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Physiological synaptic signals initiate sequential spikes at soma of cortical pyramidal neurons.

Ge R, Qian H, Wang JH - Mol Brain (2011)

Bottom Line: In dual recordings from the soma vs. axon, the signals recorded in vivo induce somatic spikes with higher capacity, which is associated with lower somatic thresholds and shorter refractory periods mediated by voltage-gated sodium channels.The introduction of these parameters from the soma and axon into NEURON model simulates sequential spikes being somatic in origin.Physiological signals integrated from synaptic inputs primarily trigger the soma to encode neuronal digital spikes.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Lab for Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

ABSTRACT
The neurons in the brain produce sequential spikes as the digital codes whose various patterns manage well-organized cognitions and behaviors. A source for the physiologically integrated synaptic signals to initiate digital spikes remains unknown, which we studied at pyramidal neurons of cortical slices. In dual recordings from the soma vs. axon, the signals recorded in vivo induce somatic spikes with higher capacity, which is associated with lower somatic thresholds and shorter refractory periods mediated by voltage-gated sodium channels. The introduction of these parameters from the soma and axon into NEURON model simulates sequential spikes being somatic in origin. Physiological signals integrated from synaptic inputs primarily trigger the soma to encode neuronal digital spikes.

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Latencies between somatic spikes and axonal ones favor somatic origins of sequential spikes. A) Top panel shows an electrical circuit for cellular membrane, Cm, membrane capacitance; Rin input resistance and Rv, voltage-gated conductance. Middle panel illustrates sequential spikes (black line) subtracted from the responses (gray dot-line) by depolarization and hyperpolarization. Bottom shows the derivative of spike potentials with respect to time (dv/dt). B) shows the expanded waveforms of dv/dt vs. time for a somatic spike (red trace) and axonal one (blue). A vertical line shows a location of spike initiation, which is defined as a time point of minimal dv/dt but larger than zero. C) illustrates latencies between somatic spikes and axonal ones (ΔT = Tsoma-Taxon) versus spikes. D) shows the measurement in the amplitudes of spike dv/dt and the time of minimal dv/dt to peak in the intracellular use of QX-314 (0.5 mM). E) shows the proportional correlation between the amplitudes of spike dv/dt and the time of minimal dv/dt to peak (36 spikes from three cells) in the partial inactivation of VGSCs. F) The rising phase of spikes is better fitted into two exponentials under the control (r2 = 0.99), and a single exponential (r2 = 0.99) under QX-314 application.
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Figure 3: Latencies between somatic spikes and axonal ones favor somatic origins of sequential spikes. A) Top panel shows an electrical circuit for cellular membrane, Cm, membrane capacitance; Rin input resistance and Rv, voltage-gated conductance. Middle panel illustrates sequential spikes (black line) subtracted from the responses (gray dot-line) by depolarization and hyperpolarization. Bottom shows the derivative of spike potentials with respect to time (dv/dt). B) shows the expanded waveforms of dv/dt vs. time for a somatic spike (red trace) and axonal one (blue). A vertical line shows a location of spike initiation, which is defined as a time point of minimal dv/dt but larger than zero. C) illustrates latencies between somatic spikes and axonal ones (ΔT = Tsoma-Taxon) versus spikes. D) shows the measurement in the amplitudes of spike dv/dt and the time of minimal dv/dt to peak in the intracellular use of QX-314 (0.5 mM). E) shows the proportional correlation between the amplitudes of spike dv/dt and the time of minimal dv/dt to peak (36 spikes from three cells) in the partial inactivation of VGSCs. F) The rising phase of spikes is better fitted into two exponentials under the control (r2 = 0.99), and a single exponential (r2 = 0.99) under QX-314 application.

Mentions: The initiation of spikes was defined at a time point of minimal dv/dt but larger than zero (Figure 3A~B and Methods). Latencies between somatic spikes and axonal ones (ΔT) were calculated. Figure 3C shows that ΔT values for spikes 1~3 are -2.5 ± 87, -311 ± 226.5 and -471 ± 215.8 μs (n = 20), respectively. In spite of big variation for ΔT values, sequential spikes recorded at the soma appear ahead of those at the axon.


