Emma, Blog #5, A close to the summer

After ten weeks in the lab, my summer at the Siegel lab has officially come to a close. It is so weird to be saying those words, as the last ten weeks have flown by so quickly.

I ended up finishing my two projects, one with the other high school student Meghan doing immunohistochemistries on ketamine and saline treated brain slices, and another running TMazes (a working memory paradigm) on mice with a Dexras1 abscission.

The results from both of my projects endeed up yielding publishable results which I am ecstatic about. I will not be an author of either of the two papers my results will be featured in, but I will be acknowledged in the reference section. The first paper I expect to be sent out for review will be the one about Dexras1 abscission's in mice, and whether this specific genetic manipulation cause schizophrenic-like endophenotypes. Below is the final report I gave to the post-doc writing the paper on what I found out about working memory in mice with the Dexras1 abscission.
Note: I couldn't paste the graphs I made on Statistica into this blog because they are not compatible.

T Maze Report

Dexras Mice

12 mice total

Wildtype Mice

14 mice total

Possible point of interest for future studies (?): Dexras mice on average ran 8.33 trials in T-Maze across 3 days, whereas the wildtype ran 10.067 during the same time period.

95% confidence interval for % of correct choices for Dexras mice: (.5, .65)

95% confidence interval for % of correct choices for WT mice: (.58, .72)

Null hypothesis: The % of correct choices is the same for Dexras and Wildtype mice.

Alternative Hypothesis: The % of correct choices is different for Dexras and Wildtype mice.

P-value: .104

With an alpha level of .05: Because the p-value is so high, we fail to reject the null hypothesis in favor of the alternative. Evidence to suggest that there is no difference in the % of correct choices in the T maze between Dexras and Wildtype mice.

This data supports the claim that there is no difference in working memory between Dexras and Wildtype mice.

My second project was about whether or not the number of neurons (measured by density and area) were different between the brains of ketamine treated mice and saline treated mice, This relates to schizophrenia because ketamine is an NMDA antagonist and produces symptoms in people similar to those that schizophrenics experience. We were in effect, trying to figure out if the cause of these schizophrenic like symptoms had to do with a difference in neurons in the prefrontal cortext. 

Immunohistochemistry Report

Ketamine Mice: 3429 (6 sections), 3425 (6 sections), 3418(6 sections). 18 sections total

Saline Mice: 3422 (5 sections), 3413 (6 sections), 3412 (6 sections). 17 sections total

Two ways we measured whether or not the amount of neurons differ in ketamine or saline exposed mice: Density & % Area of neurons in brain slices

Density: 

95% confidence interval for density of neurons in ketamine brain slices: (~.00018, ~.00026)

95% confidence interval for density of neurons in saline brain slices: (~.00016, ~.00023)

Null hypothesis: Density of neurons will be the same between ketamine and saline treated mice.

Alternative hypothesis: Density of neurons will be different between ketamine and saline treated mice.

P-value: .285

With an alpha level of .05: Because the p-value is so high, we fail to reject the null hypothesis in favor of the alternative. Evidence to suggest that there is no difference in neuronal density between ketamine and saline treated mice.

This data supports the claim that ketamine does not alter the amount of neurons in the brain in the long term (in this case 6 months after receiving treatment).

% Area:

95% confidence interval for % area of neurons in ketamine treated brains: (~5.2, ~9.5)

95% confidence interval for % area of neurons in saline treated brains: (~3.1, ~7.75)

Null hypothesis: % Area of neurons will be the same between ketamine and saline brain slices

Alternative hypothesis:  % Area of neurons will be different between ketamine and saline treated brains.

P-value: .195

With an alpha level of .05: Because the p-value is so high, we fail to reject the null hypothesis in favor of the alternative. Evidence to suggest that there is no difference in % Area of neurons between ketamine and saline treated mice.

This data supports the claim that ketamine does not alter the amount of neurons in the brain in the long term (in this case 6 months after receiving treatment).