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Excitotoxicity in Traumatic Brain Injury

Permanent Link: http://ncf.sobek.ufl.edu/NCFE003814/00001

Material Information

Title: Excitotoxicity in Traumatic Brain Injury
Physical Description: Book
Language: English
Creator: MacLean, Dell
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2007
Publication Date: 2007

Subjects

Subjects / Keywords: Brain
Trauma
Excitotoxicity
Mitochondrial Permeability Transition Injury
Medical Calcium
Ca2+
NMDAR
AMPA
NMDA
Kainate Channel
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Traumatic brain injury (TBI) is a common and devastating condition. Excitotoxicity, one of the most harmful aspects of cellular injury that occurs as a result of TBI, is a biological cascade of events that frequently culminates in neuronal death. A crucial factor in excitotoxicity is entry of calcium (Ca2+) into neurons. However, Ca2+ that enters through N-methyl- D-aspartate receptors (NMDARs) is more harmful than Ca2+ entering through other channels. This finding gave rise to the source specificity hypothesis, the idea that calcium entry through some receptors may be physically coupled to damaging processes Another key feature of excitotoxic cell death is Ca2+ uptake by mitochondria, an excess of which leads to the deadly mitochondrial permeability transition (MPT). MPT in neuronal mitochondria may be the cause of delayed Ca2+ deregulation (DCD), a secondary spike in intracellular Ca2+ load that is invariably followed by cell death. Since NMDARs are the primary contributor to excitotoxic cell death, NMDAR antagonists have held much promise as a TBI treatment, and have been successful in animal trials. However, clinical trials using NMDAR antagonist drugs for TBI have uniformly failed to show benefit, possibly due to differences in animal and clinical trial design or to the inherent unsuitability of the drugs or of animal models for human TBI. However, lessons learned from these trials can be applied to new antiexcitotoxic therapies, such as drugs that only partially block NMDARs, or that downmodulate their function. These new treatments could prevent death and disability for countless people.
Statement of Responsibility: by Dell MacLean
Thesis: Thesis (B.A.) -- New College of Florida, 2007
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Local: Faculty Sponsor: Walstrom, Katherine

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2007 M16
System ID: NCFE003814:00001

Permanent Link: http://ncf.sobek.ufl.edu/NCFE003814/00001

Material Information

Title: Excitotoxicity in Traumatic Brain Injury
Physical Description: Book
Language: English
Creator: MacLean, Dell
Publisher: New College of Florida
Place of Publication: Sarasota, Fla.
Creation Date: 2007
Publication Date: 2007

Subjects

Subjects / Keywords: Brain
Trauma
Excitotoxicity
Mitochondrial Permeability Transition Injury
Medical Calcium
Ca2+
NMDAR
AMPA
NMDA
Kainate Channel
Genre: bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Traumatic brain injury (TBI) is a common and devastating condition. Excitotoxicity, one of the most harmful aspects of cellular injury that occurs as a result of TBI, is a biological cascade of events that frequently culminates in neuronal death. A crucial factor in excitotoxicity is entry of calcium (Ca2+) into neurons. However, Ca2+ that enters through N-methyl- D-aspartate receptors (NMDARs) is more harmful than Ca2+ entering through other channels. This finding gave rise to the source specificity hypothesis, the idea that calcium entry through some receptors may be physically coupled to damaging processes Another key feature of excitotoxic cell death is Ca2+ uptake by mitochondria, an excess of which leads to the deadly mitochondrial permeability transition (MPT). MPT in neuronal mitochondria may be the cause of delayed Ca2+ deregulation (DCD), a secondary spike in intracellular Ca2+ load that is invariably followed by cell death. Since NMDARs are the primary contributor to excitotoxic cell death, NMDAR antagonists have held much promise as a TBI treatment, and have been successful in animal trials. However, clinical trials using NMDAR antagonist drugs for TBI have uniformly failed to show benefit, possibly due to differences in animal and clinical trial design or to the inherent unsuitability of the drugs or of animal models for human TBI. However, lessons learned from these trials can be applied to new antiexcitotoxic therapies, such as drugs that only partially block NMDARs, or that downmodulate their function. These new treatments could prevent death and disability for countless people.
Statement of Responsibility: by Dell MacLean
Thesis: Thesis (B.A.) -- New College of Florida, 2007
Electronic Access: RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE
Bibliography: Includes bibliographical references.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Local: Faculty Sponsor: Walstrom, Katherine

Record Information

Source Institution: New College of Florida
Holding Location: New College of Florida
Rights Management: Applicable rights reserved.
Classification: local - S.T. 2007 M16
System ID: NCFE003814:00001

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