The role of intracellular calcium in axonal injury

R. M. Dastgheyb; K. A. Barbee; G. Gallo

doi:10.1109/NEBEC.2014.6972768

The role of intracellular calcium in axonal injury

R. M. Dastgheyb, K. A. Barbee, G. Gallo

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Abstract

Increased levels of axonal calcium have been found after Traumatic Brain injury. Calcium can enter the cell from an extracellular source or be released from intracellular stores. Here, we investigate the importance of intracellular calcium in axonal pathology by chelating intracellular calcium and isolating components of the injury pathway such as membrane damage, calcium influx, mitochondrial injury, and increased oxidative stress. The findings were that chelating intracellular calcium with BAPTA-AM was neuroprotective after increasing membrane permeability with melittin, damaging mitochondria with CCCP, and increasing oxidative stress with TbHp. Chelating intracellular calcium was not neuroprotective after injuring cells by selectively increasing axonal calcium with A23187.

Original language	English (US)
Title of host publication	Proceedings - 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014
Publisher	Institute of Electrical and Electronics Engineers Inc.
ISBN (Electronic)	9781479937288
DOIs	https://doi.org/10.1109/NEBEC.2014.6972768
State	Published - Dec 2 2014
Externally published	Yes
Event	2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014 - Boston, United States Duration: Apr 25 2014 → Apr 27 2014

Publication series

Name	Proceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC
Volume	2014-December
ISSN (Print)	1071-121X
ISSN (Electronic)	2160-7001

Other

Other	2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014
Country/Territory	United States
City	Boston
Period	4/25/14 → 4/27/14

ASJC Scopus subject areas

Bioengineering

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10.1109/NEBEC.2014.6972768

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Dastgheyb, R. M., Barbee, K. A., & Gallo, G. (2014). The role of intracellular calcium in axonal injury. In Proceedings - 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014 Article 6972768 (Proceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC; Vol. 2014-December). Institute of Electrical and Electronics Engineers Inc.. https://doi.org/10.1109/NEBEC.2014.6972768

The role of intracellular calcium in axonal injury. / Dastgheyb, R. M.; Barbee, K. A.; Gallo, G.
Proceedings - 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014. Institute of Electrical and Electronics Engineers Inc., 2014. 6972768 (Proceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC; Vol. 2014-December).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

Dastgheyb, RM, Barbee, KA & Gallo, G 2014, The role of intracellular calcium in axonal injury. in Proceedings - 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014., 6972768, Proceedings of the IEEE Annual Northeast Bioengineering Conference, NEBEC, vol. 2014-December, Institute of Electrical and Electronics Engineers Inc., 2014 40th Annual Northeast Bioengineering Conference, NEBEC 2014, Boston, United States, 4/25/14. https://doi.org/10.1109/NEBEC.2014.6972768

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abstract = "Increased levels of axonal calcium have been found after Traumatic Brain injury. Calcium can enter the cell from an extracellular source or be released from intracellular stores. Here, we investigate the importance of intracellular calcium in axonal pathology by chelating intracellular calcium and isolating components of the injury pathway such as membrane damage, calcium influx, mitochondrial injury, and increased oxidative stress. The findings were that chelating intracellular calcium with BAPTA-AM was neuroprotective after increasing membrane permeability with melittin, damaging mitochondria with CCCP, and increasing oxidative stress with TbHp. Chelating intracellular calcium was not neuroprotective after injuring cells by selectively increasing axonal calcium with A23187.",

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N2 - Increased levels of axonal calcium have been found after Traumatic Brain injury. Calcium can enter the cell from an extracellular source or be released from intracellular stores. Here, we investigate the importance of intracellular calcium in axonal pathology by chelating intracellular calcium and isolating components of the injury pathway such as membrane damage, calcium influx, mitochondrial injury, and increased oxidative stress. The findings were that chelating intracellular calcium with BAPTA-AM was neuroprotective after increasing membrane permeability with melittin, damaging mitochondria with CCCP, and increasing oxidative stress with TbHp. Chelating intracellular calcium was not neuroprotective after injuring cells by selectively increasing axonal calcium with A23187.

AB - Increased levels of axonal calcium have been found after Traumatic Brain injury. Calcium can enter the cell from an extracellular source or be released from intracellular stores. Here, we investigate the importance of intracellular calcium in axonal pathology by chelating intracellular calcium and isolating components of the injury pathway such as membrane damage, calcium influx, mitochondrial injury, and increased oxidative stress. The findings were that chelating intracellular calcium with BAPTA-AM was neuroprotective after increasing membrane permeability with melittin, damaging mitochondria with CCCP, and increasing oxidative stress with TbHp. Chelating intracellular calcium was not neuroprotective after injuring cells by selectively increasing axonal calcium with A23187.

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The role of intracellular calcium in axonal injury

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