Acetyl-L-carnitine arginine amide prevents beta 25-35-induced
neurotoxicity in cerebellar granule cells
Cerebellar granule cells (CGC) at different stages of maturation
in vitro (1 or 6 DIV), were treated with beta 25-35 and acetyl-L-carnitine
arginine amide (ST857) in presence of 25 mM KCl in the culture
medium, and neuronal viability was assessed. Three days of
treatment slightly modified the survival of 1 DIV-treated
cells, which degenerate and die five days later beta-amyloid
matching. Similarly, a significative neurotoxic effect was
observed on 6 DIV treated-cells after 5 days of exposure to
the peptide, while the death occurred within 8 days. ST857
coincubated with beta 25-35 was able to rescue neurons from
beta 25-35-induced neurotoxicity. We also studied the changes
in Ca2+ homeostasis following glutamate stimulation, in control
and beta-amyloid treated single cells, either in presence
or in absence of ST857. beta 25-35 did not affect basal [Ca2+]i,
while modified glutamate-induced [Ca2+]i increase, causing
a sustained plateau phase of [Ca2+]i, that persisted after
the removal of the agonist. ST857 pretreatment completely
reverted this effect suggesting that, in CGC chronically treated
with beta 25-35, ST857 could protect the cells by neurotoxic
insults of the peptide likely interfering with the cellular
mechanisms involved in the control of Ca2+ homeostasis. Scorziello
A, Meucci O, Calvani M, Schettini G. Neurochem Res. 1997 Mar;22(3):257-65.
The preceding abstract was obtained from the Medline service maintained by the
National Institutes of Health.
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