TrkB-dependent disinhibition of the nucleus accumbens is enhanced by ethanol
Male
0301 basic medicine
Membrane Glycoproteins
Ethanol
Long-Term Synaptic Depression
Central Nervous System Depressants
Neural Inhibition
Protein-Tyrosine Kinases
Nucleus Accumbens
Mice, Inbred C57BL
Mice
03 medical and health sciences
0302 clinical medicine
Animals
Female
Signal Transduction
DOI:
10.1038/s41386-019-0341-8
Publication Date:
2019-02-13T15:09:04Z
AUTHORS (8)
ABSTRACT
The nucleus accumbens is a critical integration center for reward-related circuitry and is comprised primarily of medium spiny projection neurons. The dynamic balance of excitation and inhibition onto medium spiny neurons determines the output of this structure. While nucleus accumbens excitatory synaptic plasticity is well-characterized, inhibitory synaptic plasticity mechanisms and their potential relevance to shaping motivated behaviors is poorly understood. Here we report the discovery of long-term depression of inhibitory synaptic transmission in the mouse nucleus accumbens core. This long-term depression is postsynaptically expressed, tropomyosin kinase B (TrkB) receptor-mediated, and augmented in the presence of ethanol. Our findings support the emerging view that TrkB signaling regulates inhibitory synaptic plasticity and suggest this mechanism in the nucleus accumbens as a target for ethanol modulation of reward.
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