Re: [DIYbio] Re: THC legislation is next week

On Thu, Nov 1, 2012 at 11:57 AM, Josiah Zayner <josiah.zayner@gmail.com> wrote:
> It is great that you want to study this plant scientifically apart from the
> millions of others that can be studied legally. The benefit is that we have
> the Cannabis genome/transcriptome, what genes are you interested in
> studying? Have you tried to clone them recombinantly?

I never said I wanted to study it, but I do think there are people out
there that would... well established neuroscientists who could
theorize more than me. I'm primarily interested in DNA as a
chemical/molecule, rather than the much higher level neuroscience
field.

> What do you think about using synthetic cannibinoids? Why not just use that
> for treatment?

Sure, but I think I read a while ago that we have signatures for more
than 80 biosynthetic active molecules in marijuana, and probably about
the same number or more in a synthetic library that the JWH guy came
up. So if the whole political atmosphere changed from 'hippies' to '1
of a million things that has some effect on your brain' I think
progress would be less hindered for sure.

>
> You say marijuana could perhaps be used to help brain plasticity, what
> signalling pathway/mechanism do you suggest this works by and how would you
> suggest one plan on testing it?

There are tons of results if you type marijuana plasticity into google
or google scholar, lots this year even. To cherry pick an open one:
Allele-specific Differences in Activity of a Novel Cannabinoid
Receptor 1 (CNR1) Gene Intronic Enhancer in Hypothalamus, Dorsal Root
Ganglia, and Hippocampus*
http://www.jbc.org/content/287/16/12828.short

Polymorphisms within intron 2 of the CNR1 gene, which encodes
cannabinoid receptor 1 (CB1), have been associated with addiction,
obesity, and brain volume deficits. We used comparative genomics to
identify a polymorphic (rs9444584-C/T) sequence (ECR1) in intron 2 of
the CNR1 gene that had been conserved for 310 million years. The
C-allele of ECR1 (ECR1(C)) acted as an enhancer in hypothalamic and
dorsal root ganglia cells and responded to MAPK activation through the
MEKK pathway but not in hippocampal cells. However, ECR1(T) was
significantly more active in hypothalamic and dorsal root ganglia
cells but, significantly, and in contrast to ECR1(C), was highly
active in hippocampal cells where it also responded strongly to
activation of MAPK. Intriguingly, rs9444584 is in strong linkage
disequilibrium with two other SNPs (rs9450898 (r2 = 0.841) and
rs2023239 (r2 = 0.920)) that have been associated with addiction,
obesity (rs2023239), and reduced fronto-temporal white matter volumes
in schizophrenia patients as a result of cannabis misuse (rs9450898).
Considering their high linkage disequilibrium and the increased
response of ECR1(T) to MAPK signaling when compared with ECR1(C), it
is possible that the functional effects of the different alleles of
rs9444584 may play a role in the conditions associated with rs9450898
and rs2023239. Further analysis of the different alleles of ECR1 may
lead to a greater understanding of the role of CNR1 gene misregulation
in these conditions as well as chronic inflammatory pain.

-----

I guess I would suggest testing it on those people who don't seem to
have any reliable or clear cut options in the existing repertoire of
medicine, or on mice or monkeys. If the political and social taboo was
removed, some decent survey association studies could be done, but as
it stands I doubt self-reporting is complete and true.

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