Abstract
The dopaminergic modulation of long-term potentiation (LTP) has been studied well, but the mechanism by which dopamine induces LTP (DA-LTP) in CA1 pyramidal neurons is unknown. Here, we report that DA-LTP in basal dendrites is dependent while in apical dendrites it is independent of activation of L-type voltage-gated calcium channels (VDCC). Activation via NMDAR is critical for the induction of DA-LTP in both apical and basal dendrites, but only BDNF is required for the induction and maintenance of DA-LTP in apical dendrites. We report that dopaminergic modulation of LTP is lamina-specific at the Schaffer collateral/commissural synapses in the CA1 region.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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2-Amino-5-phosphonovalerate / pharmacology
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Animals
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Biophysics
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Brain-Derived Neurotrophic Factor / metabolism*
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Brain-Derived Neurotrophic Factor / pharmacology
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Calcium Channel Blockers / pharmacology
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Calcium Channels / metabolism*
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Dendrites / drug effects*
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Dopamine / pharmacology*
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Electric Stimulation
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / drug effects
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Hippocampus / cytology
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In Vitro Techniques
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Long-Term Potentiation / drug effects*
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Male
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Neurons / cytology*
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Neurons / drug effects
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Nifedipine / pharmacology
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Rats
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Receptor, trkB / pharmacology
Substances
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Brain-Derived Neurotrophic Factor
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Calcium Channel Blockers
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Calcium Channels
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Excitatory Amino Acid Antagonists
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2-Amino-5-phosphonovalerate
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Receptor, trkB
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Nifedipine
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Dopamine