Today we took blood samples from the mice before sending them back to their home cage. We put the blood samples into a water and propanol solution. The propanol acts as an internal matrix (something we can compare the ethanol in their blood to) when we assay it using GC. We then cleaned the cages that were in the chambers. Underneath each cage was a large rectangular diaper thing that catches all their food crumbs and poop. I got the lovely job of gathering these diaper things and throwing them away. I then had to wipe down all three chambers using, ironically, ethanol as a cleaning solution. We then filled up the water bottles to give the mice for this weekend. They will not be given bottles with ethanol until Monday. The ethanol chambers promote neuroplasticity. The receptors involved with multiple withdrawal lead to increased voluntary consumption of ethanol.

We cleaned their chamber cages with bleach and as a side note I learned from Chris that the reason bleach takes color out of things is that it oxidizes the bonds on they dye, which prevents the fabric from absorbing any color. Because of this it reflects ALL colors making the bleach stain appear white.

So here is what I learned today about purpose of this lab:

Prep Phase

All the mice have a baseline drinking level. Through involuntary exposure (the ethanol chambers), a multiple withdrawal group emerges. This is in hopes to proliferate GABA and the change of the subunits that will expose the MW group to increased dependence. The mice go through a cycle of evaluation, chamber time, and then abstinence which will solidify neuroadaptations. We want to prove that there is divergent drinking in the MW group from the control group.

Treatment Phase

We will use GABA modulators on the lateral septum (bilaterally). We will use an agonist and antagonist on the GABAb, which is a metatrophic receptor. To agonize GABAb we will use Baclofen. This makes the mice tired and has the same affect as EtOH. This makes the mice drink less. To antagonize the GABAb we will use saclofen, which acts as a hyperstimulant and makes the mice want to drink more. On the GABAa receptors we will use muscinol to agonize. This will cause decreased drinking. To antagonize we will use bicuculline which will cause increased drinking. 

The question of the lab is this: Does GABA play a role in dependency in the lateral septum?