Methyl-beta-cyclodextrin induced cholesterol depletion facilitates synaptic transmission at the crayfish neuromuscular junction
Methyl-beta-cyclodextrin (MβCD) is a toxin that has been found to act as a cholesterol inhibitor within the cell membrane. Research has indicated that the removal of cholesterol from the cellular membrane causes an increase in excitatory postsynaptic potentials (EPSPs) in neuromuscular junctions when the presynaptic cell is stimulated. This rise in EPSPs is due to the increase of calcium within the presynaptic cell when the membrane becomes more fluid. We investigated the effects of increasing membrane fluidity by removing cholesterol from the cellular membrane and the consequences of doing such within the crayfish neuromuscular junction (NMJ). This research is important due to its possible insights into neurodegenerative diseases such as Niemann-Picks disease. Based on prior research, we hypothesized that increasing membrane fluidity by removing cholesterol from the presynaptic membrane will increase the amplitude of the first EPSP in paired-pulse stimulation therefore creating a short term plasticity, via an increase of calcium within the cell. Our second hypothesis was that there would be a decrease in paired-pulse facilitation, coming from a diminished second EPSP caused by a lack of readily-releasable pool of neurotransmitter. Contradictory to our hypotheses, our results showed an increase in facilitation when paired-pulse stimulation was used in combination with MβCD.