Abstract

Spike timing dependent plasticity (STDP) has been demonstrated in various neural systems of many
animals. It has been shown that STDP depends on the target and the location of the synapse and
is dynamically regulated by the activity of adjacent synapses, the presence of postsynaptic calcium,
presynaptic GABA inhibition or the action of neuromodulators. Recent experimental evidence has
reported that the profile of STDP in the CA1 pyramidal neuron can be classified into two types depending
on its dendritic location: (1) A symmetric STDP profile in the proximal to the soma dendrites, and (2)
an asymmetric one in the distal dendrites. Bicuculline application revealed that GABAA is responsible
for the symmetry of the STDP curve. We investigate via computer simulations how GABAA shapes the
STDP profile in the CA1 pyramidal neuron dendrites when it is driven by excitatory spike pairs (doublets).
The model constructed uses calcium as the postsynaptic signaling agent for STDP and is shown to
be consistent with classical long-term potentiation (LTP) and long-term depression (LTD) induced by
several doublet stimulation paradigms in the absence of inhibition. Overall, simulation results provide
computational evidence for the first time that the switch between the symmetrical and the asymmetrical
STDP operational modes is indeed due to GABA inhibition. Furthermore, gamma frequency inhibition and
not theta one is responsible for the transition from asymmetry-to-symmetry. The resulted symmetrical
STDP profile is centered at+10 ms with two distinct LTD tails at−10 and+40 ms. Finally, the asymmetryto-
symmetry transition is strongly dependent on the strength (conductance) of inhibition and its relative
onset with respect to pre- and postsynaptic spike stimulation.