Letter To The Editor
Reply to Meredith and Groen: Role of AMPA and NMDA Receptors and
Back-Propagating Action Potentials in Spike Timing–Dependent Plasticity
Marco Fuenzalida,3David Ferna ´ndez de Sevilla,2Alejandro Couve,3and Washington Bun ˜o1
1Instituto Cajal, Consejo Superior de Investigaciones Cientı ´ficas;2Departamento de Anatomı ´a, Histologı ´a y Neurociencia, Facultad de
Medicina, Universidad Auto ´noma de Madrid, Madrid, Spain; and3Centro de Neurobiologı ´a y Plasticidad del Desarrollo, Facultad de
Ciencias, Universidad Valparaiso, Valparaiso, Chile
REPLY: In their letter Meredith and Groen (2010) emphasize the
role of GABAergic inhibition in controlling dendritic excitabil-
ity and depolarization in pyramidal neurons and, consequently,
in regulating the induction threshold of long-term potentiation
(LTP). In particular they stress the requirement of a burst of
postsynaptic back-propagating action potentials in the induc-
tion of spike timing–dependent plasticity (STDP) when inhi-
bition is functional in vitro. We totally agree with their view.
Indeed countless reports show that LTP is more readily in-
duced when dendritic excitability and depolarization are not
regulated by inhibition.
In our experiments GABAergic inhibition was blocked to
analyze the role of glutamatergic excitatory postsynaptic po-
tentials (EPSPs) and back-propagating action potentials in the
genesis of LTP by STDP (Fuenzalida et al. 2007, 2010). In
these reports a single action potential was sufficient to induce
LTP with STDP protocols.
We point out that recently Kwag and Paulsen (2009) re-
ported that an STDP-like protocol—which simulates the theta
rhythm and generates a single back-propagating action poten-
tial per theta cycle added to an EPSP—was able to induce LTP
not only with intact inhibition but also without inhibition in
CA1 pyramidal cells in vitro.
Therefore the degree of postsynaptic depolarization needed
for back-propagation of action potentials and dendritic Ca2?
spike generation required for STDP may be attained in special
conditions without the need of postsynaptic action potential
R E F E R E N C E S
Fuenzalida M, Ferna ´ndez de Sevilla D, Bun ˜o W. Changes of the EPSP
waveform regulate the temporal window for spike-timing-dependent plas-
ticity. J Neurosci 27: 11940–11948, 2007.
Fuenzalida M, Ferna ´ndez de Sevilla D, Couve A, Bun ˜o W. Role of AMPA
and NMDA receptors and back-propagating action potentials in spike
timing–dependent plasticity. J Neurophysiol 103: 47–54, 2010.
Kwag J, Paulsen O. The timing of external input controls the sign of plasticity
at local synapses. Nat Neurosci 12: 1219–1221, 2009.
Meredith RM, Groen MR. Inhibition of action potential backpropagation
during postnatal development of the hippocampus. J Neurophysiol 103:
Address for reprint requests and other correspondence: W. Bun ˜o, Instituto
Cajal, Consejo Superior de Investigaciones Cientı ´ficas, Avenida Doctor Arce
37, 28002 Madrid, Spain (E-mail: email@example.com).
J Neurophysiol 103: 2314, 2010.
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