| | Models | Description |
| 1. |
Calcium influx during striatal upstates (Evans et al. 2013)
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"...
To
investigate the mechanisms that underlie the relationship between
calcium and AP timing, we have developed a realistic biophysical
model of a medium spiny neuron (MSN).
...
Using this model, we found that either the slow inactivation of
dendritic sodium channels (NaSI) or the calcium inactivation of
voltage-gated calcium channels (CDI) can cause high calcium corresponding
to early APs and lower calcium corresponding to later APs.
We found that only CDI can account for the experimental observation
that sensitivity to AP timing is dependent on NMDA receptors.
Additional simulations demonstrated a mechanism by which MSNs
can dynamically modulate their sensitivity to AP timing and show that
sensitivity to specifically timed pre- and postsynaptic pairings (as in
spike timing-dependent plasticity protocols) is altered by the timing of
the pairing within the upstate.
…" |
| 2. |
NMDA subunit effects on Calcium and STDP (Evans et al. 2012)
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Effect of NMDA subunit on spike timing dependent plasticity. |
| 3. |
VTA dopamine neuron (Tarfa, Evans, and Khaliq 2017)
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In our model of a midbrain VTA dopamine neuron, we show that the decay kinetics of the A-type potassium current can control the timing of rebound action potentials. |
