VK: I have come to know that you have done research with KYNA, what study was the

most interesting?
AB: I think the research study having to do with sleep deprivation we are currently working on is
really interesting. Just the relevance of sleep deprivation has on college students like me (haha
J) and the various aspects and angles it can be studied from, are very interesting as well. Its
quite intriguing how sleep deprivation over such a brief period of time can have such a big
impact on the test subjects in a study and how it portrays expected human behavior in animals
as well.
VK: Which study in your opinion produced a set of data closest to the hypothesis? Could
you describe it please?
AB: The ongoing study with the EKYNs (the prenatally muted mice). We have the pregnant
moms who were treated with Kynurenine, and the offspring who for the rest of their life will have
elevated KYNA levels. So were currently doing a project, studying their performance in the
Barnes maze, which is a hippocampal dependent memory task. And we knew that they were
already impaired in another behavior task having to do with passive avoidance; and so we
expected them to be impaired in the Barnes maze task as well. However something distinct we
observed in this study is gender differences in the EKYNs themselves, although were still
gathering data for that. But yeah, we expected the learning and memory deficit in EKYNs.

VK: So which gender did worse? Do you know why this might be?
AB: So actually, what were seeing is that both of them did worse. So the first part of the task is
all hippocampal-dependent. You know, trying to find the escape cagethe females were doing
worse on that, but at the end of the task you reverse the maze so the escape cage is 180 rotated
(away), and the males were actually doing worse on that, which is more of a prefrontal cortex

dependent problem: executive functioning, allowing mental flexibility, being able to search your
search pattern, etc.

VK: So brain elasticity?

AB: Yeah! So well see if their elasticity improves, and they form new neural pathways to help
them solve the Barnes maze and such hippocampal dependent problems.
VK: Which study in your opinion produced a set of data furthest from what the hypothesis
predicted? Could you describe it please?
AB: The study that started before I started working at MPRC and got involved with after
produced different than expected results. Its just a characterization of genetically modified mice;
we looked at the Kynurenine pathway. In the Kynurenine pathway, from Kynurenine its either
converted into KYNA using KAT, or 3HK using another enzyme called KMO. And so, there were
mice that had the knockout for KAT or the knockout for KMO, and so they [researchers] said,
hey lets do genetic modification and knockout BOTH! And so they went in and looked
biochemically, and Ive been bolstering that data. Unlike they expected, what was really
interesting, in the mice that had both KAT and KMO knockout was that the KYNA levels were in
between the single KAT (lots of KYNA) knockout or KMO knockout (no KYNA), which was really
interesting and nothing we had initially expected.

VK: Could I have your thoughts on why the study didn't produce the predicted results?

AB: I dont know too much about what caused that, as we are still researching, however it could
maybe be a form of non-enzymatic production, so like other factors could have been involved
when producing that KYNA.
VK: Are you researching any other neurotransmitters?
AB: Currently, those are the only ones we are looking at, but we have discussed researching
possibly serotonin or dopamine.
VK: Would that be for schizophrenia related research, possibly depression?
AB: Yeah! Actually we thought of a study linking EKYNs to depression. It would qualitatively
and indirectly measure serotonin levels in mice based on how the react to being suspended by
tail in the air. So, serotonin levels in those who have depression are very low and it makes them
passive which makes them give up earlier compared to the mice with normal levels of serotonin
who fight back to being suspended by the tail. This would theoretically mean that the mice are
more depressed which lets us allow mental disorders in mice and link the abnormalities to
neurotransmitters.
VK: Are you participating in any research pertaining to neurodegenerative diseases?
AB: No, not currently, however I am interested in doing that in the future.
VK: What is a typical day in your life in the lab like?
AB: There is no set procedure, I just do what is needed. One day I could be running samples on
the HPLC, and an other I could be doing surgeries on mice and rats for the whole day, or I could
be recording data from the wave machine that shows sleep cycles. So, there is no typical just
atypical.

VK: For how long have you been interested in the field of research (if you were before)?
Was scientific research your ultimate goal?
AB: I took Biology and Psychology AP in high school and I loved them both. So, when I got into
college, I discovered neuroscience which is a combination of both of those subjects, and I really
appreciated just the research aspect of it, so thats what I do now!
VK: Do clinical trials produce more results for what you're researching or do assays
provide more insight? Why?
AB: On humans, clinical trials are generally better because they can communicate back to us.
However, on animals, preclinical and assays are better for research data and information on
animals like we are doing. For example, we cant use clinical to tell us the concentration of a
certain enzyme or protein in a liver, however an assay would be very helpful with that!