Journal
NEURON
Volume 93, Issue 2, Pages 425-440Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2016.12.030
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Funding
- Intramural Research Program of the National Institute on Drug Abuse (NIDA) at NIH [P50DA000266]
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Fear learning is a fundamental behavioral process that requires dopamine (DA) release. Experience-dependent synaptic plasticity occurs on DA neurons while anorganism is engagedin aversive experiences. However, whether synaptic plasticity onto DA neurons is causally involved in aversion learning is unknown. Here, we show that a stress priming procedure enhances fear learning by engaging VTA synaptic plasticity. Moreover, we took advantage of the ability of the ATPase Thorase to regulate the internalization of AMPA receptors (AMPARs) in order to selectively manipulate glutamatergic synaptic plasticity on DA neurons. Genetic ablation of Thorase in DAT(+) neurons produced increased AMPAR surface expression and function that lead to impaired induction of both longterm depression (LTD) and long-term potentiation (LTP). Strikingly, animals lacking Thorase inDAT(+) neurons expressed greater associative learning in a fear conditioning paradigm. In conclusion, our data provide a novel, causal link between synaptic plasticity onto DA neurons and fear learning.
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