Abstract
We have previously shown that a metabolically stable analogue of MPF, the C-terminal tetrapeptide of human beta-endorphin of structure Lys-Lys-Gly-Glu, reduces the turning behaviour of rats with unilateral lesions of their nigro-striatal pathways. Transmission electron microscopy (TEM) has now revealed that this effect is related to reversal of the mitochondrial damage to substantia nigra (SN) neurones induced by the lesion. The results are consistent with the concept that an inherited defect in components of the mitochondrial enzyme system is the initial step in the genesis of Parkinson's disease (PD). They also, in conjunction with known neurotropic properties of MPF, and our unpublished finding of high concentrations of an MPF-like peptide in human basal ganglia, suggest that MPF may have physiological significance in the development and regeneration of the human CNS.
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