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Interneuron activity controls endocannabinoid-mediated presynaptic plasticity through calcineurin.

Boris D Heifets1, Vivien Chevaleyre, Pablo E Castillo

  • 1Dominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

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Endocannabinoid signaling (eCBs) induces long-term depression (LTD) at synapses. In the hippocampus, interneuron activity during eCB signaling is crucial for this synaptic plasticity, involving calcium and calcineurin.

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Signaling

Background:

  • Endocannabinoids (eCBs) mediate long-term depression (LTD) at synapses by reducing neurotransmitter release.
  • In the hippocampus, eCB-LTD at interneuron-pyramidal cell synapses (I-LTD) requires cannabinoid receptor 1 (CB1R) activation and reduced cAMP/PKA signaling.
  • The role of interneuron (IN) activity during eCB-LTD induction remains unclear.

Purpose of the Study:

  • To investigate whether GABAergic terminals actively contribute to I-LTD induction.
  • To determine the role of spontaneous interneuron activity during the eCB signaling window.
  • To elucidate the presynaptic mechanisms, including calcium dynamics and phosphatase activity, involved in I-LTD.

Main Methods:

  • Cell-pair recordings in the hippocampus to assess I-LTD.
  • Manipulation of spontaneous interneuron firing rates.
  • Disruption of presynaptic calcium dynamics.
  • Pharmacological inhibition of specific phosphatases (calcineurin).

Main Results:

  • Reducing spontaneous IN firing blocked I-LTD, which was rescued by stimulating inhibitory afferents.
  • I-LTD was induced in an IN onto a pyramidal cell only if the IN was active during eCB signaling.
  • Disrupting presynaptic Ca(2+) dynamics blocked I-LTD, indicating IN spikes regulate it via presynaptic Ca(2+).
  • Inhibition of calcineurin, but not another phosphatase, fully blocked I-LTD.

Conclusions:

  • Interneuron activity during the eCB signaling period is essential for inducing I-LTD.
  • Presynaptic Ca(2+) influx, triggered by IN spikes, is a critical regulatory step.
  • CB1R signaling and IN activity cooperatively modulate presynaptic kinase/phosphatase balance to induce I-LTD, with calcineurin playing a key role.