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]
Citations  Citation Browser
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 GLU 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 GLU 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  H-current that uses Na ions

NEURON {
	SUFFIX h
        RANGE  gbar,vhalf, K, taun, ninf, g  
	USEION na READ ena WRITE ina      
:	NONSPECIFIC_CURRENT i
}

UNITS {
	(um) = (micrometer)
	(mA) = (milliamp)
	(uA) = (microamp)
	(mV) = (millivolt)
	(pmho) = (picomho)
	(mmho) = (millimho)
}



PARAMETER {              : parameters that can be entered when function is called in cell-setup
        dt             (ms)
	v              (mV)
        ena    = 50    (mV)
        eh     = -10   (mV)
	K      = 8.5   (mV)
	gbar   = 0     (mho/cm2)  : initialize conductance to zero
	:vhalf  = -90   (mV)       : half potential
      vhalf  = -81   (mV)       : half potential
     

}	


STATE {                : the unknown parameters to be solved in the DEs
	n
}

ASSIGNED {             : parameters needed to solve DE
	ina (mA/cm2)
	ninf
	taun (ms)
	g
}

        


INITIAL {               : initialize the following parameter using states()
	states()	
	n = ninf
	g = gbar*n
	ina = g*(v-eh)
}


BREAKPOINT {
	SOLVE h METHOD derivimplicit
	g = gbar*n
	ina = g*(v-eh)  
}

DERIVATIVE h {
	states()
        n' = (ninf - n)/taun
}

PROCEDURE states() {  
 
 	if (v > -30) {
	   taun = 1
	} else {
           :taun = 2*(1/(exp((v+145)/-17.5)+exp((v+16.8)/16.5)) + 5) :h activation tau
           taun = 5*(1/(exp((v+145)/-17.5)+exp((v+16.8)/16.5)) + 5) :h activation tau


	}  
         ninf = 1 - (1 / (1 + exp((vhalf - v)/K)))                  :steady state value
}