Electrostimulation to reduce synaptic scaling driven progression of Alzheimers (Rowan et al. 2014)

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Accession:154096
"... As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. ... The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, ... Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. ... "
Reference:
1 . Rowan MS, Neymotin SA, Lytton WW (2014) Electrostimulation to reduce synaptic scaling driven progression of Alzheimer's disease. Front Comput Neurosci 8:39 [PubMed]
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 V1 pyramidal corticothalamic L6 cell; Neocortex V1 pyramidal intratelencephalic L2-5 cell; Neocortex V1 interneuron basket PV cell; Neocortex fast spiking (FS) interneuron; Neocortex spiny stellate cell; Neocortex spiking regular (RS) neuron; Neocortex spiking low threshold (LTS) neuron;
Channel(s):
Gap Junctions:
Receptor(s): GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON; Python;
Model Concept(s): Long-term Synaptic Plasticity; Aging/Alzheimer`s; Deep brain stimulation; Homeostasis;
Implementer(s): Lytton, William [billl at neurosim.downstate.edu]; Neymotin, Sam [samn at neurosim.downstate.edu]; Rowan, Mark [m.s.rowan at cs.bham.ac.uk];
Search NeuronDB for information about:  Neocortex V1 pyramidal corticothalamic L6 cell; Neocortex V1 pyramidal intratelencephalic L2-5 cell; Neocortex V1 interneuron basket PV cell; GabaA; AMPA; NMDA; Gaba; Glutamate;
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RowanEtAl2014
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//  $Header: /usr/site/nrniv/simctrl/hoc/RCS/local.hoc,v 1.15 2003/02/13 15:32:06 billl Exp $
//
//  This file contains local modifications to nrnoc.hoc and default.hoc
//
//  Users should not edit nrnoc.hoc or default.hoc.  Any local 
//  changes to these files should be made in this file.

// ------------------------------------------------------------
//* MODIFICATIONS TO NRNOC.HOC
// The procedures declared here will overwrite any duplicate
// procedures in nrnoc.hoc.
// ------------------------------------------------------------

//*MODIFICATIONS TO DEFAULT.HOC
//
// Vars added here may not be handled properly within nrnoc.hoc
//------------------------------------------------------------

//** String defaults

//** Simulation defaults

long_dt     = .001      // msec 

objref sfunc,tmpfile
sfunc = hoc_sf_   // needed to use is_name()
tmpfile = new File()  // check for existence before opening a user's local.hoc file

proc write_comment () {
  tmpfile.aopen("index")
  tmpfile.printf("%s\n",$s1)
  tmpfile.close()  
}

func asin () { return atan($1/sqrt(1-$1*$1)) }
func acos () { return atan(sqrt(1-$1*$1)/$1) }

objref mt[2]
mt = new MechanismType(0)
proc uninsert_all () { local ii
  forall for ii=0,mt.count()-1 {
    mt.select(ii)
    mt.selected(temp_string_)
    if (strcmp(temp_string_,"morphology")==0) continue
    if (strcmp(temp_string_,"capacitance")==0) continue
    if (strcmp(temp_string_,"extracellular")==0) continue
    if (sfunc.substr(temp_string_,"_ion")!=-1) continue
    mt.remove()
    // print ii,temp_string_
  }
}

condor_run = 0  // define for compatability

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