapses between inhibitory interneurons and excitatory principal neurons (PNs) in a sub‐region of the amygdala. The described LTP i is heavily dependent on the production and diffusion of the volatile gas nitric oxide (NO), produced by PNs during stages of increased activity. These findings indicate that NO‐mediated long‐term regulation of inhibitory transmission in the amygdala might contribute to the learning of fear.