Intracortical synaptic potential modulation by presynaptic somatic potential (Shu et al. 2006, 2007)

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Accession:135787
" ... Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca21- dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals."
References:
1 . Shu Y, Duque A, Yu Y, Haider B, McCormick DA (2007) Properties of action-potential initiation in neocortical pyramidal cells: evidence from whole cell axon recordings. J Neurophysiol 97:746-60 [PubMed]
2 . Shu Y, Hasenstaub A, Duque A, Yu Y, McCormick DA (2006) Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential. Nature 441:761-5 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Axon;
Brain Region(s)/Organism:
Cell Type(s): Neocortex V1 pyramidal corticothalamic L6 cell;
Channel(s): I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I_AHP; I_KD;
Gap Junctions:
Receptor(s): GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Detailed Neuronal Models; Action Potentials; Synaptic Integration;
Implementer(s):
Search NeuronDB for information about:  Neocortex V1 pyramidal corticothalamic L6 cell; GabaA; AMPA; NMDA; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I_AHP; I_KD;
/
ShuEtAl20062007
readme.txt
ampa5.mod *
ca.mod *
cad.mod
caL3d.mod *
capump.mod
gabaa5.mod *
Gfluct.mod *
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iahp.mod *
iahp2.mod *
ih.mod
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NMDA_Mg.mod *
nmda5.mod *
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2006_Nature.pdf
2006_Nature_supp.pdf
best_full_axon_decay.hoc
best_full_axon_spike_init.hoc
best_full_axon_spike_init.hoc'A=0
decay_constant.gif
for_decay.m
for_initiation.m
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j4a_removedendrite.hoc
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mosinit.hoc
spike_initiation.gif
                            
TITLE hyperpolarization-activated current (H-current) 

COMMENT
	Two distinct activation gates are assumed with the same asymptotic 
	opening values, a fast gate (F) and a slow gate (S). The following 
	kinetic scheme is assumed

	s0  --(Alpha)--> s1 + n Cai  --(k1)--> s2
           <--(Beta)---             <--(k2)--
 
 	f0  --(Alpha)--> f1 + n Cai  --(k1)--> f2
           <--(Beta)---             <--(k2)--

	where s0/f0, s1/f1, and s2/f2 are resp. fraction of closed slow/fast 
	gates, fraction of open unbound slow/fast gates, and fraction of open 
	calcium-bound slow/fast	gates, n is taken 2, and k1 = k2*C where 
	C = (cai/cac)^n and cac is the critical value at which Ca2+ binding 
	is half-activated.
	
	The total current is computed according

	ih = ghbar * (s1+s2) * (f1+f2) * (v-eh)

        *********************************************
        reference:      Destexhe, Babloyantz & Sejnowski (1993)
			Biophys.J. 65, 1538-1552
        found in:       thalamocortical neurons
        *********************************************
	Maxim Bazhenov's first mod file
        Rewritten for MyFirstNEURON by Arthur Houweling 
ENDCOMMENT

INDEPENDENT {t FROM 0 TO 1 WITH 1 (ms)}

NEURON {
	SUFFIX iH
	USEION h READ eh WRITE ih VALENCE 1
	USEION ca READ cai
        RANGE ghbar, tau_s, tau_f, tau_c, ih
	GLOBAL cac
}

UNITS {
	(mA) 	= (milliamp)
	(mV) 	= (millivolt)
	(molar)	= (1/liter)
	(mM) 	= (millimolar)
}

PARAMETER {
	v		(mV)
	cai		(mM)
	celsius		(degC)
:	eh	= -63	(mV)
	eh	= -43	(mV)
	ghbar	= 4e-6	(mho/cm2)
:	ghbar	= 4e-5	(mho/cm2)
	cac 	= 5e-4	(mM)
}

STATE {
	s1			: fraction of open unbound slow gates 
	s2 			: fraction of open calcium-bound slow gates
	f1	 		: fraction of open unbound fast gates
	f2			: fraction of open calcium-bound fast gates
}

ASSIGNED {
	ih		(mA/cm2)
        h_inf
        tau_s		(ms)	: time constant slow gate
        tau_f 		(ms)	: time constant fast gate
	tau_c		(ms)	: time constant calcium binding 
        alpha_s		(1/ms)
        alpha_f 	(1/ms)
        beta_s 		(1/ms)
        beta_f		(1/ms)
	C
	k2		(1/ms)
	tadj
	s0			: fraction of closed slow gates 
	f0			: fraction of closed fast gates
}

BREAKPOINT { 
	SOLVE states METHOD derivimplicit : see http://www.neuron.yale.edu/phpBB/viewtopic.php?f=28&t=592
	ih = ghbar * (s1+s2) * (f1+f2) * (v-eh)
}

UNITSOFF
DERIVATIVE states { 
	evaluate_fct(v,cai)

	s1' = alpha_s*s0 - beta_s*s1 + k2*(s2-C*s1)
        f1' = alpha_f*f0 - beta_f*f1 + k2*(f2-C*f1)
        s2' = -k2*(s2-C*s1)
        f2' = -k2*(f2-C*f1)

        s0 = 1-s1-s2
        f0 = 1-f1-f2
}

INITIAL {
	: Q10 assumed to be 3
	tadj = 3^((celsius-35.5)/10)
	evaluate_fct(v,cai)

	s1 = alpha_s / (beta_s+alpha_s*(1+C))
	s2 = alpha_s*C / (beta_s+alpha_s*(1+C))
	s0 = 1-s1-s2
	f1 = alpha_f / (beta_f+alpha_f*(1+C))
	f2 = alpha_f*C / (beta_f+alpha_f*(1+C))
	f0 = 1-f1-f2

	tau_c = 1 / (1+C) / k2	: for plotting purposes
}

PROCEDURE evaluate_fct( v(mV), cai(mM)) {
	h_inf = 1 / (1+exp((v+68.9)/6.5))
	tau_s = exp((v+183.6)/15.24) / tadj
	tau_f = exp((v+158.6)/11.2) / (1+exp((v+75)/5.5)) / tadj

	alpha_s = h_inf / tau_s 
	alpha_f = h_inf / tau_f 
	beta_s = (1-h_inf) / tau_s
	beta_f = (1-h_inf) / tau_f

        C = cai*cai/(cac*cac)
	k2 = 4e-4 * tadj	
}	
UNITSON







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