Pyramidal neuron conductances state and STDP (Delgado et al. 2010)

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Accession:144482
Neocortical neurons in vivo process each of their individual inputs in the context of ongoing synaptic background activity, produced by the thousands of presynaptic partners a typical neuron has. That background activity affects multiple aspects of neuronal and network function. However, its effect on the induction of spike-timing dependent plasticity (STDP) is not clear. Using the present biophysically-detailed computational model, it is not only able to replicate the conductance-dependent shunting of dendritic potentials (Delgado et al,2010), but show that synaptic background can truncate calcium dynamics within dendritic spines, in a way that affects potentiation more strongly than depression. This program uses a simplified layer 2/3 pyramidal neuron constructed in NEURON. It was similar to the model of Traub et al., J Neurophysiol. (2003), and consisted of a soma, an apical shaft, distal dendrites, five basal dendrites, an axon, and a single spine. The spine’s location was variable along the apical shaft (initial 50 μm) and apical. The axon contained an axon hillock region, an initial segment, segments with myelin, and nodes of Ranvier, in order to have realistic action potential generation. For more information about the model see supplemental material, Delgado et al 2010.
Reference:
1 . Delgado JY, Gómez-González JF, Desai NS (2010) Pyramidal neuron conductance state gates spike-timing-dependent plasticity. J Neurosci 30:15713-25 [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: Auditory cortex;
Cell Type(s): Neocortex L2/3 pyramidal GLU cell;
Channel(s): I Na,p; I Sodium; I Calcium; I Potassium; I_AHP;
Gap Junctions:
Receptor(s): AMPA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Action Potentials; STDP; Calcium dynamics; Conductance distributions; Audition;
Implementer(s): Gomez-Gonzalez, JF [jfcgomez at ull.edu.es]; Delgado JY, [jyamir at ucla.edu];
Search NeuronDB for information about:  Neocortex L2/3 pyramidal GLU cell; AMPA; NMDA; I Na,p; I Sodium; I Calcium; I Potassium; I_AHP;
TITLE decay of internal calcium concentration
:
: Internal calcium concentration calculated from calcium currents 
: and buffered by endogenous buffer and extrusion mechanism.
:
: Uses differential equations from Helmchen 1996
:dCa/dt = (dCa_T delta_t - (gamma*(dCa - Ca_rest)))/kb
: or dCa/dt = (dCa_T delta_t)/kb - (dCa - Ca_rest)/taur 
: with  taur = kb/gamma
:
: to add exogenous buffer kb = 1+kendo+kexo
: for OGB-1 kexo = concOGB1/kd = 200uM/0.2uM => kb=1020
: for OGB-6 kexo = concOGB6/kd = 200uM/3uM   => kb=80
:
: mod file was modified from original version (Destexhe 92)
: use diam/4 instead of depth to calculate [Ca]
: Units checked using "modlunit" -> factor 10000 needed in ca entry
:
: Written by B Kampa May 2006

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

NEURON {
	SUFFIX cad
	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 {
	diam		(um)
	depth	= .1	(um)		: no used anymore, uses diam/4 now
	taur	= 15	(ms)		: Ca decay from Sabatini 2002
	kb 	= 1			: buffer ratio from Sabatini 2002, Value of 20 when buffer is included
	cainf	= 60e-6(mM) 	: will be adjusted during init phase
	cai		(mM)
	gamma = 1.2	(1/ms)      : Value used by Kampa et. al.,
}

STATE {
	ca		(mM) <1e-5>
}

INITIAL {
	ca = cainf
	cai = ca
}

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

DERIVATIVE state { 
	depth = diam/4
	drive_channel =  - (10000) * ica / (2 * FARADAY * depth)
	if (drive_channel <= 0.) { drive_channel = 0. }	: cannot pump inward
	taur = kb/gamma
	ca' = (drive_channel/kb) + ((cainf-ca)/taur)
	cai = ca
}


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