Excitation and inhibition compete to control spiking during hippocampal ripples: intracellular study in behaving mice.
J. Neurosci.. 2014-12-03; 34(49): 16509-16517
DOI: 10.1523/JNEUROSCI.2600-14.2014
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1. J Neurosci. 2014 Dec 3;34(49):16509-17. doi: 10.1523/JNEUROSCI.2600-14.2014.
Excitation and inhibition compete to control spiking during hippocampal ripples:
intracellular study in behaving mice.
English DF(1), Peyrache A(1), Stark E(1), Roux L(1), Vallentin D(1), Long MA(2),
Buzsáki G(3).
Author information:
(1)NYU Neuroscience Institute, School of Medicine, and.
(2)NYU Neuroscience Institute, School of Medicine, and Center for Neural Science,
New York University, New York, New York 10016.
(3)NYU Neuroscience Institute, School of Medicine, and Center for Neural Science,
New York University, New York, New York 10016 .
High-frequency ripple oscillations, observed most prominently in the hippocampal
CA1 pyramidal layer, are associated with memory consolidation. The cellular and
network mechanisms underlying the generation of the rhythm and the recruitment of
spikes from pyramidal neurons are still poorly understood. Using intracellular,
sharp electrode recordings in freely moving, drug-free mice, we observed
consistent large depolarizations in CA1 pyramidal cells during sharp wave
ripples, which are associated with ripple frequency fluctuation of the membrane
potential (“intracellular ripple”). Despite consistent depolarization, often
exceeding pre-ripple spike threshold values, current pulse-induced spikes were
strongly suppressed, indicating that spiking was under the control of concurrent
shunting inhibition. Ripple events were followed by a prominent
afterhyperpolarization and spike suppression. Action potentials during and
outside ripples were orthodromic, arguing against ectopic spike generation, which
has been postulated by computational models of ripple generation. These findings
indicate that dendritic excitation of pyramidal neurons during ripples is
countered by shunting of the membrane and postripple silence is mediated by
hyperpolarizing inhibition.
Copyright © 2014 the authors 0270-6474/14/3316509-09$15.00/0.
DOI: 10.1523/JNEUROSCI.2600-14.2014
PMCID: PMC4252557
PMID: 25471587 [Indexed for MEDLINE]