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Dopamine Inhibits High-Frequency Stimulation-Induced Long-Term Potentiation of Intrinsic Excitability in CA1 Hippocampal Pyramidal Neurons
Author(s) -
Chunling Wei,
Yihui Liu,
Ming-Hao Yang,
Zhi-qiang Liu,
Wei Ren
Publication year - 2012
Publication title -
neurosignals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.755
H-Index - 67
eISSN - 1424-8638
pISSN - 1424-862X
DOI - 10.1159/000342435
Subject(s) - long term potentiation , neuroscience , synaptic plasticity , hippocampal formation , dopamine , chemistry , ltp induction , rheobase , long term depression , stimulation , excitatory postsynaptic potential , nmda receptor , biology , receptor , inhibitory postsynaptic potential , ampa receptor , biochemistry
The efficiency of neural circuits is modified by changes not only in synaptic strength, but also in intrinsic excitability of neurons. In CA1 hippocampal pyramidal neurons, bidirectional changes in the intrinsic excitability are often presented after induction of synaptic long-term potentiation or depression. This plasticity of intrinsic excitability has been identified as a cellular correlate of learning. Besides, behavioral learning often involves action of reinforcement or rewarding mediated by dopamine (DA). Here, we examined how DA influences the intrinsic plasticity of CA1 hippocampal pyramidal neurons when high-frequency stimulation (HFS) was applied to Schaffer collaterals. The results showed that DA inhibits the decrease in rheobase and increase in mean firing rate of pyramidal neurons induced by HFS, and that this inhibition was abolished by the D1-like receptor antagonist SCH23390 but not by the D2-like receptor antagonist sulpiride. The results suggest that DA inhibits the potentiation of excitability induced by presynaptic HFS, and that this inhibition depends on the activation of D1-like receptors.

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