Research article summary (published 23 Jun 2009):

Burst-timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons.

Full Abstract

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.

Author information

Author/s: Harnett, Mark T (MT); Bernier, Brian E (BE); Ahn, Kee-Chan (KC); Morikawa, Hitoshi (H);

Affiliation: Institute for Neuroscience, University of Texas at Austin, Austin, TX 78712, USA.

Grants: DA015687 (Agency:NIDA NIH HHS)

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural

Journal: Neuron (Neuron), published in United States. (Language: eng)

Reference: 2009-Jun; vol 62 (issue 6) : pp 826-38

Dates: Created 2009/06/26; Completed 2009/07/09;

PMID: 19555651, status: MEDLINE (last retrieval date: 7/24/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

2-Amino-5-phosphonovalerate - pharmacology Action Potentials - drug effects; physiology Animals Biophysics Calcium - metabolism Dopamine - metabolism Dose-Response Relationship, Drug Electric Stimulation - methods Enzyme Inhibitors - pharmacology Excitatory Amino Acid Antagonists - pharmacology Gene Expression Regulation - drug effects; physiology Inositol 1,4,5-Trisphosphate - analogs & derivatives; pharmacology Intracellular Signaling Peptides and Proteins - pharmacology

Intracellular Signaling Peptides and Proteins - pharmacology Long-Term Potentiation - drug effects; physiology Male Mesencephalon - cytology Methoxyhydroxyphenylglycol - analogs & derivatives; pharmacology Neural Pathways - physiology Neuronal Plasticity - drug effects; physiology Neurons - drug effects; physiology Peptide Fragments - pharmacology Rats Rats, Sprague-Dawley Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; physiology Time Factors

Associated Chemicals: Enzyme Inhibitors (0) ; Excitatory Amino Acid Antagonists (0) ; Intracellular Signaling Peptides and Proteins (0) ; Peptide Fragments (0) ; Receptors, N-Methyl-D-Aspartate (0) ; inositol 1,4,5-trisphosphate 1-(2-nitrophenyl)ethyl ester (119147-21-6) ; protein kinase inhibitor peptide (6-24) (136058-52-1) ; dihydroxyphenylethylene glycol (3343-19-9) ; Methoxyhydroxyphenylglycol (534-82-7) ; Calcium (7440-70-2) ; 2-Amino-5-phosphonovalerate (76726-92-6) ; Inositol 1,4,5-Trisphosphate (85166-31-0)

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