The Vestibular Ocular Reflex In Parkinsonian Mice

Abstract

Parkinson's disease (PD) is a progressive neurological disorder characterized by poor balance, slow movement, rigidity, and uncontrollable tremors of the hands. These symptoms result from the degeneration of dopamine-producing nerve cells in the brain, specifically in the substantia nigra and the locus coeruleus. Dopamine is a neurotransmitter that is released by the brain and stimulates motor neurons. When dopamine production is depleted, the motor system is unable to control movement and coordination and PD symptoms occur.

The goal of this experiment was to gain a better understanding of the effects of PD on the vestibular system. More specifically, the effect of the destruction of the dopamine producing cells on the vestibular ocular reflex (VOR) was investigated. The VOR is a gaze-stabilization reflex which maintains eye fixation on an object during head rotation. As the head turns, the eyes compensate by slowly turning in the opposite direction. As the eyes reach the limit of their turning range, they quickly reset by returning to their starting position. Together, the VOR (slow phase) and the resetting (quick phase) make up the vestibular nystagmus. The VOR produced during horizontal and vertical rotations by untreated mice was compared with the VOR produced by those mice that were injected with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a drug known to destroy the dopamine producing neurons in humans, primates, and rodents. In addition, the relationship between peak eye velocity and amplitude of the quick phases was analyzed to see if the quick phase was altered in MPTP-treated mice.