"... 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. …"
Model Type: Neuron or other electrically excitable cell
Region(s) or Organism(s): Striatum
Cell Type(s): Neostriatum medium spiny direct pathway GABA cell
Currents: I Na,t; I L high threshold; I N; I A; I K; I K,Ca; I A, slow; I Krp; I R
Genes: Cav1.3 CACNA1D; Cav1.2 CACNA1C; Cav2.2 CACNA1B
Model Concept(s): Oscillations; STDP; Calcium dynamics
Simulation Environment: GENESIS
Implementer(s): Evans, Rebekah [Rebekah.Evans at nih.gov]
References:
Evans RC, Maniar YM, Blackwell KT. (2013). Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates. Journal of neurophysiology. 110 [PubMed]