Mechanisms of magnetic stimulation of central nervous system neurons (Pashut et al. 2011)

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Accession:138321
Transcranial magnetic stimulation (TMS) is a widely applied tool for probing cognitive function in humans and is one of the best tools for clinical treatments and interfering with cognitive tasks. Surprisingly, while TMS has been commercially available for decades, the cellular mechanisms underlying magnetic stimulation remain unclear. Here we investigate these mechanisms using compartmental modeling. We generated a numerical scheme allowing simulation of the physiological response to magnetic stimulation of neurons with arbitrary morphologies and active properties. Computational experiments using this scheme suggested that TMS affects neurons in the central nervous system (CNS) primarily by somatic stimulation.
Reference:
1 . Pashut T, Wolfus S, Friedman A, Lavidor M, Bar-Gad I, Yeshurun Y, Korngreen A (2011) Mechanisms of magnetic stimulation of central nervous system neurons. PLoS Comput Biol 7:e1002022 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Neocortex V1 L6 pyramidal corticothalamic GLU cell; Squid axon;
Channel(s):
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON; MATLAB;
Model Concept(s): Action Potential Initiation; Magnetic stimulation;
Implementer(s): Korngreen, Alon [alon.korngreen at gmail.com]; Pashut, Tamar [tamar.pashut at gmail.com];
Search NeuronDB for information about:  Neocortex V1 L6 pyramidal corticothalamic GLU cell;
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pashut2011
TwoDimensions
Neuron
cells
cad2.mod *
child.mod *
childa.mod *
epsp.mod *
it2.mod *
kaprox.mod *
kca.mod *
km.mod *
kv.mod *
na.mod *
SlowCa.mod *
xtra.mod *
alon.ses
BACModel.hoc
BACModel_mag.hoc
Display.ses *
magstim.hoc
                            
TITLE decay of internal calcium concentration
:
: Internal calcium concentration due to calcium currents and pump.
: Differential equations.
:
: Simple model of ATPase pump with 3 kinetic constants (Destexhe 92)
:     Cai + P <-> CaP -> Cao + P  (k1,k2,k3)
: A Michaelis-Menten approximation is assumed, which reduces the complexity
: of the system to 2 parameters: 
:       kt = <tot enzyme concentration> * k3  -> TIME CONSTANT OF THE PUMP
:	kd = k2/k1 (dissociation constant)    -> EQUILIBRIUM CALCIUM VALUE
: The values of these parameters are chosen assuming a high affinity of 
: the pump to calcium and a low transport capacity (cfr. Blaustein, 
: TINS, 11: 438, 1988, and references therein).  
:
: Units checked using "modlunit" -> factor 10000 needed in ca entry
:
: VERSION OF PUMP + DECAY (decay can be viewed as simplified buffering)
:
: All variables are range variables
:
: adopted from the lower model by AS 102199
:
: This mechanism was published in:  Destexhe, A. Babloyantz, A. and 
: Sejnowski, TJ.  Ionic mechanisms for intrinsic slow oscillations in
: thalamic relay neurons. Biophys. J. 65: 1538-1552, 1993)
:
: Written by Alain Destexhe, Salk Institute, Nov 12, 1992
:

INDEPENDENT {t FROM 0 TO 1 WITH 1 (ms)}

NEURON {
	SUFFIX cad2
	USEION ca READ ica, cai WRITE cai
	RANGE ca
	GLOBAL depth,cainf,taur
}

UNITS {
	(molar) = (1/liter)			: moles do not appear in units
	(mM)	= (millimolar)
	(um)	= (micron)
	(mA)	= (milliamp)
	(msM)	= (ms mM)
	FARADAY = (faraday) (coulomb)
}


PARAMETER {
	depth	= .1	(um)		: depth of shell
	taur	= 80	(ms)		: rate of calcium removal, changed from 200 to 80 (H.Markram)
	cainf	= 100e-6(mM)
	cai		(mM)
}

STATE {
	ca		(mM) 
}

INITIAL {
	ca = cainf
}

ASSIGNED {
	ica		(mA/cm2)
	drive_channel	(mM/ms)
}
	
BREAKPOINT {
	SOLVE state METHOD euler
}

DERIVATIVE state { 

	drive_channel =  - (10000) * ica / (2 * FARADAY * depth)
	if (drive_channel <= 0.) { drive_channel = 0. }	: cannot pump inward

	ca' = drive_channel + (cainf-ca)/taur
	cai = ca
}








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