Coincident glutamatergic depolarization effects on Cl- dynamics (Lombardi et al, 2021)

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Accession:266823
"... we used compartmental biophysical models of Cl- dynamics simulating either a simple ball-and-stick topology or a reconstructed CA3 neuron. These computational experiments demonstrated that glutamatergic co-stimulation enhances GABA receptor-mediated Cl- influx at low and attenuates or reverses the Cl- efflux at high initial [Cl-]i. The size of glutamatergic influence on GABAergic Cl--fluxes depends on the conductance, decay kinetics, and localization of glutamatergic inputs. Surprisingly, the glutamatergic shift in GABAergic Cl--fluxes is invariant to latencies between GABAergic and glutamatergic inputs over a substantial interval..."
Reference:
1 . Lombardi A, Jedlicka P, Luhmann HJ, Kilb W (2021) Coincident glutamatergic depolarizations enhance GABAA receptor-dependent Cl- influx in mature and suppress Cl- efflux in immature neurons PLOS Comp Bio
Model Information (Click on a link to find other models with that property)
Model Type: Synapse; Dendrite;
Brain Region(s)/Organism:
Cell Type(s): Hippocampus CA3 pyramidal GLU cell;
Channel(s):
Gap Junctions:
Receptor(s): GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Short-term Synaptic Plasticity; Synaptic Plasticity; Chloride regulation;
Implementer(s): Jedlicka, Peter [jedlicka at em.uni-frankfurt.de]; Kilb, Werner [wkilb at uni-mainz.de];
Search NeuronDB for information about:  Hippocampus CA3 pyramidal GLU cell; GabaA; AMPA; NMDA; Gaba; Glutamate;
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_For Zip -Neuron-Models_AMPA-GABA
Suppl3_Real_Cell_Cl_1GDP_tonicGABA_Var_Cl_var-gAMPA
cldif_CA3_NKCC1_HCO3.mod *
gabaA_Cl_HCO3.mod *
tonic.mod *
vecevent.mod *
Cell1_Cl_HCO3_tonicGABA.hoc
GDP_Cl_HCO3_All_short.ses *
Single_GDP_tonicGABA_gGABA-0.789-nGABA-534_Div_gAMPA_Div_Cl.hoc
start_Single_GDP_tonicGABA_gGABA-0.789-nGABA-534_Div_gAMPA_Div_Cl.hoc
                            
COMMENT
Modified Proddutur A, Yu J, Elgammal FS, Santhakumar V (2013)
Tonic Inhibition with changing Cl- concentration
ENDCOMMENT

NEURON{
	SUFFIX tonic
	USEION cl READ ecl WRITE icl VALENCE -1
	NONSPECIFIC_CURRENT ihco3
	RANGE  icl, leak, P, e,ihco3,ehco3 
	RANGE P, HCO3e, HCO3i, i
}

UNITS {
	(uS)  = (micromho)
	(nA)  = (nanoamp)
	(mV)  = (millivolt)
	(mM)    = (milli/liter)
	F 	  = (faraday) (coulombs)
	R     = (k-mole)  (joule/degC)
}


PARAMETER {
	leak    = 0.01 (siemens/cm2) <0, 1e9>
	P    = 0.18		: HCO3/Cl relative permeability
	celsius = 31    (degC)
	HCO3e   = 26	(mM)	: extracellular HCO3- concentration
	HCO3i   = 16	(mM)	: intracellular HCO3- concentration
}

ASSIGNED{
	icl (milliamp/cm2)
	i (milliamp/cm2)
	ihco3 (milliamp/cm2)
	v	(mV)		: postsynaptic voltage 
	e	(mV)		: reversal potential for GABAR	
	ecl	(mV)		: equilibrium potential for Cl-
    ehco3	(mV)		: equilibrium potential for HCO3-	
}

INITIAL { 

	ehco3 = log(HCO3i/HCO3e)*(1000)*(celsius + 273.15)*R/F
	e = P*ehco3 + (1-P)*ecl
}


BREAKPOINT {
	icl = (1-P)*leak*(v-ecl)
	ihco3 = P*leak*(v-ehco3)
	i = icl + ihco3
	e = P*ehco3 + (1-P)*ecl
}

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