@article {6348,
	title = {Burst-timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons.},
	journal = {Neuron},
	volume = {62},
	year = {2009},
	month = {2009 Jun 25},
	pages = {826-38},
	abstract = {<p>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 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 might thus represent a potential neural substrate for conditioned dopamine neuron burst responses to environmental stimuli acquired during reward-based learning.</p>
},
	keywords = {2-Amino-5-phosphonovalerate, 4, 5-Trisphosphate, Action Potentials, Animals, Biophysics, Calcium, Dopamine, Dose-Response Relationship, Drug, Electric Stimulation, Enzyme Inhibitors, Excitatory Amino Acid Antagonists, Gene Expression Regulation, Inositol 1, Intracellular Signaling Peptides and Proteins, Long-Term Potentiation, Male, Mesencephalon, Methoxyhydroxyphenylglycol, N-Methyl-D-Aspartate, Neural Pathways, Neuronal Plasticity, Neurons, Peptide Fragments, Rats, Receptors, Sprague-Dawley, Time Factors},
	issn = {1097-4199},
	doi = {10.1016/j.neuron.2009.05.011},
	author = {Harnett, Mark T and Bernier, Brian E and Ahn, Kee-Chan and Morikawa, Hitoshi}
}