Physiological synaptic signals initiate sequential spikes at soma of cortical pyramidal neurons.

Ge R, Qian H, Wang JH - Mol Brain (2011)

Latencies between somatic spikes and axonal ones favor somatic origins of sequential spikes. A) Top panel shows an electrical circuit for cellular membrane, Cm, membrane capacitance; Rin input resistance and Rv, voltage-gated conductance. Middle panel illustrates sequential spikes (black line) subtracted from the responses (gray dot-line) by depolarization and hyperpolarization. Bottom shows the derivative of spike potentials with respect to time (dv/dt). B) shows the expanded waveforms of dv/dt vs. time for a somatic spike (red trace) and axonal one (blue). A vertical line shows a location of spike initiation, which is defined as a time point of minimal dv/dt but larger than zero. C) illustrates latencies between somatic spikes and axonal ones (ΔT = Tsoma-Taxon) versus spikes. D) shows the measurement in the amplitudes of spike dv/dt and the time of minimal dv/dt to peak in the intracellular use of QX-314 (0.5 mM). E) shows the proportional correlation between the amplitudes of spike dv/dt and the time of minimal dv/dt to peak (36 spikes from three cells) in the partial inactivation of VGSCs. F) The rising phase of spikes is better fitted into two exponentials under the control (r2 = 0.99), and a single exponential (r2 = 0.99) under QX-314 application.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3113741&req=5

Figure 3: Latencies between somatic spikes and axonal ones favor somatic origins of sequential spikes. A) Top panel shows an electrical circuit for cellular membrane, Cm, membrane capacitance; Rin input resistance and Rv, voltage-gated conductance. Middle panel illustrates sequential spikes (black line) subtracted from the responses (gray dot-line) by depolarization and hyperpolarization. Bottom shows the derivative of spike potentials with respect to time (dv/dt). B) shows the expanded waveforms of dv/dt vs. time for a somatic spike (red trace) and axonal one (blue). A vertical line shows a location of spike initiation, which is defined as a time point of minimal dv/dt but larger than zero. C) illustrates latencies between somatic spikes and axonal ones (ΔT = Tsoma-Taxon) versus spikes. D) shows the measurement in the amplitudes of spike dv/dt and the time of minimal dv/dt to peak in the intracellular use of QX-314 (0.5 mM). E) shows the proportional correlation between the amplitudes of spike dv/dt and the time of minimal dv/dt to peak (36 spikes from three cells) in the partial inactivation of VGSCs. F) The rising phase of spikes is better fitted into two exponentials under the control (r2 = 0.99), and a single exponential (r2 = 0.99) under QX-314 application.
Mentions: The initiation of spikes was defined at a time point of minimal dv/dt but larger than zero (Figure 3A~B and Methods). Latencies between somatic spikes and axonal ones (ΔT) were calculated. Figure 3C shows that ΔT values for spikes 1~3 are -2.5 ± 87, -311 ± 226.5 and -471 ± 215.8 μs (n = 20), respectively. In spite of big variation for ΔT values, sequential spikes recorded at the soma appear ahead of those at the axon.

Bottom Line: In dual recordings from the soma vs. axon, the signals recorded in vivo induce somatic spikes with higher capacity, which is associated with lower somatic thresholds and shorter refractory periods mediated by voltage-gated sodium channels.The introduction of these parameters from the soma and axon into NEURON model simulates sequential spikes being somatic in origin.Physiological signals integrated from synaptic inputs primarily trigger the soma to encode neuronal digital spikes.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Lab for Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

ABSTRACT
The neurons in the brain produce sequential spikes as the digital codes whose various patterns manage well-organized cognitions and behaviors. A source for the physiologically integrated synaptic signals to initiate digital spikes remains unknown, which we studied at pyramidal neurons of cortical slices. In dual recordings from the soma vs. axon, the signals recorded in vivo induce somatic spikes with higher capacity, which is associated with lower somatic thresholds and shorter refractory periods mediated by voltage-gated sodium channels. The introduction of these parameters from the soma and axon into NEURON model simulates sequential spikes being somatic in origin. Physiological signals integrated from synaptic inputs primarily trigger the soma to encode neuronal digital spikes.

Show MeSH
Related in: MedlinePlus