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Comment
. 2009 Aug;12(8):959-60.
doi: 10.1038/nn0809-959.

Who let the spikes out?

Chris G Dulla  1 , John R Huguenard
Affiliations
Comment

Who let the spikes out?

Chris G Dulla et al. Nat Neurosci. 2009 Aug.
No abstract available

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Figures

Figure
Figure
A New Blueprint for Action Potential Initiation in the Axon Initial Segment. Excitatory neurotransmission onto the dendrites of a layer V pyramidal cell (green oval) causes depolarization of the post-synaptic Vm. This local depolarization moves electrotonically towards the soma (green arrows), where it can be shunted by inhibitory GABAergic neurotransmission (red oval). However, with sufficient synaptic input, depolarization will spread beyond the soma and into the axon initial segment (inset). Once incoming depolarization (green arrow) reaches the AIS (1) it will first enter an area rich in NaV1.2 (blue). These channels are the “cautious” high-threshold subtype so depolarization will pass through without rapidly activating the NaV1.2 channels (green arrows with white dashes). When the wave of depolarization reaches the “trigger-happy” low-threshold NaV1.6 channels (yellow), however, they will quickly open (2) and initiate an inward sodium current (red arrow). This will rapidly depolarize Vm in the distal AIS, activating other nearby NaV1.6 channels causing a chain reaction of NaCh opening and initiating a forward-propagating action potential (3). Because NaV1.2 channels were bypassed by the initial synaptic depolarization they are available for activation, rather than in an inactivated state. When NaV1.6 channels open they drive NaV1.2 channel activation (4), inducing a secondary wave of inward sodium currents and initiating a back-propagating action potential (5). Because NaV1.6 channels will be in their inactive state, NaV1.2 channel opening will not induce a secondary forward-propagating AP.
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References

    1. Catterall WA. Localization of sodium channels in cultured neural cells. J Neurosci. 1981;1:777–783. - PMC - PubMed
    1. Coombs JS, Curtis DR, Eccles JC. The generation of impulses in motoneurones. J Physiol. 1957;139:232–249. - PMC - PubMed
    1. Katz B. The Release of Neural Transmitter Substances. Liverpool University Press; Liverpool, England: 1969.
    1. Markram H, Lubke J, Frotscher M, Sakmann B. Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs. Science. 1997;275:213–215. - PubMed
    1. Magee JC, Johnston D. A synaptically controlled, associative signal for Hebbian plasticity in hippocampal neurons. Science. 1997;275:209–213. - PubMed

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