Shaping of STDP curve by interneuron and Ca2+ dynamics
Lynsey McCabe
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2
Paolo Di Prodi
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2
Bernd Porr
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2
Florentin Wrgtter
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1
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References 1. Magee JC, Johnston D: A synaptically controlled, associative sig- nal for Hebbian plasticity in hippocampal neurons. Science 1997
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275:209-213. 2. Markram H, Lubke J, Frotscher M
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Sakmann B: Regulation of syn- aptic efficacy by coincidence of postsynaptic Aps and EPSPs.
Science 1997, 275:213-215. 3. Hebb DO:
The organization of behaviour: A neuropsycholog- ical study. Wiley Interscience
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New York; 1949. 4. Porr B, Saudargiene A
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Worgotter F: Analytical solution of spike- timing dependent plasticity based on synaptic biophysics. In Advances in neural information processing systems
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16, 2004 Cambridge MA: MIT Press. 5. Aihara Y, Abiru Y, Yamazaki Y, Wantanbe H, Fukushima Y, Tsukada M: The relation between spike-timing dependent plasticity and Ca
1
Bernstein Center for Computational Neuroscience, University of Gottingen, Bunsenstr. 10 (at the MPI)
,
D-37073 Gottingen
,
Germany
2
Department of Electronics and Electrical Engineering, University of Glasgow
,
Glasgow G12 8LT
,
UK
and is already a topic of interest in the research of schizophrenia.
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Spike-timing-dependent-plasticity (STDP)[1,2] is a
special form of Hebbian learning [3] where the relative
timing of post- and presynaptic activity determines the
change in synaptic weight. More familiarly, the
postsynaptic and presynaptic activity correspond respectively to
the derivative of the membrane potential Vm and the
NMDA channel activation [4]. We present a model where
the postsynaptic activity is modelled by the derivative of
the Ca2+ concentration. Using a model of a pyramidal cell,
attached interneuron and detailed Ca2+ dynamics, we
show that the classical STDP curve is greatly altered, in
particular, that long term depression (LTD) is markedly
reduced [5] while LTP remains close to the original
expected weight-change curve. In addition to this we have
shown that by reducing the NMDA activity in the circuit
model there is a noticeable change in the LTD/LTP
magnitude in the STDP weight-change curve. This modification
causes two effects; it reduces plasticity in the excitatory
neuron but also reduces inhibition on the excitatory
neuron. Therefore we show that by decreasing NMDA activity
there is a clear reduction in LTD and LTP. This appears
much like the "classical" STDP curve albeit scaled down in
ratio to the reduced NMDA activity. In this study we have
shown that the inhibitory interneuron reduces the LTD
part of the STDP weight change curve. The more
inhibition seen, the less LTD in the excitatory neuron. Thus, a
hypofunction of inhibitory neurons will lead to more LTD
in cortical structures and ultimately to less cortical
activity. This hypofunction could be a possible mechanism of
how administration of the NMDA antagonist PCP causes
cortical hypoactivity[6] after a time lapse of a few days,
(...truncated)