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Dendritic spikes in apical dendrites of neocortical layer 2/3 pyramidal neurons

MPG-Autoren
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Larkum,  Matthew E.
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Waters,  David Jack
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sakmann,  Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Helmchen,  Fritjof
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Zitation

Larkum, M. E., Waters, D. J., Sakmann, B., & Helmchen, F. (2007). Dendritic spikes in apical dendrites of neocortical layer 2/3 pyramidal neurons. The Journal of Neuroscience, 27(34), 8999-9008. doi:10.1523/JNEUROSCI.1717-07.2007.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002C-ABF7-E
Zusammenfassung
Layer 2/3 (L2/3) pyramidal neurons are the most abundant cells of the neocortex. Despite their key position in the cortical microcircuit, synaptic integration in dendrites of L2/3 neurons is far less understood than in L5 pyramidal cell dendrites, mainly because of the difficulties in obtaining electrical recordings from thin dendrites. Here we directly measured passive and active properties of the apical dendrites of L2/3 neurons in rat brain slices using dual dendritic-somatic patch-clamp recordings and calcium imaging. Unlike L5 cells, L2/3 dendrites displayed little sag in response to long current pulses, which suggests a low density of I(h) in the dendrites and soma. This was also consistent with a slight increase in input resistance with distance from the soma. Brief current injections into the apical dendrite evoked relatively short (half-width 2-4 ms) dendritic spikes that were isolated from the soma for near-threshold currents at sites beyond the middle of the apical dendrite. Regenerative dendritic potentials and large concomitant calcium transients were also elicited by trains of somatic action potentials (APs) above a critical frequency (130 Hz), which was slightly higher than in L5 neurons. Initiation of dendritic spikes was facilitated by backpropagating somatic APs and could cause an additional AP at the soma. As in L5 neurons, we found that distal dendritic calcium transients are sensitive to a long-lasting block by GABAergic inhibition. We conclude that L2/3 pyramidal neurons can generate dendritic spikes, sharing with L5 pyramidal neurons fundamental properties of dendritic excitability and control by inhibition.