@article {45894,
	title = {Intracellular correlate of EPSP-spike potentiation in CA1 pyramidal neurons is controlled by GABAergic modulation.},
	journal = {Hippocampus},
	volume = {13},
	year = {2003},
	month = {2003},
	pages = {801-5},
	abstract = {<p>The hippocampus has been used extensively as a model to study plastic changes in the brain{\textquoteright}s neural circuitry. Immediately after high-frequency stimulation to hippocampal Schaffer collateral axons, a dramatic change occurs in the relationship between the presynaptic CA3 and the postsynaptic CA1 pyramidal neurons. For a fixed excitatory postsynaptic potential (EPSP), there arises an increased likelihood of action potential generation in the CA1 pyramidal neuron. This phenomenon is called EPSP-spike (E-S) potentiation. We explored E-S potentiation, using patch-clamp techniques in the hippocampal slice preparation. A specific protocol was developed to measure the action potential probability for a given synaptic strength, which allowed us to quantify the amount of E-S potentiation for a single neuron. E-S potentiation was greatest when gamma-aminobutyric acid (GABA)ergic inhibition was intact, suggesting that modulation of inhibition is a major aspect of E-S potentiation. Expression of E-S potentiation also correlated with a reduced action-potential threshold, which was greatest when GABAergic inhibition was intact. Conditioning stimuli produced a smaller threshold reduction when inhibition was blocked, but some reduction also occurred in the absence of a conditioning stimulus. Together, these results suggest that E-S potentiation is caused primarily through a reduction of GABAergic inhibition, leading to larger EPSPs and reduced action potential threshold. Our findings do not rule out, however, the possibility that modulation of voltage-gated conductances also contributes to E-S potentiation.</p>
},
	keywords = {Action Potentials, Animals, Dendrites, Excitatory Postsynaptic Potentials, GABA Antagonists, GABA-A Receptor Antagonists, GABA-B Receptor Antagonists, gamma-Aminobutyric Acid, Hippocampus, In Vitro Techniques, Intracellular Fluid, Neural Inhibition, Neuronal Plasticity, Patch-Clamp Techniques, Pyramidal Cells, Rats, Rats, Wistar, Receptors, GABA-A, Receptors, GABA-B, Synaptic Transmission},
	issn = {1050-9631},
	doi = {10.1002/hipo.10129},
	author = {Staff, Nathan P and Spruston, Nelson}
}
