MPTP Parkinsonism in the Cat: Pattern of Neuronal Loss May Partially be Explained by the Distribution of MAO-B in the Brain

Abstract

Recently, it has been shown that administration of l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to cats produces a parkinsonian syndrome consisting of akinesia, rigidity, postural tremor, and decreased responsiveness to sensory stimulation (Schneider et al., 1986). While animals eventually recover from this behavioral syndrome (Schneider et al., 1986), the majority of substantia nigra pars compacta (SNc) cells are irreversibly damaged. Tyrosine hydroxylase (TH) immunohistochemistry and cresyl violet Nissl substance staining demonstrate an extensive loss of SNc cells even five months after initial MPTP treatment at a time when the animal appears to have recovered much of its behavioral functions (Schneider and Markham, 1986). While the damage to the SNc is the most prominent feature of the MPTP-induced disorder, other mesencephalic dopamine cell groups also sustain damage. The retrorubral (A-8) dopamine cell group located dorsal to the SNc experiences a much more moderate loss of neurons while the ventral tegmental area (VTA) appears to receive only reversible damage (as evidenced by an acute decrease in TH immunoreactivity within the first few weeks following MPTP administration and an eventual return of staining) (Fig. 1).