1982
DOI: 10.1016/0006-8993(82)91188-x
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Stable-isotope dilution measurement of zinc and lead in rat hippocampus and spinal cord

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Cited by 47 publications
(15 citation statements)
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“…5, it can be observed that, in general, for zinc concentrations were higher in the hippocampus than, in the other brain structures. Our results are in good agreement with those reported by Frederickson et al 30 They showed, using a stable isotope dilution mass spectrometry method, that zinc is more abundant in the hippocampus than in the spinal cord; however, preliminary data in human CNS tissue indicate that the zinc content for hippocampus is only slightly higher than in other regions. 30 Our results are also in good agreement with those reported by Takeda et al, who also determined, using high-resolution autoradiography, that Zn was concentrated in many regions, such as the hippocampal formation.…”
Section: Resultssupporting
confidence: 93%
“…5, it can be observed that, in general, for zinc concentrations were higher in the hippocampus than, in the other brain structures. Our results are in good agreement with those reported by Frederickson et al 30 They showed, using a stable isotope dilution mass spectrometry method, that zinc is more abundant in the hippocampus than in the spinal cord; however, preliminary data in human CNS tissue indicate that the zinc content for hippocampus is only slightly higher than in other regions. 30 Our results are also in good agreement with those reported by Takeda et al, who also determined, using high-resolution autoradiography, that Zn was concentrated in many regions, such as the hippocampal formation.…”
Section: Resultssupporting
confidence: 93%
“…It is well known that the staining intensity using the Timm method does not correlate with the total amount of zinc in the organs [9,10,12,30]. How ever, it does correlate with the amount of chelatable zinc as especially the mossy fibers of the hippocampus stain heav ier than the pituitary, and the amount of chelatable zinc in these fibers has been estimated to account for 10% of the total of hippocampal zinc [ 13].…”
Section: Discussionmentioning
confidence: 99%
“…Injurious stimuli promote the N-terminal proteolytic cleavage of BCL-xL to form the killer protein ⌬N-BCL-xL (Cheng et al, 1997), which induces large conductance channels in mitochondrial outer membranes (Jonas et al, 2004 and cytochrome c release (Clem et al, 1998;Fujita et al, 1998). Zn 2ϩ is normally abundant in hippocampus (Frederickson et al, 1982;Assaf and Chung, 1984;Frederickson and Danscher, 1990;Tonder et al, 1990;Danscher et al, 1997;Li et al, 2001) (but see Kay, 2003) and at high concentrations is a mediator of neuronal death (Koh et al, 1996;Choi and Koh, 1998;Weiss and Sensi, 2000;Bossy-Wetzel et al, 2004;Sensi and Jeng, 2004;Zukin et al, 2004). Global ischemia elicits a delayed rise in Zn 2ϩ in CA1 neurons before death (Koh et al, 1996;Choi and Koh, 1998;Calderone et al, 2004); evidence suggests that Zn 2ϩ enters through GluR2 (glutamate receptor subunit 2)-lacking AMPA receptors (Sensi et al, 1999;Yin et al, 2002) and is released from intracellular stores (Aizenman et al, 2000;Lee et al, 2000;Sensi et al, 2003a;Bossy-Wetzel et al, 2004).…”
Section: Introductionmentioning
confidence: 99%