PLOSOne, 4/18/2013
Bee venom has recently been suggested to possess beneficial
effects in the treatment of Parkinson disease (PD). For instance, it has been
observed that bilateral acupoint stimulation of lower hind limbs with bee venom
was protective in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)
mouse model of PD. In particular, a specific component of bee venom, apamin,
has previously been shown to have protective effects on dopaminergic neurons in
vitro. However, no information regarding a potential protective action of
apamin in animal models of PD is available to date.
The specific goals of the present study were to (i)
establish that the protective effect of bee venom for dopaminergic neurons is
not restricted to acupoint stimulation, but can also be observed using a more
conventional mode of administration and to (ii) demonstrate that apamin can
mimic the protective effects of a bee venom treatment on dopaminergic neurons.
Using the chronic mouse model of MPTP/probenecid, we show
that bee venom provides sustained protection in an animal model that mimics the
chronic degenerative process of PD. Apamin, however, reproduced these
protective effects only partially, suggesting that other components of bee
venom enhance the protective action of the peptide.
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