Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: an intracellular and computational study.
The effect of synaptic inputs on somatodendritic interactions during action potentials was investigated, in the cat, using in vivo intracellular recording and computational models of neocortical pyramidal cells. An array of 10 microelectrodes, each ending at a different cortical depth, was used to preferentially evoke synaptic inputs to different somatodendritic regions. Relative to action potentials evoked by current injection, spikes elicited by cortical microstimuli were reduced in amplitude and duration, with stimuli delivered at proximal (somatic) and distal (dendritic) levels evoking the largest and smallest decrements, respectively. When the inhibitory postsynaptic potential reversal was shifted to around -50 mV by recording with KCl pipettes, synaptically-evoked spikes were significantly less reduced than with potassium acetate or cesium acetate pipettes, suggesting that spike decrements are not only due to a shunt, but also to voltage-dependent effects. Computational models of neocortical pyramidal cells were built based on available data on the distribution of active currents and synaptic inputs in the soma and dendrites. The distribution of synapses activated by extracellular stimulation was estimated by matching the model to experimental recordings of postsynaptic potentials evoked at different depths. The model successfully reproduced the progressive spike amplitude reduction as a function of stimulation depth, as well as the effects of chloride and cesium. The model revealed that somatic spikes contain an important contribution from proximal dendritic sodium currents up to approximately 100 microm and approximately 300 microm from the soma under control and cesium conditions, respectively. Proximal inhibitory postsynaptic potentials can present this dendritic participation thus reducing the spike amplitude at the soma. The model suggests that the somatic spike amplitude and shape can be used as a "window" to infer the electrical participation of proximal dendrites. Thus, our results suggest that inhibitory postsynaptic potentials can control the participation of proximal dendrites in somatic sodium spikes.
Paré
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Département de Physiologie, Faculté de Médecine, Université Laval, Québec, Canada.
Lang
E J
EJ
Destexhe
A
A
D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D002415:Cats; D003712:Dendrites / Q000502:physiology*; D004553:Electric Conductivity; D004558:Electric Stimulation; D007473:Ion Channels / Q000502:physiology*; D008433:Mathematics; D008839:Microelectrodes; D008959:Models, Neurological; D019579:Neocortex / Q000166:cytology / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D017966:Pyramidal Cells / Q000166:cytology / Q000502:physiology*; D011930:Reaction Time; D015222:Sodium Channels / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
D015220:Calcium Channels; D007473:Ion Channels; D015221:Potassium Channels; D015222:Sodium Channels