Another reference to follow:
Grzywacz and Zucker, Modeling Starburst Cell's GABA(B) Receptors and their
putative role in motion sensitivity, Biophysical Journal 91, 2006, 473-486.
The introduction starts:
"One of the most important unanswered questions in retinal neurobiology is
why the Starburst cholinergic amacrine cells have two neurotransmitters."
--Stephen
On 20 Jan 2007 13:22:41 -0800, Zachary Tong <polyfractal At gmail.com> wrote:
>> Thanks again to everyone who replied to me. This is thoroughly
> interesting and I find the material fascinating (despite only being an
> undergrad just getting into this work).
>> >>Can't be sure but know of one example that highlights what you're
> >>driving at. CB 1 receptors - cannabinoid receptor. Cannabinoid
> >>consumption slowly leads to the retraction of these receptor from the
> >>cell surface. In one study the degree of cannabinoid tolerance was
> >>found to be directly related to the loss of these receptors(mice). It
> >>has been suggested that these receptors are then degraded and never
> >>find their way back to the cell membrane, thus requiring gene
> >>transcription to create new receptors. Hence, long continual pot
> >>smoking radically alters the number of CB 1 receptors. Cessation, will,
> >>hopefully, restore the receptor balance but that could take weeks if
> >>not months.
>> Thats exactly the idea I was thinking. I wasn't sure, however, if it
> the loss of sensitivity was a "choice" of the neuron, or if it was
> because of molecular actions. Based off your comment about the CB1
> receptors, it appears that it is based in molecular limitations. Then
> again, it appears that the brain has evolved to use these limitations
> to its advantage, so perhaps its not a limitation as I first assumed.
>> >>I doubt there would be a way to select between the transmitters for
> >>release - after all an action potential is an action potential. However
> >>I could imagine that secondary transmitters leaking back across the
> >>synaptic cleft could influence the releasability of presynaptic vesicles
> >>of different kinds. That's just a guess though.
>> This makes sense. The interplay of secondary transmitters and reuptake
> of primary neurotransmitters with the presynaptic end probably adds
> another layer of complexity to the brain, allowing for complex
> behaviors to arrise from a fairly simplistic subunit (relatively
> speaking of course, the neuron is fascinatingly complex in its own
> right)
>> >>For example, SSVs (containing e.g.,
> >>ACh, glutamate, GABA) are released after single spikes, whereas high
> >>frequency trains are required to mobilize and release LDCVs containing
> >>peptides.
>> Thats really interesting stuff. The fast and slow actions of the
> different vesicles add yet another layer of complexity. I'd imagine
> that, despite being complex, each neuron fires its various transmitters
> in a predicatable manner depending on the input. I'd assume the key to
> understanding higher cognitive function is understanding the complex
> firing patters, which in turn would mean knowing the exact reasons for
> various neurotransmitter release.
>> Thanks for the papers, I'm about to go read them. They look
> fascinating :)
>>> Lastly, I was curious on the technicalities of conducting "research".
> I'm a comp. sci major, but have been highly interested and motivated in
> learning about neuroscience. I've been drafting a prototype brain
> simulation, based off of brain structure (particularly the neocortex)
> and theories of how the the neocortex works (collection of several
> authors). Anyhow, it should be "functional" (although entirely
> possible it not useful) soon, and I'm curious how I should go about
> documenting my results. Take lots of data and date all material?
> Should I record observations in a formal manner?
>> Basically, should I stumble across something publication worthy, how
> should I go about documenting my work so that if that time comes, I'm
> ready? Thanks.
>> -Zachary Tong
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