Region-specific phosphorylation of ERK5-MEF2C in the rat frontal cortex and hippocampus after electroconvulsive shock

Chang Yoon Se; Min Ahn Yong; Ja Jun Sook; Yeni Kim; Gu Kang Ung; Joo Bae Park; Sik Kim Yong

doi:10.1016/j.pnpbp.2005.04.006

Region-specific phosphorylation of ERK5-MEF2C in the rat frontal cortex and hippocampus after electroconvulsive shock

Chang Yoon Se, Min Ahn Yong, Ja Jun Sook, Yeni Kim, Gu Kang Ung, Joo Bae Park, Sik Kim Yong

Department of Medicine

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

ERK5-MEF2C has been implicated in many aspects of neuronal survival and neuroprotection. Neurotrophic effects have been considered as one of the mechanisms in therapeutic electroconvulsive shock (ECS). To investigate whether ECS activates ERK5-MEF2C, we examined the phosphorylation of ERK5, along with its downstream molecule MEF2C, after ECS in the rat frontal cortex and hippocampus. Increased phosphorylation of ERK5 was observed immediately after ECS, but was barely detectable from 2 min after ECS in both the frontal cortex and the hippocampus. The level of MEF2C phosphorylation was decreased immediately after ECS in both regions. It was increased from 2 min and maintained until 10 min after ECS in the frontal cortex, but it returned to the basal level from 2 min after ECS in the hippocampus. Taken together, these results suggest that ECS can regulate the region-specific activity of ERK5-MEF2C pathways in the rat brain.

Original language	English
Pages (from-to)	749-753
Number of pages	5
Journal	Progress in Neuro-Psychopharmacology and Biological Psychiatry
Volume	29
Issue number	5
DOIs	https://doi.org/10.1016/j.pnpbp.2005.04.006
State	Published - Jun 2005

Keywords

ECS
ERK5
MEF2C
Neuronal survival
Neuroprotection
Signal transduction

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10.1016/j.pnpbp.2005.04.006

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title = "Region-specific phosphorylation of ERK5-MEF2C in the rat frontal cortex and hippocampus after electroconvulsive shock",

abstract = "ERK5-MEF2C has been implicated in many aspects of neuronal survival and neuroprotection. Neurotrophic effects have been considered as one of the mechanisms in therapeutic electroconvulsive shock (ECS). To investigate whether ECS activates ERK5-MEF2C, we examined the phosphorylation of ERK5, along with its downstream molecule MEF2C, after ECS in the rat frontal cortex and hippocampus. Increased phosphorylation of ERK5 was observed immediately after ECS, but was barely detectable from 2 min after ECS in both the frontal cortex and the hippocampus. The level of MEF2C phosphorylation was decreased immediately after ECS in both regions. It was increased from 2 min and maintained until 10 min after ECS in the frontal cortex, but it returned to the basal level from 2 min after ECS in the hippocampus. Taken together, these results suggest that ECS can regulate the region-specific activity of ERK5-MEF2C pathways in the rat brain.",

keywords = "ECS, ERK5, MEF2C, Neuronal survival, Neuroprotection, Signal transduction",

author = "Se, {Chang Yoon} and Yong, {Min Ahn} and Sook, {Ja Jun} and Yeni Kim and Ung, {Gu Kang} and Park, {Joo Bae} and Yong, {Sik Kim}",

year = "2005",

month = jun,

doi = "10.1016/j.pnpbp.2005.04.006",

language = "English",

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T1 - Region-specific phosphorylation of ERK5-MEF2C in the rat frontal cortex and hippocampus after electroconvulsive shock

AU - Se, Chang Yoon

AU - Yong, Min Ahn

AU - Sook, Ja Jun

AU - Kim, Yeni

AU - Ung, Gu Kang

AU - Park, Joo Bae

AU - Yong, Sik Kim

PY - 2005/6

Y1 - 2005/6

N2 - ERK5-MEF2C has been implicated in many aspects of neuronal survival and neuroprotection. Neurotrophic effects have been considered as one of the mechanisms in therapeutic electroconvulsive shock (ECS). To investigate whether ECS activates ERK5-MEF2C, we examined the phosphorylation of ERK5, along with its downstream molecule MEF2C, after ECS in the rat frontal cortex and hippocampus. Increased phosphorylation of ERK5 was observed immediately after ECS, but was barely detectable from 2 min after ECS in both the frontal cortex and the hippocampus. The level of MEF2C phosphorylation was decreased immediately after ECS in both regions. It was increased from 2 min and maintained until 10 min after ECS in the frontal cortex, but it returned to the basal level from 2 min after ECS in the hippocampus. Taken together, these results suggest that ECS can regulate the region-specific activity of ERK5-MEF2C pathways in the rat brain.

AB - ERK5-MEF2C has been implicated in many aspects of neuronal survival and neuroprotection. Neurotrophic effects have been considered as one of the mechanisms in therapeutic electroconvulsive shock (ECS). To investigate whether ECS activates ERK5-MEF2C, we examined the phosphorylation of ERK5, along with its downstream molecule MEF2C, after ECS in the rat frontal cortex and hippocampus. Increased phosphorylation of ERK5 was observed immediately after ECS, but was barely detectable from 2 min after ECS in both the frontal cortex and the hippocampus. The level of MEF2C phosphorylation was decreased immediately after ECS in both regions. It was increased from 2 min and maintained until 10 min after ECS in the frontal cortex, but it returned to the basal level from 2 min after ECS in the hippocampus. Taken together, these results suggest that ECS can regulate the region-specific activity of ERK5-MEF2C pathways in the rat brain.

KW - ECS

KW - ERK5

KW - MEF2C

KW - Neuronal survival

KW - Neuroprotection

KW - Signal transduction

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U2 - 10.1016/j.pnpbp.2005.04.006

DO - 10.1016/j.pnpbp.2005.04.006

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AN - SCOPUS:21244505125

SN - 0278-5846

VL - 29

SP - 749

EP - 753

JO - Progress in Neuro-Psychopharmacology and Biological Psychiatry

JF - Progress in Neuro-Psychopharmacology and Biological Psychiatry

IS - 5

ER -

Region-specific phosphorylation of ERK5-MEF2C in the rat frontal cortex and hippocampus after electroconvulsive shock

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