Abstract
Preface
The present PhD-thesis is based on the following two articles referred to in the text by their Roman
numerals. The articles have never been part of a PhD or Doctoral thesis before.
List of papers:
І. Changes in the Vesicular Zinc Pattern Following Traumatic Brain Injury. Doering P,
Danscher G, Larsen A, Bruhn M, Søndergaard C, Stoltenberg M.
Neuroscience. 2007 Nov 30;150(1):93-103. Epub 2007 Oct 9.
ІІ. Chemical Blocking of Zinc Ions in CNS Increases Neuronal Damage Following Traumatic
Brain Injury (TBI) in mice. Peter Doering, Meredin Stoltenberg, Milena Penkowa, Jørgen
Rungby, Agnete Larsen and Gorm Danscher. PLoS One. 2010 Apr 9;5(4):e10131.
Hypotheses
The involvement of vesicular zinc in neuronal cell damage and cell death in an array of pathological
scenarios including Traumatic Brain Injury, Seizure and Ischemia has been defined in the
Translocation Theory; The theory states that a presynaptic release of vesicular zinc ions
transcends the synaptic cleft and aggravate damage of the post-synaptic neurons
(Frederickson et al., 1989; Koh et al., 1996; Sørensen et al., 1998; Suh et al., 2001) after the
above mentioned pathological events. However, other studies, suggest that a decrease in the
amount of zinc ions, established either by chelation or genetic manipulation, will increase the
extent of brain damage following pathological circumstances (Yeiser et al., 2002; Takeda et
al., 2005B-C; Li et al., 2010) and that the “toxic” transsynaptic zinc signal defined in the
translocation theory could come from a non-vesicular zinc pool (Cole et al., 2000; Lee et al.,
2002; Li et al., 2010). We speculate that this zinc signal can be traced with the ZnSeAMG
method and that either genetic removal of vesicular zinc (using a KO model) or chemical
binding of the vesicular zinc pool will have profound, and according to the translocation
theory neuroprotective effects
The present PhD-thesis is based on the following two articles referred to in the text by their Roman
numerals. The articles have never been part of a PhD or Doctoral thesis before.
List of papers:
І. Changes in the Vesicular Zinc Pattern Following Traumatic Brain Injury. Doering P,
Danscher G, Larsen A, Bruhn M, Søndergaard C, Stoltenberg M.
Neuroscience. 2007 Nov 30;150(1):93-103. Epub 2007 Oct 9.
ІІ. Chemical Blocking of Zinc Ions in CNS Increases Neuronal Damage Following Traumatic
Brain Injury (TBI) in mice. Peter Doering, Meredin Stoltenberg, Milena Penkowa, Jørgen
Rungby, Agnete Larsen and Gorm Danscher. PLoS One. 2010 Apr 9;5(4):e10131.
Hypotheses
The involvement of vesicular zinc in neuronal cell damage and cell death in an array of pathological
scenarios including Traumatic Brain Injury, Seizure and Ischemia has been defined in the
Translocation Theory; The theory states that a presynaptic release of vesicular zinc ions
transcends the synaptic cleft and aggravate damage of the post-synaptic neurons
(Frederickson et al., 1989; Koh et al., 1996; Sørensen et al., 1998; Suh et al., 2001) after the
above mentioned pathological events. However, other studies, suggest that a decrease in the
amount of zinc ions, established either by chelation or genetic manipulation, will increase the
extent of brain damage following pathological circumstances (Yeiser et al., 2002; Takeda et
al., 2005B-C; Li et al., 2010) and that the “toxic” transsynaptic zinc signal defined in the
translocation theory could come from a non-vesicular zinc pool (Cole et al., 2000; Lee et al.,
2002; Li et al., 2010). We speculate that this zinc signal can be traced with the ZnSeAMG
method and that either genetic removal of vesicular zinc (using a KO model) or chemical
binding of the vesicular zinc pool will have profound, and according to the translocation
theory neuroprotective effects
| Original language | English |
|---|---|
| Publication status | Published - 13 Sept 2010 |
| Externally published | Yes |