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Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
Published on: August 11, 2019
Inhibitory synaptic plasticity regulates pyramidal neuron spiking in the rodent hippocampus
F Saraga1, T Balena, T Wolansky
1Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada.
Neuroscience
|June 20, 2008
Summary
Inhibitory synaptic plasticity, which shifts the GABA reversal potential (E(GABA)), enhances CA1 pyramidal neuron firing and improves signal transmission in the hippocampus. This plasticity increases action potential frequency and reliability.
Area of Science:
- Neuroscience
- Computational Neuroscience
- Synaptic Plasticity
Background:
- Synaptic plasticity, particularly spike-timing-dependent plasticity, modifies synaptic efficacy in hippocampal CA1 pyramidal neurons.
- Repetitive presynaptic stimulation before postsynaptic firing induces inhibitory synaptic plasticity, leading to a depolarization of the reversal potential for GABA (E(GABA)).
Purpose of the Study:
- To investigate how inhibitory synaptic plasticity, specifically the depolarization of E(GABA), regulates the spiking activity of CA1 pyramidal neurons in the rat hippocampus.
- To elucidate the mechanisms by which altered E(GABA) influences action potential generation, spike latency, and the excitatory input required for spiking.
Main Methods:
- Electrophysiological recordings from cultured hippocampal neurons to measure spontaneous action potential firing frequency.
- Single-compartment computational modeling of a CA1 pyramidal neuron to simulate the effects of E(GABA) depolarization on neuronal output.
- Analysis of spike latency, inter-spike intervals, and spike count in response to simulated synaptic input trains.
Main Results:
- Depolarizing E(GABA) by 24.7 mV significantly increased spontaneous firing frequency by 254% in cultured neurons.
- Computational models showed that depolarizing E(GABA) at both feedforward and feedback inhibitory synapses reduced spike latency more than acting alone.
- Weakening inhibition through E(GABA) depolarization enhanced the reliability of input-output transmission by increasing spike number and decreasing inter-spike intervals in a frequency-dependent manner.
- Simulated theta rhythm inputs demonstrated that depolarizing E(GABA) increased spiking during specific phases of the rhythm without altering the preferred firing phase.
Conclusions:
- Depolarization of the GABA reversal potential (E(GABA)) through inhibitory synaptic plasticity effectively weakens inhibition onto CA1 pyramidal neurons.
- This weakening of inhibition enhances neuronal excitability, leading to increased firing rates, reduced spike latency, and improved signal transmission reliability.
- The findings provide a mechanistic explanation for how inhibitory synaptic plasticity dynamically regulates CA1 pyramidal neuron output during network oscillations like theta rhythm.
