@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}
}
@article {45915,
	title = {Dendritic spikes as a mechanism for cooperative long-term potentiation.},
	journal = {Nature},
	volume = {418},
	year = {2002},
	month = {2002 Jul 18},
	pages = {326-31},
	abstract = {<p>Strengthening of synaptic connections following coincident pre- and postsynaptic activity was proposed by Hebb as a cellular mechanism for learning. Contemporary models assume that multiple synapses must act cooperatively to induce the postsynaptic activity required for hebbian synaptic plasticity. One mechanism for the implementation of this cooperation is action potential firing, which begins in the axon, but which can influence synaptic potentiation following active backpropagation into dendrites. Backpropagation is limited, however, and action potentials often fail to invade the most distal dendrites. Here we show that long-term potentiation of synapses on the distal dendrites of hippocampal CA1 pyramidal neurons does require cooperative synaptic inputs, but does not require axonal action potential firing and backpropagation. Rather, locally generated and spatially restricted regenerative potentials (dendritic spikes) contribute to the postsynaptic depolarization and calcium entry necessary to trigger potentiation of distal synapses. We find that this mechanism can also function at proximal synapses, suggesting that dendritic spikes participate generally in a form of synaptic potentiation that does not require postsynaptic action potential firing in the axon.</p>
},
	keywords = {Action Potentials, Animals, Axons, Calcium, Calcium Signaling, Dendrites, Excitatory Postsynaptic Potentials, Long-Term Potentiation, Pyramidal Cells, Rats, Rats, Wistar, Synapses, Theta Rhythm},
	issn = {0028-0836},
	doi = {10.1038/nature00854},
	author = {Golding, Nace L and Staff, Nathan P and Spruston, Nelson}
}
