Rescue of dying neurons: a new action for deprenyl in MPTP parkinsonism.

摘要: Deprenyl slows the progression of disabling symptoms in Parkinson's disease (PD) by an unknown mechanism. It can block action MPTP on substantia nigra compacta (SNc) neurons inhibiting monoamine oxidase B necessary to mediate conversion MPP+, its active metabolite, astroglia. Mice were pretreated with saline or PD-producing toxin, (30 mg/kg) daily for 5 days and then after a further 3 (to allow metabolism excretion MPTP) treated deprenyl (0.25 10 mg/kg ) times weekly 20 days. In three series mice alone MPTP-saline, serial sections through SNc showed that averages 37–42% tyrosine hydroxylase (TH) immunoreactive lost gradually over Joint counts numbers TH-immunoreactive Nissl-stained somata from immediately adjacent established reductions TH at treatment represented neuronal death. reduced loss 14–16% 10-mg/kg 0.25-mg/kg doses, respectively, joint Nissl/ reduction soma rescue would have died The gradual following exposure may reflect toxin's axotomy-like effects prolonged sequestered MPP+. either case, research shows increase survival mechanism is independent blockade MPTP's MPP+ be responsible slowing progressioon PD.