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Two different Ca 2+ ‐dependent inhibitory mechanisms of spontaneous firing by glutamate in dopamine neurons
Author(s) -
Kim Shin Hye,
Choi Yu Mi,
Chung Sungkwon,
Uhm Dae Yong,
Park Myoung Kyu
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02783.x
Subject(s) - kainate receptor , glutamate receptor , metabotropic glutamate receptor , inhibitory postsynaptic potential , excitatory postsynaptic potential , neuroscience , stimulation , metabotropic receptor , nmda receptor , dopamine , ampa receptor , bursting , chemistry , biophysics , biology , receptor , biochemistry
The excitatory neurotransmitter, glutamate, generates a characteristic burst‐pause type of firing in midbrain dopamine neurons in association with the reward behavior, but the cellular mechanism by which glutamate generates these bursts is unknown. Here, we show that the bursts in spontaneously firing dopamine neurons can be generated by the combinative actions of the brief stimulatory and the subsequent Ca 2+ ‐dependent inhibitory signals in response to glutamate stimulation. The two Ca 2+ ‐dependent firing‐extinction signals are activated by different glutamate receptors. Although the activation of metabotropic glutamate receptors rapidly stopped the enhanced firing through the Ca 2+ release from intracellular stores, the activation of NMDA and AMPA/kainate receptors abolished the firing immediately after termination of the stimulation due to the Ca 2+ accumulation in the cell. These two Ca 2+ ‐dependent inhibitory mechanisms appear to participate in the generation of characteristic bursts in dopamine neurons by controlling the maximum firing number of single bursts and the duration of post‐firing pauses.