The Cellular Mechanisms of Dopamine Modulation on the Neuronal Network Oscillations in the CA3 Area of Rat Hippocampal Slices
•Dopamine (DA) increased kainate-induced γ oscillations in the CA3 area of rat hippocampal slices.•DA-mediated increase in γ power is associated with dopamine receptor (DR) 1 and 2 activation.•Receptor tyrosine kinase (RTK) and ERK are the main intracellular kinases that mediate DA enhancement of γ....
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Veröffentlicht in: | Neuroscience 2021-11, Vol.475, p.83-92 |
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Sprache: | eng |
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Zusammenfassung: | •Dopamine (DA) increased kainate-induced γ oscillations in the CA3 area of rat hippocampal slices.•DA-mediated increase in γ power is associated with dopamine receptor (DR) 1 and 2 activation.•Receptor tyrosine kinase (RTK) and ERK are the main intracellular kinases that mediate DA enhancement of γ.•DA-mediated enhancement of γ oscillation is involved in the activation of DR1/2-RTK-ERK signaling pathway.
Network oscillations at γ frequency band (30–80 Hz), generated by the interaction between inhibitory interneurons and excitatory neurons, have been proposed to be associated with higher brain functions such as learning and memory. Dopamine (DA), one of the major CNS transmitters, modulates hippocampal γ oscillations but the intracellular mechanisms involved remain elusive. In this study, we recorded kainate-induced γ oscillations in the CA3 area of rat hippocampal slices, and found that DA strongly enhanced γ power, which was largely blocked by dopamine receptor 1 (DR1) antagonist SCH23390, receptor tyrosine kinase (RTK) inhibitor UNC569 and ERK inhibitor U0126, partially blocked by D2/3R antagonist raclopride, PKA inhibitor H89 and PI3K inhibitor wortmannin, but not affected by AKT inhibitor TCBN or NMDAR antagonist D-AP5. Our results indicate that DA-mediated γ enhancement is involved in the activation of signaling pathway of DR1/2-RTK-ERK. Our data demonstrate a strong, rapid modulation of DA on hippocampal γ oscillations and provide a new insight into cellular mechanisms of DA-mediated γ oscillations. |
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ISSN: | 0306-4522 1873-7544 |
DOI: | 10.1016/j.neuroscience.2021.09.005 |