Feedback mechanism in depolarization-induced sustained activation of extracellular signal-regulated kinase in the hippocampus.

Chinmoyee Maharana, Kaushik P Sharma, Shiv K Sharma

Scientific reports 2013

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Phosphorylation plays important roles in several processes including synaptic plasticity and memory. The critical role of extracellular signal-regulated kinase (ERK) in these processes is well established. ERK is activated in a sustained manner by different stimuli. However, the mechanisms of sustained ERK activation are not completely understood. Here we show that KCl depolarization-induced sustained ERK activation in the hippocampal slices is critically dependent on protein synthesis and transcription. In addition, the sustained ERK activation requires receptor tyrosine kinase(s) activity. In support of a role for a growth factor in sustained ERK activation, KCl depolarization enhances the level of brain-derived neurotrophic factor (BDNF). Furthermore, BDNF antibody blocks KCl-induced sustained ERK activation. These results suggest a positive feed-back loop in which depolarization-induced BDNF maintains ERK activation in the sustained phase.

Citation

Chinmoyee Maharana, Kaushik P Sharma, Shiv K Sharma. Feedback mechanism in depolarization-induced sustained activation of extracellular signal-regulated kinase in the hippocampus. Scientific reports. 2013;3:1103