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Intracellular correlate of EPSP‐spike potentiation in CA1 pyramidal neurons is controlled by GABAergic modulation
Author(s) -
Staff Nathan P.,
Spruston Nelson
Publication year - 2003
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.10129
Subject(s) - long term potentiation , neuroscience , excitatory postsynaptic potential , post tetanic potentiation , schaffer collateral , chemistry , postsynaptic potential , ltp induction , inhibitory postsynaptic potential , hippocampal formation , biology , biochemistry , receptor
The hippocampus has been used extensively as a model to study plastic changes in the brain'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 γ‐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. © 2003 Wiley‐Liss, Inc.