NMDA receptor saturation (Chen et al 2001)

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Accession:7988
Experiments and modeling reported in the paper Chen N, Ren J, Raymond LA, and Murphy T (2001) support the hypothesis that glutamate has a relatively lower potency at NMDARs than previously thought from agonist application under equilibrium conditions. Further information and reprint requests are available from Dr T.H. Murphy thmurphy at interchange.ubc.ca
Reference:
1 . Chen N, Ren J, Raymond LA, Murphy TH (2001) Changes in agonist concentration dependence that are a function of duration of exposure suggest N-methyl-D-aspartate receptor nonsaturation during synaptic stimulation. Mol Pharmacol 59:212-9 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Synapse;
Brain Region(s)/Organism:
Cell Type(s):
Channel(s):
Gap Junctions:
Receptor(s): NMDA;
Gene(s): NR2A GRIN2A; NR2B GRIN2B;
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Ion Channel Kinetics;
Implementer(s): Murphy, Tim H [THMurphy at interchange.ubc.ca];
Search NeuronDB for information about:  NMDA; Glutamate;
TITLE transmitter release


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

NEURON {
	SUFFIX glurel
	RANGE dur, cmax, T, Twait
}

UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(mM) = (milli/liter)
}

PARAMETER {
	dur = 2000 (ms)
	cmax = 1 (mM)
	Twait = 10 (ms)
}

ASSIGNED {
	T (mM)
}


INITIAL {
	T = 0
}

BREAKPOINT {
        if(t < Twait) {
                T = 0
        }
	
        if ( (t >= Twait)&&(t <= (Twait + dur))) {
		T = cmax
        }
	  if (t > (Twait + dur)) {
		T = 0
	  }

}


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