Dopaminergic neurons of the substantia nigra pars compacta (SNc) are selectively vulnerable in Parkinson’s disease, while closely related neurons in the ventral tegmental area (VTA) are comparatively spared. Although mitochondrial dysfunction, calcium stress, and α-synuclein aggregation have each been implicated, none alone explains why anatomically similar populations exhibit such different fates. Here we develop a
minimal two-variable energetic model
that captures only mitochondrial functional capacity, energetic reserve, and the combined load from axonal arborization and calcium handling. Despite its simplicity, the model reveals that increasing structural load deforms the energetic landscape until a
saddle-node bifurcation
emerges, producing coexisting healthy-energy and collapsed-energy states. SNc-like neurons, which bear extreme axonal and calcium-handling demands, reside
inside
this bistable regime, operating near a separatrix that renders them vulnerable to even modest metabolic perturbations. In contrast, VTA-like neurons lie
outside
the bistable window and robustly return to their high-energy state following similar disturbances. The model reproduces hallmark features of Parkinsonian degeneration—long periods of stability, sudden irreversible collapse, and population-specific susceptibility—using only the geometry of load-dependent energy regulation. These findings suggest that selective SNc vulnerability arises not from unique molecular defects, but from the
fundamental dynamical structure
imposed by their extraordinary anatomical and physiological load.