Fronto-parietal visuospatial WM model with HH cells (Edin et al 2007)

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Accession:98017
1) J Cogn Neurosci: 3 structural mechanisms that had been hypothesized to underlie vsWM development during childhood were evaluated by simulating the model and comparing results to fMRI. It was concluded that inter-regional synaptic connection strength cause vsWM development. 2) J Integr Neurosci: Given the importance of fronto-parietal connections, we tested whether connection asymmetry affected resistance to distraction. We drew the conclusion that stronger frontal connections are beneficial. By comparing model results to EEG, we concluded that the brain indeed has stronger frontal-to-parietal connections than vice versa.
Reference:
1 . Edin F, Macoveanu J, Olesen P, Tegnér J, Klingberg T (2007) Stronger synaptic connectivity as a mechanism behind development of working memory-related brain activity during childhood. J Cogn Neurosci 19:750-60 [PubMed]
2 . Edin F, Klingberg T, Stödberg T, Tegnér J (2007) Fronto-parietal connection asymmetry regulates working memory distractibility. J Integr Neurosci 6:567-96 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism: Neocortex;
Cell Type(s): Neocortex U1 L2/6 pyramidal intratelencephalic GLU cell; Abstract Wang-Buzsaki neuron;
Channel(s):
Gap Junctions: Gap junctions;
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Working memory; Attractor Neural Network;
Implementer(s):
Search NeuronDB for information about:  Neocortex U1 L2/6 pyramidal intratelencephalic GLU cell;
COMMENT
Summating nmda synapse. This synapse is modified from the standard
Neuron exp2syn mechanism. Changes are restricted to a Mg2+ block.
It can be used to represent several different non-summating synapses
provided their firing rate is not too large and provided they are
close spatially.

Author: Fredrik Edin, 2003
Address: freedin@nada.kth.se

Original comment:
------------------------------------------------------
Two state kinetic scheme synapse described by rise time tau1,
decay time constant tau2, and peak conductance gtrig.
Decay time MUST be greater than rise time.

The solution of A->G->bath with rate constants 1/tau1 and 1/tau2 is
 A = a*exp(-t/tau1) and
 G = a*tau2/(tau2-tau1)*(-exp(-t/tau1) + exp(-t/tau2))
	where tau1 < tau2

(Notice if tau1 -> 0 then we have just single exponential decay.)
The factor is evaluated in the
initial block such that the peak conductance is gtrig.

Because the solution is a sum of exponentials, the
coupled equations can be solved as a pair of independent equations
by the more efficient cnexp method.

Specify an incremental delivery event
(synapse starts delay after the source
crosses threshold. gtrig is incremented by the amount specified in
the delivery event, onset will be set to the proper time)
--------------------------------------------------------
ENDCOMMENT

NEURON {
	POINT_PROCESS nmdaSUM
	RANGE tau1, tau2, e, i
	NONSPECIFIC_CURRENT i

	RANGE g, s
	GLOBAL total
}

UNITS {
	(nA) = (nanoamp)
	(mV) = (millivolt)
	(umho) = (micromho)
}

PARAMETER {
	tau1 	= .1	(ms)
	tau2 	= 10	(ms)
	e	= 0	(mV)
	mag     = 1     (mM)
	eta	= 3.57  (mM)
	gamma   = 0.062 (/mV)
}

ASSIGNED {
	v (mV)
	i (nA)
	g (umho)
	s
	factor
	total (umho)
}

STATE {
	A (umho)
	B (umho)
}

INITIAL {
	LOCAL tp
	total = 0
	A = 0
	B = 0
	tp = (tau1*tau2)/(tau2 - tau1) * log(tau2/tau1)
	factor = -exp(-tp/tau1) + exp(-tp/tau2)
	factor = 1/factor
}

BREAKPOINT {
	SOLVE state METHOD cnexp
	s = B - A
	g = s * 1(umho) /(1 + mag * exp( - (gamma * v)) / eta )
	i = g * (v - e)
}

DERIVATIVE state {
	A' = -A/tau1
	B' = -B/tau2
}

NET_RECEIVE(weight (umho)) {
	state_discontinuity(A, A + weight*factor)
	state_discontinuity(B, B + weight*factor)
	total = total+weight
}