Occurrence of Gap Junctions in the Basal Ganglia of a Rat Model for Parkinson's Disease
Background and problem statement
Parkinson's disease patients show different neural activity compared to healthy subjects, including enhanced synchrony and bursting of neurons as well as oscillations in different frequency bands. The origin of these activity changes after dopamine depletion is still a big matter of debate.
Gap junctional coupling in the basal ganglia could in large parts explain the activity changes during Parkinson's disease. Dopamine may act as a gap junction blocker and its depletion may therefore enhance gap junctional coupling.
The major protein bilding neural gap junctions is Connexin-36 (Cx36) and can be visualized by confocal mircoscopy.
- Is the gap junction protein Cx36 enhanced in the GPe, GPi and/ or STN of a rat rotenone model compared to control rats?
Gap junctions (green) between GABAergic neurons (red)
From Cellular Mechanisms to Neural Circuit Behavior
Principal Investigator track
Stephan van Gils / Richard van Wezel
Supervision and info
Brain tissue of rats treated with rotenone should be stained fluorescently and imaged by confocal microscopy. The amount of Cx36 should be quantified and compared to Cx36 levels from tissue of healthy rats.
Eventually, experiments of Neurobiotin dye coupling can be added to study the functionality of the detected gap junctions.
−Thesis writing, final presentation