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

This paper also looks pretty good, but I can't get it:
http://www.annualreviews.org/doi/pdf/10.1146/annurev.neuro.29.051605.112834

ENDOCANNABINOID-MEDIATED SYNAPTIC PLASTICITY IN THE CNS
Annual Review of Neuroscience
Vol. 29: 37-76 (Volume publication date July 2006)
First published online as a Review in Advance on March 15, 2006
DOI: 10.1146/annurev.neuro.29.051605.112834
Vivien Chevaleyre, Kanji A. Takahashi, and Pablo E. Castillo
Department of Neuroscience, Albert Einstein College of Medicine,
Bronx, New York 10461; email: pcastill@aecom.yu.edu

Changes in synaptic efficacy are thought to be crucial to
experience-dependent modifications of neural function. The diversity
of mechanisms underlying these changes is far greater than previously
expected. In the last five years, a new class of use-dependent
synaptic plasticity that requires retrograde signaling by
endocannabinoids (eCB) and presynaptic CB1 receptor activation has
been identified in several brain structures. eCB-mediated plasticity
encompasses many forms of transient and long-lasting synaptic
depression and is found at both excitatory and inhibitory synapses. In
addition, eCBs can modify the inducibility of non-eCB-mediated forms
of plasticity. Thus, the eCB system is emerging as a major player in
synaptic plasticity. Given the wide distribution of CB1 receptors in
the CNS, the list of brain structures and synapses expressing
eCB-mediated plasticity is likely to expand.

On Thu, Nov 1, 2012 at 12:52 PM, Nathan McCorkle <nmz787@gmail.com> wrote:
> 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.



--
-Nathan

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