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Evaluation of passive component of propagating AP in mossy fiber axons (Ohura & Kamiya 2018)

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"Action potentials propagating along axons are often followed by prolonged afterdepolarization (ADP) lasting for several tens of milliseconds. Axonal ADP is thought to be an important factor in modulating the fidelity of spike propagation during repetitive firings. However, the mechanism as well as the functional significance of axonal ADP remain unclear, partly due to inaccessibility to small structures of axon for direct electrophysiological recordings. Here, we examined the ionic and electrical mechanisms underlying axonal ADP using whole-bouton recording from mossy fiber terminals in mice hippocampal slices. ADP following axonal action potentials was strongly enhanced by focal application of veratridine, an inhibitor of Na+ channel inactivation. In contrast, tetrodotoxin (TTX) partly suppressed ADP, suggesting that a Na+ channel–dependent component is involved in axonal ADP. The remaining TTX-resistant Na+ channel–independent component represents slow capacitive discharge reflecting the shape and electrical properties of the axonal membrane. We also addressed the functional impact of axonal ADP on presynaptic function. In paired-pulse stimuli, we found that axonal ADP minimally affected the peak height of subsequent action potentials, although the rising phase of action potentials was slightly slowed, possibly due to steady-state inactivation of Na+ channels by prolonged depolarization. Voltage clamp analysis of Ca2+ current elicited by action potential waveform commands revealed that axonal ADP assists short-term facilitation of Ca2+ entry into the presynaptic terminals. Taken together, these data show that axonal ADP maintains reliable firing during repetitive stimuli and plays important roles in the fine-tuning of short-term plasticity of transmitter release by modulating Ca2+ entry into presynaptic terminals."
1 . Ohura S, Kamiya H (2018) Sodium Channel-Dependent and -Independent Mechanisms Underlying Axonal Afterdepolarization at Mouse Hippocampal Mossy Fibers. eNeuro [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Axon;
Brain Region(s)/Organism: Hippocampus; Dentate gyrus;
Cell Type(s): Dentate gyrus granule GLU cell;
Channel(s): I Sodium; I K;
Gap Junctions:
Simulation Environment: NEURON;
Model Concept(s): Action Potentials;
Implementer(s): Kamiya, Haruyuki [kamiya at];
Search NeuronDB for information about:  Dentate gyrus granule GLU cell; I K; I Sodium;
TITLE: mfbhh.mod    Sodium and potassium channels of mossy fiber boutons

  This is the Hodgkin-Huxley treatment for the set of sodium, potassium, 
  and leakage channels found in the hippocampal mossy fiber boutons.
  ("Presynaptic action potential amplification by voltage-gated Na+ channels in 
  hippocampal mossy fiber boutons" Neuron 45:405-417 (2005).)
  Global activation & inactivation shift; make vShift (Donnan) global by 12 mV.  
  "Engel & Jonas model (2005)" reconstructed by Kamiya 
        (mA) = (milliamp)
        (mV) = (millivolt)
	    (S) = (siemens)
? interface
        SUFFIX mfbhh
        USEION na READ ena WRITE ina
        USEION k READ ek WRITE ik
        RANGE gnabar, gkbar, gl, el, gna, gk
        GLOBAL minf, hinf, ninf, rinf, mtau, htau, ntau, rtau
	THREADSAFE : assigned GLOBALs will be per thread
        gnabar = 0.05 (S/cm2)
        gkbar = 0.036 (S/cm2)
        gl = .0001 (S/cm2)
        el = -81 (mV)
        m h n r
        v (mV)
        celsius (degC)
        ena (mV)
        ek (mV)

	    gna (S/cm2)
	    gk (S/cm2)
        ina (mA/cm2)
        ik (mA/cm2)
        il (mA/cm2)
        minf hinf ninf rinf
	mtau (ms) htau (ms) ntau (ms) rtau (ms)
? currents
        SOLVE states METHOD cnexp
    gna = gnabar*m*m*m*h
	ina = gna*(v - ena)
    gk = gkbar*n*n*n*n*r
	ik = gk*(v - ek)      
    il = gl*(v - el)
	m = minf
	h = hinf
	n = ninf
    r = rinf

? states
DERIVATIVE states {  
        m' = (minf-m)/mtau
        h' = (hinf-h)/htau
        n' = (ninf-n)/ntau
        r' = (rinf-r)/rtau
:LOCAL q10

? rates
PROCEDURE rates(v(mV)) {  :Computes rate and other constants at current v.
                      :Call once from HOC to initialize inf at resting v.
        LOCAL  alpha, beta, sum, q10
        TABLE minf, mtau, hinf, htau, ninf, ntau, rinf, rtau DEPEND celsius FROM -100 TO 100 WITH 200

        q10 = 3^((celsius - 23)/10)
	 :"m" sodium activation system
        alpha = 93.8285*vtrap(-(v-12-105.023),17.7094)
        beta =  0.168396*exp(-(v-12)/23.2707)
        sum = alpha + beta
	    mtau = 1/(q10*sum)
        minf = alpha/sum
     :"h" sodium inactivation system
        alpha = 0.000354*exp(-(v-12)/18.706)
        beta = 6.62694/(exp(-(v-12+17.6769)/13.3097)+1)
        sum = alpha + beta
	    htau = 1/(q10*sum)
        hinf = alpha/sum
     :"n" potassium activation system
        alpha = .01*vtrap(-(v+55),10) 
        beta = .125*exp(-(v+65)/80)
	    sum = alpha + beta
        ntau = 1/(q10*sum)
        ninf = alpha/sum
     :"r" potassium inactivation system
        alpha = 0.0000256077*exp(-v/45.4217)
        beta = 0.0330402/(exp(-(v+45.6599)/2.30235)+1)  :Recombinant Kv1.4
        sum = alpha + beta
	    rtau = 1/(q10*sum)
        rinf = alpha/sum
FUNCTION vtrap(x,y) {  :Traps for 0 in denominator of rate eqns.
        if (fabs(x/y) < 1e-6) {
                vtrap = y*(1 - x/y/2)
                vtrap = x/(exp(x/y) - 1)

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