Effects of somatosensory electrical stimulation on neuronal injury after global hypoxia-ischemia

Manuel M. Buitrago; Andreas R. Luft; Nitish V. Thakor; Mary E. Blue; Daniel F. Hanley

doi:10.1007/s00221-004-1906-1

Effects of somatosensory electrical stimulation on neuronal injury after global hypoxia-ischemia

Manuel M. Buitrago, Andreas R. Luft, Nitish V. Thakor, Mary E. Blue, Daniel F. Hanley

School of Medicine

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

14 Scopus citations

Abstract

Electrical stimulation (ES) is used after cardiac arrest (CA) for diagnostic and therapeutic purposes. The effects of ES on brain damage induced by hypoxic-ischemic brain injury (HI) has not been investigated. Stimulation of afferent pathways by ES may increase neural injury by releasing excitatory neurotransmitters (glutamate) and thereby exacerbating excitotoxicity. To test this hypothesis, ES was applied to the median nerve (2 h) of adult male Wistar rats after 5 min of asphyxic CA and cardiopulmonary resuscitation. Control animals received no ES. Assessment of neuronal damage in five regions of interest was performed in survivors (ES_n=15, Control N=10, Sham n=3) after 48 h using H&E, Cresyl-Violet, and TUNEL stains, and Caspase-3 and activated ERK 1/2 immunohistochemistry. Ratios of injured to normal cells were calculated. Most injury was found in hippocampus and cerebellum. ES animals showed significantly lower injury ratios in bilateral hippocampus as compared with controls (F=20.8,p<0.00001). TUNEL staining, caspase-3 and activated ERK 1/2 showed no differences between groups. It is concluded that ES during the acute phase of HI does not amplify neuronal damage at 48 h, but may have a protective effect that requires further investigation.

Original language	English (US)
Pages (from-to)	336-344
Number of pages	9
Journal	Experimental Brain Research
Volume	158
Issue number	3
DOIs	https://doi.org/10.1007/s00221-004-1906-1
State	Published - Oct 2004

Keywords

ERK
Global ischemia
Hippocampus
Hypoxia
Neuronal injury
Somatosensory stimulation

ASJC Scopus subject areas

General Neuroscience

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10.1007/s00221-004-1906-1

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@article{88966042d1e84d7fab8bccc63837c707,

title = "Effects of somatosensory electrical stimulation on neuronal injury after global hypoxia-ischemia",

abstract = "Electrical stimulation (ES) is used after cardiac arrest (CA) for diagnostic and therapeutic purposes. The effects of ES on brain damage induced by hypoxic-ischemic brain injury (HI) has not been investigated. Stimulation of afferent pathways by ES may increase neural injury by releasing excitatory neurotransmitters (glutamate) and thereby exacerbating excitotoxicity. To test this hypothesis, ES was applied to the median nerve (2 h) of adult male Wistar rats after 5 min of asphyxic CA and cardiopulmonary resuscitation. Control animals received no ES. Assessment of neuronal damage in five regions of interest was performed in survivors (ESn=15, Control N=10, Sham n=3) after 48 h using H&E, Cresyl-Violet, and TUNEL stains, and Caspase-3 and activated ERK 1/2 immunohistochemistry. Ratios of injured to normal cells were calculated. Most injury was found in hippocampus and cerebellum. ES animals showed significantly lower injury ratios in bilateral hippocampus as compared with controls (F=20.8,p<0.00001). TUNEL staining, caspase-3 and activated ERK 1/2 showed no differences between groups. It is concluded that ES during the acute phase of HI does not amplify neuronal damage at 48 h, but may have a protective effect that requires further investigation.",

keywords = "ERK, Global ischemia, Hippocampus, Hypoxia, Neuronal injury, Somatosensory stimulation",

author = "Buitrago, {Manuel M.} and Luft, {Andreas R.} and Thakor, {Nitish V.} and Blue, {Mary E.} and Hanley, {Daniel F.}",

