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Activity-dependent modulation of hippocampal synaptic plasticity via PirB and endocannabinoids
Maja Djurisic1, Barbara K Brott2, Nay L Saw3
1Departments of Biology and Neurobiology, and Bio-X, Stanford University, Stanford, CA, 94305, USA. djurisic@stanford.edu.
Molecular Psychiatry
|April 20, 2018
Summary
Paired Immunoglobulin-like receptor B (PirB) deletion impairs endocannabinoid signaling, affecting synaptic plasticity and learning. PirB is crucial for maintaining bidirectional Hebbian plasticity and memory through NMDA receptor-mediated signaling.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Molecular and Cellular Biology
Background:
- Hebbian synaptic plasticity in the central nervous system (CNS) is regulated by prior activity.
- Endocannabinoids are involved in modulating plasticity at adult CA3-CA1 synapses.
- The precise mechanisms by which activity engages and sustains retrograde endocannabinoid signaling remain unclear.
Purpose of the Study:
- To investigate the role of Paired Immunoglobulin-like receptor B (PirB) in regulating synaptic plasticity and endocannabinoid signaling at CA3-CA1 synapses.
- To elucidate the molecular mechanisms underlying PirB's influence on NMDA receptor (NMDAR)-dependent signaling pathways.
Main Methods:
- Conditional deletion of PirB in adult mouse hippocampal pyramidal neurons.
- Electrophysiological recordings to assess long-term depression (LTD) and long-term potentiation (LTP) at CA3-CA1 synapses.
- Analysis of NMDAR, CB1R, and group I mGluR dependent signaling pathways.
- Measurement of miniature excitatory postsynaptic current (mEPSC) frequency.
- Behavioral testing for learning and memory.
Main Results:
- PirB deletion resulted in deficient LTD and enhanced LTP at CA3-CA1 synapses.
- This phenotype was attributed to the disengagement of retrograde endocannabinoid signaling.
- NMDAR-dependent regulation of endocannabinoid signaling was lost in PirB-deficient mice, while CB1R and group I mGluR regulation remained intact.
- Elevated mEPSC frequency in PirB mutant cells suggests increased excitatory synapse density and altered synapse pruning.
- Mice lacking PirB exhibited improved performance in learning and memory tasks.
Conclusions:
- PirB is essential for maintaining bidirectional Hebbian plasticity and learning.
- PirB acts as a key component in an NMDAR-mediated synaptic mechanism.
- Activity-dependent endocannabinoid signaling, regulated by PirB, is critical for synaptic plasticity and cognitive function.
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