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
mod
infot.mod *
intf6.mod *
intfsw.mod *
misc.mod *
myfft.mod *
nstim.mod *
place.mod *
sampen.mod *
staley.mod *
stats.mod *
tsa.mod *
updown.mod *
vecst.mod *
bpf.h *
misc.h *
mkmod *
parameters.multi *
                            
: $Id: nstim.mod,v 1.24 2006/04/03 19:18:18 billl Exp $

NEURON	{ 
  ARTIFICIAL_CELL NStim
  RANGE interval, number, start, end
  RANGE noise,type,id
}

PARAMETER {
  interval	= 10 (ms) <1e-9,1e9>: time between spikes (msec)
  number	= 10 <0,1e9>	: number of spikes
  start		= 50 (ms)	: start of first spike
  noise		= 0 <0,1>	: amount of randomeaness (0.0 - 1.0)
  end		= 1e9 (ms)	: time to terminate train
}

ASSIGNED {
  event (ms)
  on
  endt (ms)
  type
  id
}

CONSTRUCTOR {
  VERBATIM 
  { if (ifarg(1)) { id= *getarg(1); } else { id= -1; }
    if (ifarg(2)) { type= *getarg(2); } else { type= 1; }
  }
  ENDVERBATIM
}

PROCEDURE seed (x) {
  set_seed(x)
}

INITIAL {
  on = 0
  if (noise < 0) { noise = 0 }
  if (noise > 1) { noise = 1 }
  if (interval <= 0.) { interval = .01 (ms) }
  if (start>=0 && number>0 && end>0) {
    event = start + invl(interval) - interval*(1. - noise)
    if (event < 0) { event = 0 }
    net_send(event, 3)
  }
}	

PROCEDURE init_sequence (t(ms)) {
  if (number > 0) {
    on = 1
    event = t
    endt = t + 1e-6 + interval*(number-1)
  }
}

FUNCTION invl (mean (ms)) (ms) {
  if (noise == 0) {
    invl = mean
  } else {
    invl = (1. - noise)*mean + noise*mean*exprand(1)
  }
}

NET_RECEIVE (w) {
  if (flag == 0) { : external event
    if (w > 0 && on == 0) { : turn on spike sequence
      init_sequence(t)
      net_send(0, 1)
    } else if (w < 0 && on == 1) { : turn off spiking
      on = 0
    }
  }
  if (flag == 3) { : from INITIAL
    if (on == 0) {
      init_sequence(t)
      net_send(0, 1)
    }
  }
  if (flag == 1 && on == 1) {
    net_event(t)
    event = event + invl(interval)
    if (event > endt || event > end) {
      on = 0
    } else {
      net_send(event - t, 1)
    }
  }
}

FUNCTION fflag () { fflag=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]

References and models cited by this paper

References and models that cite this paper

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