Burst-timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons.
Burst-timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons.
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DOI：
10.1016/j.neuron.2009.05.011
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发表时间：
2009-06-25
期刊：
影响因子：
16.2
通讯作者：
Morikawa, Hitoshi
中科院分区：
文献类型：
--
作者：
Harnett, Mark T.;Bernier, Brian E.;Ahn, Kee-Chan;Morikawa, Hitoshi
Bursts of spikes triggered by sensory stimuli in midbrain dopamine neurons evoke phasic release of dopamine in target brain areas, driving reward-based reinforcement learning and goal-directed behavior. NMDA-type glutamate receptors (NMDARs) play a critical role in the generation of these bursts. Here we report LTP of NMDAR-mediated excitatory transmission onto dopamine neurons in the substantia nigra. Induction of LTP requires burst-evoked Ca2+ signals amplified by preceding metabotropic neurotransmitter inputs in addition to the activation of NMDARs themselves. PKA activity gates LTP induction by regulating the magnitude of Ca2+ signal amplification. This novel form of plasticity is associative, input specific, reversible, and depends on the relative timing of synaptic input and postsynaptic bursting in a manner analogous to the timing rule for cue-reward learning paradigms in behaving animals. NMDAR plasticity may thus represent a potential neural substrate for conditioned dopamine neuron burst responses to environmental stimuli acquired during reward-based learning.
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