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;
BK.g *
CaT.g *
gaba_channel.g *
KaF.g *
KaFnew.g *
Kir.g *
NaF.g *
NaFslowinact.g *
SK.g *
tabchanforms.g *
/***************************		MS Model, Version 9.1 *********************
**************************** 	    	Kirg 			*********************
						Rebekah Evans updated 3/22/12 

function make_KIR_channel

 //initial parameters for making tab channel
	float Erev = -0.09
	int m_power = 1
    int h_power = 0
//units are mV, ms
	float mA_rate = 1e-5
	float mA_slope = -11
	float mB_rate = 1.2
	float mB_vhalf = 30
	float mB_slope = -50

	str path = "KIR_channel" 

    float xmin  = -0.15  /* minimum voltage we will see in the simulation */     // V
    float xmax  = 0.05  /* maximum voltage we will see in the simulation */      // V
    int xdivsFiner = 4000
    int c = 0

   float increment = (xmax - xmin)*1e3/xdivsFiner  // mV
   float x = -150.00 
    create tabchannel {path} 
    call {path} TABCREATE X {xdivsFiner} {xmin} {xmax}  // activation   gate

    /* Defines the powers of m Hodgkin-Huxley equation*/
    setfield {path} Ek {Erev} Xpower {m_power} Ypower {h_power}

    /* fill the tables with the values of tau and minf/hinf
     * calculated from tau and minf/hinf
	for (c = 0; c < {xdivsFiner} + 1; c = c + 1)
		float m_alpha = {exp_form {mA_rate} {mA_slope} {-x}}
		float m_beta = {sig_form {mB_rate} {mB_vhalf} {mB_slope} {x}}
		float mtau = {1e-3}/{{m_alpha}+{m_beta}}

		setfield {path} X_A->table[{c}] {({mtau}*2)/{qfactorKir}}
		setfield {path} X_B->table[{c}] {{m_alpha}/({m_alpha}+{m_beta})}
		x = x + increment
    tweaktau {path} X

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