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. …"
1 . Evans RC, Maniar YM, Blackwell KT (2013) Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates. J Neurophysiol 110:1631-45 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Striatum;
Cell Type(s): Neostriatum medium spiny direct pathway GABA cell;
Channel(s): I Na,t; I L high threshold; I N; I A; I K; I K,Ca; I A, slow; I Krp; I R;
Gap Junctions:
Receptor(s): AMPA; NMDA; Gaba;
Gene(s): Cav1.3 CACNA1D; Cav1.2 CACNA1C; Cav2.2 CACNA1B;
Simulation Environment: GENESIS;
Model Concept(s): Oscillations; STDP; Calcium dynamics;
Implementer(s): Evans, Rebekah [Rebekah.Evans at];
Search NeuronDB for information about:  Neostriatum medium spiny direct pathway GABA cell; AMPA; NMDA; Gaba; I Na,t; I L high threshold; I N; I A; I K; I K,Ca; I A, slow; I Krp; I R;

/***************************		MS Model, Version 8	*********************
**************************** 	      MScellqfact.g 	*********************
	Avrama Blackwell
	Wonryull Koh
	Rebekah Evans
	Tom Sheehan	

	MS_cell.g has only one externally called function: make_MS_cell. That primary 
	function uses the services of the following two local subroutines:

include MScell/MScellshort.g                 //MScell without synapses
include MScell/SynParamsCtx.g               //parameters on synaptic channels
include MScell/channels/nmda_channel.g   //function to make nmda channel, either GHK or not, in library
include MScell/channels/synaptic_channel.g // function to make non nmda synaptic channels in library
include MScell/AddSynapticChannels.g	// contains functions to add channels to compartments
include MScell/AddCaSpines.g		//includes calcium channels 
include MScell/CaDifshellSpine.g        //new calcium dynamics (difshell objects w/buffers etc)
include MScell/spines.g           //creates spines, puts channels & calcium in spines

function make_MS_cell_spine (cellname,pfile)
   str cellname,pfile

   str CompName

   make_MS_cell {cellname} {pfile}

	//************* create synaptic channels in library *********
	pushe /library

  	make_synaptic_channel  {AMPAname} {AMPAtau1} {AMPAtau2} {AMPAgmax} {EkAMPA}
  	make_NMDA_channel    {NMDAname} {EkNMDA} {Kmg} {NMDAtau2} {NMDAgmax} {ghk_yesno}
	make_synaptic_channel  {GABAname} {GABAtau1} {GABAtau2} {GABAgmax} {EkGABA}


        pope {cellname}
   //********************* end synaptic channels in library **************

    /* these functions needs to be modified.  The following 3 should be optional
        1. allow for putting synaptic channels on spines in library
        2. use new calcium functions and optionally create such in spine
        3. possibly vdep channels in the spines

	add_spines_evenly  {cellname} spine   26.1e-6   300.0e-6       0.1


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