note = "Funding Information: Acknowledgements This work was supported by grants from the National Institutes of Health (1RO1 NS 24282-08 NIH/ NINDS, NIH SBIR-1R43N55380167-0), the France Merrick Foundation, and the Eleanor Naylor Dana Foundation. We are indebted to Dr. Carlos Pardo V., from the Department of Neurology, Johns Hopkins University, for his constant advice on pathological assessment of neuronal injury and Mollie Lange, from the Kennedy Krieger Institute, for her help with histology and immunohistochemistry.",

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AU - Luft, Andreas R.

AU - Thakor, Nitish V.

AU - Blue, Mary E.

AU - Hanley, Daniel F.

N1 - Funding Information: Acknowledgements This work was supported by grants from the National Institutes of Health (1RO1 NS 24282-08 NIH/ NINDS, NIH SBIR-1R43N55380167-0), the France Merrick Foundation, and the Eleanor Naylor Dana Foundation. We are indebted to Dr. Carlos Pardo V., from the Department of Neurology, Johns Hopkins University, for his constant advice on pathological assessment of neuronal injury and Mollie Lange, from the Kennedy Krieger Institute, for her help with histology and immunohistochemistry.

PY - 2004/10

Y1 - 2004/10

N2 - Electrical stimulation (ES) is used after cardiac arrest (CA) for diagnostic and therapeutic purposes. The effects of ES on brain damage induced by hypoxic-ischemic brain injury (HI) has not been investigated. Stimulation of afferent pathways by ES may increase neural injury by releasing excitatory neurotransmitters (glutamate) and thereby exacerbating excitotoxicity. To test this hypothesis, ES was applied to the median nerve (2 h) of adult male Wistar rats after 5 min of asphyxic CA and cardiopulmonary resuscitation. Control animals received no ES. Assessment of neuronal damage in five regions of interest was performed in survivors (ESn=15, Control N=10, Sham n=3) after 48 h using H&E, Cresyl-Violet, and TUNEL stains, and Caspase-3 and activated ERK 1/2 immunohistochemistry. Ratios of injured to normal cells were calculated. Most injury was found in hippocampus and cerebellum. ES animals showed significantly lower injury ratios in bilateral hippocampus as compared with controls (F=20.8,p<0.00001). TUNEL staining, caspase-3 and activated ERK 1/2 showed no differences between groups. It is concluded that ES during the acute phase of HI does not amplify neuronal damage at 48 h, but may have a protective effect that requires further investigation.

AB - Electrical stimulation (ES) is used after cardiac arrest (CA) for diagnostic and therapeutic purposes. The effects of ES on brain damage induced by hypoxic-ischemic brain injury (HI) has not been investigated. Stimulation of afferent pathways by ES may increase neural injury by releasing excitatory neurotransmitters (glutamate) and thereby exacerbating excitotoxicity. To test this hypothesis, ES was applied to the median nerve (2 h) of adult male Wistar rats after 5 min of asphyxic CA and cardiopulmonary resuscitation. Control animals received no ES. Assessment of neuronal damage in five regions of interest was performed in survivors (ESn=15, Control N=10, Sham n=3) after 48 h using H&E, Cresyl-Violet, and TUNEL stains, and Caspase-3 and activated ERK 1/2 immunohistochemistry. Ratios of injured to normal cells were calculated. Most injury was found in hippocampus and cerebellum. ES animals showed significantly lower injury ratios in bilateral hippocampus as compared with controls (F=20.8,p<0.00001). TUNEL staining, caspase-3 and activated ERK 1/2 showed no differences between groups. It is concluded that ES during the acute phase of HI does not amplify neuronal damage at 48 h, but may have a protective effect that requires further investigation.

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ER -

Effects of somatosensory electrical stimulation on neuronal injury after global hypoxia-ischemia

Abstract

Keywords

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