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Updated: Aug 14, 2026
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Real-time Electrophysiology: Using Closed-loop Protocols to Probe Neuronal Dynamics and Beyond
Published on: June 24, 2015
Postsynaptic depolarization scales quantal amplitude in cortical pyramidal neurons
K R Leslie1, S B Nelson, G G Turrigiano
1Department of Biology and Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454, USA.
Summary
Pyramidal neurons use two signals for synaptic scaling: brain-derived neurotrophic factor (BDNF) to strengthen synapses and depolarization to weaken them, stabilizing neural firing rates during plasticity.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Homeostatic Regulation
Background:
- Pyramidal neurons globally adjust excitatory synapse strength to stabilize firing rates.
- Homeostatic plasticity is crucial for learning and development, but its regulatory signals are unclear.
- Brain-derived neurotrophic factor (BDNF) partially explains activity-dependent synaptic scaling.
Purpose of the Study:
- To investigate the distinct roles of postsynaptic depolarization and receptor activation in synaptic scaling.
- To identify the specific signaling pathways involved in activity-dependent synaptic strength regulation.
Main Methods:
- Pyramidal neurons were subjected to chronic depolarization using elevated KCl and ionotropic receptor blockade.
- Quantal amplitude of excitatory synapses was measured under various depolarization levels.
- The involvement of specific receptors (AMPA, NMDA, GABA(A)), action potentials, and metabotropic glutamate receptors was assessed.
Main Results:
- Chronic depolarization (48 hr, -62 to -36 mV) parametrically reduced excitatory synapse quantal amplitude.
- This depolarization-induced scaling down was independent of BDNF.
- The effect was not mediated by AMPA, NMDA, GABA(A) receptors, action potentials, or metabotropic glutamate receptors.
Conclusions:
- Two independent signals regulate synaptic scaling in pyramidal neurons: BDNF promotes scaling up, while depolarization induces scaling down.
- Depolarization acts as a BDNF-independent signal to decrease excitatory synaptic strength.
- These findings clarify mechanisms underlying homeostatic plasticity and neural network stability.
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