Superior paraolivary nucleus neuron (Kopp-Scheinpflug et al. 2011)

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Accession:139657
This is a model of neurons in the brainstem superior paraolivary nucleus (SPN), which produce very salient offset firing during sound stimulation. Rebound offset firing is triggered by IPSPs coming from the medial nucleus of the trapezoid body (MNTB). This model shows that AP firing can emerge from inhibition through integration of large IPSPs, driven by an extremely negative chloride reversal potential, combined with a large hyperpolarization- activated non-specific cationic current (IH), with a secondary contribution from a T-type calcium conductance (ITCa). As a result, tiny gaps in sound stimuli of just 3-4ms can elicit reliable APs that signal such brief offsets.
Reference:
1 . Kopp-Scheinpflug C, Tozer AJ, Robinson SW, Tempel BL, Hennig MH, Forsythe ID (2011) The sound of silence: ionic mechanisms encoding sound termination. Neuron 71:911-25 [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:
Cell Type(s): Superior paraolivary nucleus neuron;
Channel(s): I T low threshold; I h;
Gap Junctions:
Receptor(s): Glycine;
Gene(s): HCN Cnga1;
Transmitter(s): Glycine;
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Action Potentials; Rebound firing;
Implementer(s): Hennig, Matthias H [mhhennig at gmail.com];
Search NeuronDB for information about:  Glycine; I T low threshold; I h; Glycine;
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Kopp-Scheinpflug2011
index.html
ht.mod *
lt.mod *
lva.mod
mhh_Gfluct.mod
netstims.mod *
sjg_ih.mod
sjg_na.mod
trigstim.mod *
allgraphs.hoc
conductance_noise.hoc
current_inj.hoc
mosinit.hoc
run_spn_model.hoc
simcontrols.hoc
spn_neuron.hoc
spnmodel1.png
synapses.hoc
                            
COMMENT
This T-type calcium current was originally reported in Wang XJ et al 1991
This file supplies a version of this current identical to Quadroni and Knopfel 1994
except for gbar and Erev (see notes below).
ENDCOMMENT

NEURON {
	SUFFIX lva
	: NONSPECIFIC_CURRENT i
	USEION ca WRITE  ica
	RANGE Erev,g, gbar, i
	RANGE k, alpha_1, alpha_2, beta_1, beta_2, V_s, taum, minf
	GLOBAL mytaum, myminf
}

UNITS {
	(S)	=	(siemens)
	(mV)	=	(millivolt)
	(mA)	=	(milliamp)
}

PARAMETER {
	gbar = 0.4e-3	(S/cm2) < 0, 1e9 > : Quadroni and Knopfel use 166e-6
	Erev = 120 (mV)	: orig from Wang XJ et al 1991 was 120
	: note: Quadroni and Knopfel 1994 table 1 use 80 instead
	V_s = 0 (mV)	: used to describe effect of changing extracellular [Ca]
			: 0 corresponds to [Ca]outside = 3 mM (p 841)
}

ASSIGNED {
	ica (mA/cm2)
	i (mA/cm2)
	v (mV)
	g (S/cm2)
	k
	alpha_1 (1)
	alpha_2	(1)
	beta_1 (1)
	beta_2 (1)
	mytaum (ms)
	myminf (1)
}

STATE {	m h d }

BREAKPOINT {
	SOLVE states METHOD cnexp
	g = gbar * m^3 * h
	ica = g * (v - Erev)
	i = ica	: used only to display the value of the current (section.i_lva(0.5))
}

INITIAL {
	LOCAL C, E
	: assume that v has been constant for a long time
	: (derivable from rate equations in DERIVATIVE block at equilibrium)
	rates(v)
	m = minf(v)
	: h and d are intertwined so more complex than above equilib state for m
	C =  beta_1 / alpha_1
	E =  alpha_2 / beta_2
	h = E / (E * C + E + C)
	d = 1 - (1 + C) * h
}

DERIVATIVE states{ 
	rates(v)
	m' = (minf(v) - m)/taum(v)		: alpham(v) * (1 - m) - betam(v) * m
	h' = alpha_1 * (1 - h - d) - beta_1 * h
	d' =  beta_2 * (1 - h - d) - alpha_2 * d
}

FUNCTION minf(Vm (mV)) (1) {
	minf = 1.0 / (1.0 + exp(-(Vm + V_s + 63)/7.8))
	myminf = minf
}

FUNCTION taum(Vm (mV)) (ms) {
	taum = (1.7 + exp( -(Vm + V_s + 28.8)/13.5 )) / (1.0 + exp( -(Vm + V_s + 63)/7.8) )
	mytaum = taum
}

PROCEDURE rates(Vm(mV)) { LOCAL tau_2
	k = (0.25 + exp((Vm + V_s + 83.5)/6.3))^0.5 - 0.5
	tau_2 = 240.0 / (1 + exp((Vm + V_s + 37.4)/30)) : same as tau2 p 842 equation (15)
	alpha_1 = exp( -(Vm + V_s +160.3)/17.8 )	: p 842  equation (14)
	beta_1 = k * alpha_1
	alpha_2 = 1.0 / ( tau_2 * (1.0 + k) )
	beta_2 = k * alpha_2
}

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