Dataset Information

Irregular Ca(2+) oscillations regulate transcription via cumulative spike duration and spike amplitude.

ABSTRACT:

Background

[Ca(2+)](i) oscillations are irregular and heterogeneous.

Results

The correlations between NF?B/STAT3-GFP transcription and [Ca(2+)](i) spike amplitude/cumulative spike duration are revealed by simultaneous monitoring in single cells and validated in cell population.

Conclusion

[Ca(2+)](i) oscillations regulate transcription through [Ca(2+)](i) spike amplitude and cumulative spike duration.

Significance

How irregular [Ca(2+)](i) oscillations control transcription is crucial for understanding biological [Ca(2+)](i) signal-regulated events. Agonist-stimulated [Ca(2+)](i) oscillations are universally irregular in their kinetics. How irregular [Ca(2+)](i) oscillations dynamically regulate agonist-stimulated downstream events has not been studied. To overcome the obstacles of irregularity and heterogeneity of [Ca(2+)](i) oscillations, agonist-stimulated [Ca(2+)](i) signaling and NF?B/STAT3-GFP nuclear translocation were simultaneously monitored in each single cell examined. The cause-effect relationship between [Ca(2+)](i) oscillation parameters and transcriptional activities was validated in cell populations through irregular [Ca(2+)](i) oscillations with varied parameters. The time duration of cumulative [Ca(2+)](i) elevations reaching the threshold [Ca(2+)](i) level for a transcriptional factor activation and [Ca(2+)](i) spike amplitude was found to control agonist-stimulated transcription and gene expression.

SUBMITTER: Song S

PROVIDER: S-EPMC3504741 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Irregular Ca(2+) oscillations regulate transcription via cumulative spike duration and spike amplitude.

Song Shanshan S Li Jiansha J Zhu Liping L Cai Lei L Xu Qian Q Ling Chen C Su Yuan Y Hu Qinghua Q

The Journal of biological chemistry 20121015 48

<h4>Background</h4>[Ca(2+)](i) oscillations are irregular and heterogeneous.<h4>Results</h4>The correlations between NFκB/STAT3-GFP transcription and [Ca(2+)](i) spike amplitude/cumulative spike duration are revealed by simultaneous monitoring in single cells and validated in cell population.<h4>Conclusion</h4>[Ca(2+)](i) oscillations regulate transcription through [Ca(2+)](i) spike amplitude and cumulative spike duration.<h4>Significance</h4>How irregular [Ca(2+)](i) oscillations control transc ...[more]

PMID: 23071118

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Project description:Neuronal oscillatory activity has been reported in relation to a wide range of cognitive processes including the encoding of external stimuli, attention, and learning. Although the specific role of these oscillations has yet to be determined, it is clear that neuronal oscillations are abundant in the central nervous system. This raises the question of the origin of these oscillations: are the mechanisms for generating these oscillations genetically hard-wired or can they be acquired via a learning process? Here, we study the conditions under which oscillatory activity emerges through a process of spike timing dependent plasticity (STDP) in a feed-forward architecture. First, we analyze the effect of oscillations on STDP-driven synaptic dynamics of a single synapse, and study how the parameters that characterize the STDP rule and the oscillations affect the resultant synaptic weight. Next, we analyze STDP-driven synaptic dynamics of a pre-synaptic population of neurons onto a single post-synaptic cell. The pre-synaptic neural population is assumed to be oscillating at the same frequency, albeit with different phases, such that the net activity of the pre-synaptic population is constant in time. Thus, in the homogeneous case in which all synapses are equal, the post-synaptic neuron receives constant input and hence does not oscillate. To investigate the transition to oscillatory activity, we develop a mean-field Fokker-Planck approximation of the synaptic dynamics. We analyze the conditions causing the homogeneous solution to lose its stability. The findings show that oscillatory activity appears through a mechanism of spontaneous symmetry breaking. However, in the general case the homogeneous solution is unstable, and the synaptic dynamics does not converge to a different fixed point, but rather to a limit cycle. We show how the temporal structure of the STDP rule determines the stability of the homogeneous solution and the drift velocity of the limit cycle.

Dataset Information

Irregular Ca(2+) oscillations regulate transcription via cumulative spike duration and spike amplitude.

Background

Results

Conclusion

Significance

Publications

Irregular Ca(2+) oscillations regulate transcription via cumulative spike duration and spike amplitude.

Similar Datasets

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