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A decrease in firing threshold observed after induction of the EPSP-spike (E-S) component of long-term potentiation
L E Chavez-Noriega1, J V Halliwell, T V Bliss
1Division of Neurophysiology and Neuropharmacology, National Institute for Medical Research, Mill Hill, London, U.K.
Experimental Brain Research
|January 1, 1990
Summary
Long-term potentiation (LTP) involves synaptic and EPSP-Spike (E-S) components. This study reveals that E-S potentiation in CA1 pyramidal neurons is linked to decreased neuronal firing thresholds, not just synaptic changes.
Area of Science:
- Neuroscience
- Cellular and Molecular Neuroscience
Background:
- Long-term potentiation (LTP) is a key mechanism for learning and memory.
- LTP comprises distinct synaptic and EPSP-Spike (E-S) components.
- The underlying mechanisms of the E-S component remain incompletely understood.
Purpose of the Study:
- To investigate the intracellular correlates of E-S potentiation.
- To test the hypothesis that increased postsynaptic excitability underlies E-S potentiation.
Main Methods:
- Extracellular and intracellular recordings in CA1 pyramidal neurons.
- Synaptic activation from stratum radiatum.
- Analysis of synaptic potentials and neuronal firing thresholds.
Main Results:
- LTP was associated with a decreased amplitude and slope of excitatory postsynaptic potentials (PSPs) required for firing.
- A reduction in the threshold for direct neuronal activation was observed.
- These excitability changes were specific to E-S potentiation and not the synaptic component.
Conclusions:
- Distinct mechanisms underlie the synaptic and E-S components of LTP.
- Reduced neuronal discharge threshold is a key factor in tetanus-induced E-S potentiation.
- Increased excitation/inhibition ratio and reduced GABAA-mediated inhibition may contribute to E-S potentiation.