Deconstruction of cortical evoked potentials generated by subthalamic DBS (Kumaravelu et al 2018)

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Accession:244262
"... High frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) suppresses parkinsonian motor symptoms and modulates cortical activity. ... Cortical evoked potentials (cEP) generated by STN DBS reflect the response of cortex to subcortical stimulation, and the goal was to determine the neural origin of cEP using a two-step approach. First, we recorded cEP over ipsilateral primary motor cortex during different frequencies of STN DBS in awake healthy and unilateral 6-OHDA lesioned parkinsonian rats. Second, we used a biophysically-based model of the thalamocortical network to deconstruct the neural origin of the cEP. The in vivo cEP included short (R1), intermediate (R2) and long-latency (R3) responses. Model-based cortical responses to simulated STN DBS matched remarkably well the in vivo responses. R1 was generated by antidromic activation of layer 5 pyramidal neurons, while recurrent activation of layer 5 pyramidal neurons via excitatory axon collaterals reproduced R2. R3 was generated by polysynaptic activation of layer 2/3 pyramidal neurons via the cortico-thalamic-cortical pathway. Antidromic activation of the hyperdirect pathway and subsequent intracortical and cortico-thalamo-cortical synaptic interactions were sufficient to generate cEP by STN DBS, and orthodromic activation through basal ganglia-thalamus-cortex pathways was not required. These results demonstrate the utility of cEP to determine the neural elements activated by STN DBS that might modulate cortical activity and contribute to the suppression of parkinsonian symptoms."
Reference:
1 . Kumaravelu K, Oza CS, Behrend CE, Grill WM (2018) Model-based deconstruction of cortical evoked potentials generated by subthalamic nucleus deep brain stimulation. J Neurophysiol 120:662-680 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism: Neocortex; Thalamus;
Cell Type(s): Neocortex M1 L6 pyramidal corticothalamic GLU cell; Neocortex M1 L5B pyramidal pyramidal tract GLU cell; Neocortex M1 L4 stellate GLU cell; Hodgkin-Huxley neuron; Neocortex layer 4 neuron; Neocortex fast spiking (FS) interneuron; Neocortex primary motor area pyramidal layer 5 corticospinal cell;
Channel(s): I Na,p; I K; I Sodium; I_KD; I Calcium; I T low threshold; I L high threshold; I_AHP;
Gap Junctions: Gap junctions;
Receptor(s): AMPA; Gaba; NMDA;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Deep brain stimulation; Evoked LFP;
Implementer(s): Kumaravelu, Karthik [kk192 at duke.edu];
Search NeuronDB for information about:  Neocortex M1 L6 pyramidal corticothalamic GLU cell; Neocortex M1 L5B pyramidal pyramidal tract GLU cell; Neocortex M1 L4 stellate GLU cell; AMPA; NMDA; Gaba; I Na,p; I L high threshold; I T low threshold; I K; I Sodium; I Calcium; I_AHP; I_KD; Gaba; Glutamate;
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cEP_stndbs_4.5hz
cells
dat
data_stndbs_4.5hz
hoc
net
readme.txt
alphasyndiffeq.mod *
alphasynkin.mod *
alphasynkint.mod *
ampa.mod *
ar.mod *
cad.mod *
cal.mod *
cat.mod *
cat_a.mod *
gabaa.mod *
iclamp_const.mod *
k2.mod *
ka.mod *
ka_ib.mod *
kahp.mod *
kahp_deeppyr.mod *
kahp_slower.mod *
kc.mod *
kc_fast.mod *
kdr.mod *
kdr_fs.mod *
km.mod *
naf.mod *
naf_tcr.mod *
naf2.mod *
nap.mod *
napf.mod *
napf_spinstell.mod *
napf_tcr.mod *
par_ggap.mod
pulsesyn.mod *
rampsyn.mod *
rand.mod *
ri.mod *
traub_nmda.mod *
balanal.hoc *
balcomp.hoc *
cell_templates.hoc *
clear.hoc *
finit.hoc *
fortmap.hoc *
gidcell.hoc *
gidcell.ses *
Iintra.dat
init_stndbs_4.5hz.hoc
manage_setup_stndbs_4.5hz.hoc
onecell.hoc *
onecell.ses *
perf.dat
prcellstate.hoc *
printcon.hoc *
run_stndbs_4.5hz.q
spkplt.hoc *
vclampg.hoc *
vcompclamp.hoc *
vcompsim.hoc *
                            
TITLE Calcium low threshold T type current version a for RD Traub 2005

COMMENT
	This current is found in the model deepLTS cells
	Traub made this model modifying Huguenard and Prince 1992 as
	appeared on Destexhe et al 1996 (in vivo in vitro ...)
	Modification by Tom Morse for Traub et al 2005
	modified from
	Implementation by Maciej Lazarewicz 2003 (mlazarew@seas.upenn.edu)
	RD Traub, J Neurophysiol 89:909-921, 2003
ENDCOMMENT

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

UNITS { 
	(mV) = (millivolt) 
	(mA) = (milliamp) 
}
 
NEURON { 
	SUFFIX cat_a
	NONSPECIFIC_CURRENT i   : not causing [Ca2+] influx
	RANGE gbar, i, m, h, alphah, betah 	: m,h, alphah, betah for comparison with FORTRAN
}

PARAMETER { 
	gbar = 0.0 	(mho/cm2)
	v 		(mV)  
}
 
ASSIGNED { 
	i 		(mA/cm2) 
	minf hinf 	(1)
	mtau (ms) htau 	(ms) 
	alphah (/ms) betah	(/ms)
}
 
STATE {
	m h
}

BREAKPOINT { 
	SOLVE states METHOD cnexp 
	i = gbar * m * m * h * ( v - 125 ) 
	alphah = hinf/htau
	betah = 1/htau - alphah
}
 
INITIAL { 
	settables(v) 
:	m  = minf
	h  = hinf
	m  = 0
} 

DERIVATIVE states { 
	settables(v) 
	m' = ( minf - m ) / mtau 
	h' = ( hinf - h ) / htau
}

UNITSOFF 

PROCEDURE settables(v(mV)) { 
	TABLE minf, mtau,hinf, htau FROM -120 TO 40 WITH 641
        minf  = 1 / ( 1 + exp( ( -v - 52 ) / 7.4 ) )
        mtau  = 1 + .33 / ( exp( ( v + 27.0 ) / 10.0 ) + exp( ( - v - 102 ) / 15.0 ) )

        hinf  = 1 / ( 1 + exp( ( v + 80 ) / 5 ) )
        htau = 28.30 +.33 / (exp(( v + 48.0)/ 4.0) + exp( ( -v - 407.0) / 50.0 ) )

}

UNITSON