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November 1, 2000Journal of NeuroscienceOpen Access

Long-Term Potentiation Induced by θ Frequency Stimulation Is Regulated by a Protein Phosphatase-1-Operated Gate

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Authors

GBGeorge P. BrownRBRobert D. BlitzerJCJohn H. Connor

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Overview

Electrophysiological study demonstrates that cAMP pathway activation enables theta-frequency synaptic potentiation in rat hippocampal slices, indicating that protein phosphatase-1 acts as a...

Key Points

  • Investigate the molecular mechanisms through which cAMP signaling facilitates theta-frequency-induced long-term potentiation at hippocampal Schaffer collateral–CA1 synapses.
  • Conducted electrophysiological recordings in rat hippocampal slices using theta pulse stimulation (150 pulses at 10 Hz) at Schaffer collateral–CA1 synapses.
  • Administered pharmacological agents including the beta-adrenergic agonist isoproterenol, the cAMP analog 8-bromo-cAMP, and selective inhibitors of PKA and CaMKII.
  • Introduced activated inhibitor-1 intracellularly into postsynaptic CA1 neurons and biochemically assayed protein phosphatase-1 and CaMKII activation.
  • Theta pulse stimulation alone failed to induce LTP but reliably elicited potentiation when paired with either isoproterenol or 8-bromo-cAMP via postsynaptic PKA activation.
  • Postsynaptic injection of activated inhibitor-1 mimicked cAMP-mediated LTP gating, confirming that suppression of protein phosphatase-1 is necessary for synaptic potentiation.
  • Inhibition of protein phosphatase-1 coupled with theta stimulation drove autonomous CaMKII activation, which was strictly required for the induction of potentiation.

Cite This Study

Brown et al. (2000) studied this question.

synapsesocial.com/papers/6aacb36a696769727593d623https://doi.org/10.1523/jneurosci.20-21-07880.2000
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