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TITLE: Retrograde degeneration of neurite membrane structural
integrity of nerve growth cones following in vitro exposure to
mercury
JOURNAL: NeuroReport VOLUME: 12 ISSUE: 04 PAGES: 0733-0737
RECEIVED: 6 December 2000
ACCEPTED: 21 December 2000
AUTHOR: Christopher C. W. Leong*, Naweed I. Syed†, Fritz L.
Lorscheider‡
ADDRESS: *Faculty of Medicine, Department of Physiology and
Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary,
Alberta, Canada T2N 4N1; †Faculty of Medicine, Department of
Physiology and Biophysics, University of Calgary, 3330 Hospital Drive
NW, Calgary, Alberta, Canada T2N 4N1; ‡Faculty of Medicine, Department
of Physiology and Biophysics, University of Calgary, 3330 Hospital
Drive NW, Calgary, Alberta, Canada T2N 4N1
Inhalation of mercury vapor (Hg0) inhibits binding of GTP to rat brain
tubulin, thereby inhibiting tubulin polymerization into microtubules.
A similar molecular lesion has also been observed in 80% of brains
from patients with Alzheimer disease (AD) compared to age-matched
controls. However the precise site and mode of action of Hg ions
remain illusive. Therefore, the present study examined whether Hg ions
could affect membrane dynamics of neurite growth cone morphology and
behavior. Since tubulin is a highly conserved cytoskeletal protein in
both vertebrates and invertebrates, we hypothesized that growth cones
from animal species could be highly susceptible to Hg ions. To test
this possibility, the identified, large Pedal A (PeA) neurons from the
central ring ganglia of the snail Lymnaea stagnalis were cultured for
48 h in 2 ml brain conditioned medium (CM). Following neurite
outgrowth, metal chloride solution (2 ml) of Hg, Al, Pb, Cd, or Mn (10-
7 M) was pressure applied directly onto individual growth cones. Time-
lapse images with inverted microscopy were acquired prior to, during,
and after the metal ion exposure. We demonstrate that Hg ions markedly
disrupted membrane structure and linear growth rates of imaged
neurites in 77% of all nerve growth cones. When growth cones were
stained with antibodies specific for both tubulin and actin, it was
the tubulin/microtubule structure that disintegrated following Hg
exposure. Moreover, some denuded neurites were also observed to form
neurofibrillary aggregates. In contrast, growth cone exposure to other
metal ions did not effect growth cone morphology, nor was their
motility rate compromised. To determine the growth suppressive effects
of Hg ions on neuronal sprouting, cells were cultured either in the
presence or absence of Hg ions. We found that in the presence of Hg
ions, neuronal somata failed to sprout, whereas other metalic ions did
not effect growth patterns of cultured PeA cells. We conclude that
this visual evidence and previous biochemical data strongly implicate
Hg as a potential etiological factor in neurodegeneration.
KEYWORDS: Mercury, Microtubules, Neurite growth cone,
Neurodegeneration, Neurofibrillary aggregates, Tubulin
http://www.bcd.com.au/AmalgamDocs/Ne...generation.htm
On Dec 18, 11:40 am, Vaccine-man wrote:
On Dec 18, 7:15 am, Ilena Rose wrote:
Note from Ilena Rosenthal ...
Oh, and here's the reference for you:
http://www.ncbi.nlm.nih.gov/sites/entrez
See? Mercury chloride, a highly ionic and reactive form of mercury
that can readily enter cells, such as neurons. Not thimerosal or its
metabolic byproduct, ethylmercury, which is highly stable because of
its covalent bonds and which cannot pass through a cell membrane
without active transport.
You do know something about cell physiology, don't you. We wouldn't
want to think you're talking out of your ass.