Amyloid-beta effects on release probability and integration at CA3-CA1 synapses (Romani et al. 2013)

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Accession:147757
The role of amyloid beta (Aß) in brain function and in the pathogenesis of Alzheimer’s disease remains elusive. Recent publications reported that an increase in Aß concentration perturbs presynaptic release in hippocampal neurons, in particular by increasing release probability of CA3-CA1 synapses. The model predics how this alteration can affect synaptic plasticity and signal integration. The results suggest that the perturbation of release probability induced by increased Aß can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during Alzheimer’s disease.
Reference:
1 . Romani A, Marchetti C, Bianchi D, Leinekugel X, Poirazi P, Migliore M, Marie H (2013) Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses. Front Comput Neurosci 7:1 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Synapse;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal cell;
Channel(s): I Na,t; I A; I K; I M; I h; I Calcium; I_AHP;
Gap Junctions:
Receptor(s): AMPA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Synaptic Plasticity; Short-term Synaptic Plasticity; Facilitation; Depression; Synaptic Integration; Aging/Alzheimer`s;
Implementer(s): Bianchi, Daniela [danielabianchi12 -at- gmail.com]; Romani, Armando [romani.armando -at- gmail.com];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal cell; AMPA; I Na,t; I A; I K; I M; I h; I Calcium; I_AHP; Glutamate;
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RomaniEtAl2013
experiment
cad.mod *
cagk.mod *
cal.mod *
calH.mod *
car.mod *
cat.mod *
d3.mod *
h.mod *
kadist.mod *
kaprox.mod *
kca.mod *
kdr.mod *
km.mod *
na3.mod *
na3dend.mod *
na3notrunk.mod *
nap.mod *
nax.mod *
netstimmm.mod *
somacar.mod *
tmgsyn.mod
vecevent.mod
cell-setup.hoc
createNewSyn4.hoc
loadBasicModel.hoc
mosinit.hoc
session.ses
simulation.hoc
                            
TITLE  Na persistent channel
: used in distal oblique dendrites to assist Ca spike initiation  
: 
: modified to use CVode --Carl Gold 08/12/03
:  Updated by YiotaPoirazi   26/1/05

NEURON {
	SUFFIX nap
	USEION na READ ena WRITE ina
        RANGE  gnabar,vhalf, K, ina

}

UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)

}

PARAMETER {            
	K = 4.5            (1)      : slope of steady state variable
:	gnabar = 0.001e-2 (mho/cm2) : suggested conductance, 1 percent of the transient Na current
	gnabar = 0        (mho/cm2)
	vhalf  = -50.4    (mV)      : half potential
      
}	

ASSIGNED {
	v             (mV)
        ena           (mV)    
	ina           (mA/cm2)
        n_inf
        tau            (ms)
}

STATE { n }

BREAKPOINT {
	SOLVE states METHOD cnexp
	ina = gnabar*n*n*n*(v-ena)
}

INITIAL {
	rates(v)
	n = n_inf
}


DERIVATIVE states {
        rates(v)
        n' = (n_inf-n)/tau
}

PROCEDURE rates(v(mV)) {
	n_inf = 1 / (1 + (exp(vhalf - v)/K))
	tau =1
}




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