Glutamate mediated dendritic and somatic plateau potentials in cortical L5 pyr cells (Gao et al '20)

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Accession:249705
Our model was built on a reconstructed Layer 5 pyramidal neuron of the rat medial prefrontal cortex, and constrained by 4 sets of experimental data: (i) voltage waveforms obtained at the site of the glutamatergic input in distal basal dendrite, including initial sodium spikelet, fast rise, plateau phase and abrupt collapse of the plateau; (ii) a family of voltage traces describing dendritic membrane responses to gradually increasing intensity of glutamatergic stimulation; (iii) voltage waveforms of backpropagating action potentials in basal dendrites (Antic, 2003); and (iv) the change of backpropagating action potential amplitude in response to drugs that block Na+ or K+ channels (Acker and Antic, 2009). Both, synaptic AMPA/NMDA and extrasynaptic NMDA inputs were placed on basal dendrites to model the induction of local regenerative potentials termed "glutamate-mediated dendritic plateau potentials". The active properties of the cell were tuned to match the voltage waveform, amplitude and duration of experimentally observed plateau potentials. The effects of input location, receptor conductance, channel properties and membrane time constant during plateau were explored. The new model predicted that during dendritic plateau potential the somatic membrane time constant is reduced. This and other model predictions were then tested in real neurons. Overall, the results support our theoretical framework that dendritic plateau potentials bring neuronal cell body into a depolarized state ("UP state"), which lasts 200 - 500 ms, or more. Plateau potentials profoundly change neuronal state -- a plateau potential triggered in one basal dendrite depolarizes the soma and shortens membrane time constant, making the cell more susceptible to action potential firing triggered by other afferent inputs. Plateau potentials may allow cortical pyramidal neurons to tune into ongoing network activity and potentially enable synchronized firing, to form active neural ensembles.
Reference:
1 . Gao PP, Graham JW, Zhou WL, Jang J, Angulo SL, Dura-Bernal S, Hines ML, Lytton W, Antic SD (2020) Local Glutamate-Mediated Dendritic Plateau Potentials Change the State of the Cortical Pyramidal Neuron. J Neurophysiol [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Dendrite; Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Prefrontal cortex (PFC); Neocortex;
Cell Type(s): Neocortex L5/6 pyramidal GLU cell;
Channel(s): I A; I K; I h; I K,Ca;
Gap Junctions:
Receptor(s): Glutamate; NMDA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON; Python;
Model Concept(s): Action Potentials; Active Dendrites; Calcium dynamics; Axonal Action Potentials; Dendritic Bistability; Detailed Neuronal Models; Membrane Properties; Synaptic Integration;
Implementer(s): Antic, Srdjan [antic at neuron.uchc.edu]; Gao, Peng [peng at uchc.edu];
Search NeuronDB for information about:  Neocortex L5/6 pyramidal GLU cell; NMDA; Glutamate; I A; I K; I h; I K,Ca; Glutamate;
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plateau-potentials
mod
x86_64
ampa.mod
ca.mod *
Ca_HVA.mod *
Ca_LVAst.mod *
Cad.mod
CaDynamics_E2.mod *
CaT.mod
epsp.mod *
gabaa.mod
gabab.mod
glutamate.mod
h_kole.mod *
h_migliore.mod
Ih.mod
IL.mod
Im.mod *
K_Pst.mod *
K_Tst.mod *
kadist.mod
kaprox.mod
kBK.mod *
kv.mod *
na.mod
Nap_Et2.mod *
NaTa_t.mod *
NaTs2_t.mod *
NMDA.mod
NMDAeee.mod
NMDAmajor.mod
PlateauConductance.mod
SK_E2.mod *
SKv3_1.mod *
vecstim.mod
vmax.mod *
ghk.inc
                            
COMMENT
26 Ago 2002 Modification of original channel to allow variable time step and to correct an initialization error.
    Done by Michael Hines(michael.hines@yale.e) and Ruggero Scorcioni(rscorcio@gmu.edu) at EU Advance Course in Computational Neuroscience. Obidos, Portugal

ca.mod
Uses fixed eca instead of GHK eqn

HVA Ca current
Based on Reuveni, Friedman, Amitai and Gutnick (1993) J. Neurosci. 13:
4609-4621.

Author: Zach Mainen, Salk Institute, 1994, zach@salk.edu

ENDCOMMENT

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

NEURON {
	SUFFIX ca
	USEION ca READ eca WRITE ica
	RANGE m, h, gca, gbar
	RANGE minf, hinf, mtau, htau
	GLOBAL q10, temp, tadj, vmin, vmax, vshift
}

PARAMETER {
	gbar = 0.1   	(pS/um2)	: 0.12 mho/cm2
	vshift = 0	(mV)		: voltage shift (affects all)

	cao  = 2.5	(mM)	        : external ca concentration
	cai		(mM)
						
	temp = 23	(degC)		: original temp 
	q10  = 2.3			: temperature sensitivity

	v 		(mV)
	dt		(ms)
	celsius		(degC)
	vmin = -120	(mV)
	vmax = 100	(mV)
}


UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(pS) = (picosiemens)
	(um) = (micron)
	FARADAY = (faraday) (coulomb)
	R = (k-mole) (joule/degC)
	PI	= (pi) (1)
} 

ASSIGNED {
	ica 		(mA/cm2)
	gca		(pS/um2)
	eca		(mV)
	minf 		hinf
	mtau (ms)	htau (ms)
	tadj
}
 

STATE { m h }

INITIAL { 
	trates(v+vshift)
	m = minf
	h = hinf
}

BREAKPOINT {
        SOLVE states METHOD cnexp
        gca = tadj*gbar*m*m*h
	ica = (1e-4) * gca * (v - eca)
} 

LOCAL mexp, hexp

:PROCEDURE states() {
:        trates(v+vshift)      
:        m = m + mexp*(minf-m)
:        h = h + hexp*(hinf-h)
:	VERBATIM
:	return 0;
:	ENDVERBATIM
:}

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

PROCEDURE trates(v) {  
                      
        
        TABLE minf, hinf, mtau, htau 
	DEPEND  celsius, temp
	
	FROM vmin TO vmax WITH 199

	rates(v): not consistently executed from here if usetable == 1

:        tinc = -dt * tadj

:        mexp = 1 - exp(tinc/mtau)
:        hexp = 1 - exp(tinc/htau)
}


PROCEDURE rates(vm) {  
        LOCAL  a, b

        tadj = q10^((celsius - temp)/10)

	a = 0.055*(-27 - vm)/(exp((-27-vm)/3.8) - 1)
	b = 0.94*exp((-75-vm)/17)
	
	mtau = 1/tadj/(a+b)
	minf = a/(a+b)

		:"h" inactivation 

	a = 0.000457*exp((-13-vm)/50)
	b = 0.0065/(exp((-vm-15)/28) + 1)

	htau = 1/tadj/(a+b)
	hinf = a/(a+b)
}

FUNCTION efun(z) {
	if (fabs(z) < 1e-4) {
		efun = 1 - z/2
	}else{
		efun = z/(exp(z) - 1)
	}
}

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