Freethought & Rationalism Archive

scigirl · 06-30-2003, 03:05 PM

Quote:

Originally posted by Koyaanisqatsi
For those of you unfamiliar with them, they attempt to link car crashes with pot by stating something tenuous, like "a percentage of accident victims last year tested positive for marijuana;"

WHAT??!! You mean you don't believe that correlation proves causation?

scigirl

Gurdur · 06-30-2003, 03:11 PM

Just some small quibbles.

Quote:

Originally posted by Mageth
....
Those nerve cells are in Reeve's spinal cord, not brain neurons.

*cough* *cough*
The two are not necessarily exclusive. When in the spinal cord, think axons.

Quote:

And what sometimes heals are the interconnections between nerve cells; nerve cells (specifically brain cells) are not replaced when destroyed (not to my knowledge, anyways). New interconnections may sometimes form when damaged, but dead cells are not replaced.

*cough* ?

This seems a bit confused.
We're either talking CNS neurons and whatnot, or we're talking Peripheral NS nerves.
IIRC, what "heals" in the PNS is that the nerves regrow using the old cut-off connections as guide-ropes, so to speak; there is no re-connection, simply growth along the physical pathway provided.

tribalbeeyatch · 06-30-2003, 03:50 PM

Quote:

Originally posted by Koyaanisqatsi
Has anybody heard or seen this argument/research before?

Yes, it's called "state-dependent learning" and is pretty commonly accepted.

Quote:

And one final note, when I smoked from a bong, I got much higher than from a pipe, typically off of just one full hit and any head knows that you can scrape your bong during times of drought and smoke the "resin," which typically gives one a very strong high for a much shorter period, followed usually by a fairly prominent headache, which would seem to me to contradict the notion (or at least bring it into question) that smoking from a bong removes the "good stuff." If the good stuff were removed (by and large) then wouldn't one expect the bong hit to be of low quality and the resin smoking to be of higher, longer lasting quality (with no headache; presumably as a result of toxins stripped along with some active THC)?

Keep in mind that the "highness" imparted by smoking pot is extremely subjective and depends very much upon one's mindset and setting. In fact, I recall that in Reese Jones' work his "frequent user" group reported an identical level of intoxication when smoking 9%THC joints vs. placebo joints. The physiological changes like increased pulse and dry mouth associated with THC ingestion were only seen with subjects smoking the THC-containing joints, though. So it seems that subjective expectation plays such a large role in marijuana-induced intoxication that it might be a pretty unreliable guide for comparing smoking methods.

tribalbeeyatch · 06-30-2003, 04:02 PM

Quote:

Originally posted by theyeti
I didn't see anything about THC acting as an antagonist. Rather it seems to function as an agonist, meaning that it causes receptors to activate by binding in a manner similar to other neurotransmitters. So from what I can tell, it's not blocking or interfering with anything. Rather, it appears to be stimulating the effects of domamine at some point along the pathway. Unfortunately, that site has precious little info.

theyeti

Absolutely. Cannabinoids are neuromodulators that act via activation of endogenous cannabinoid receptors in the brain. They don't antagonize any receptors that I can think of. It is sort of true that they "interfere" with something. That is, their receptors are coupled to inhibitory G-proteins which downregulate adenylyl cyclase activity and intracellular cAMP production. This is very much a normal intracellular signaling event, though, and not something that those neurons need "recover from" -- at least not in the 'recuperating from some mortal wound' sense of the word.

tribalbeeyatch · 06-30-2003, 04:14 PM

Quote:

Originally posted by Mageth
[B]Those nerve cells are in Reeve's spinal cord, not brain neurons. And what sometimes heals are the interconnections between nerve cells; nerve cells (specifically brain cells) are not replaced when destroyed (not to my knowledge, anyways). New interconnections may sometimes form when damaged, but dead cells are not replaced.

You are mostly right in that large areas of brain damage are not completely replaced, but I did want to point out that there is neurogenesis in the adult brain. There is also evidence that brain trauma or neuron death can stimulate neurogenesis, but the rate of neurogenesis is quite slow and hence unable to compensate for profound losses of CNS neurons.

Gurdur · 06-30-2003, 04:34 PM

Quote:

Originally posted by tribalbeeyatch
....
but I did want to point out that there is neurogenesis in the adult brain. There is also evidence that brain trauma or neuron death can stimulate neurogenesis, but the rate of neurogenesis is quite slow and hence unable to compensate for profound losses of CNS neurons.

IIRC, isn't neurogenesis shown in recent research to be actually inhibited by the non-neuronal cells (astro-, etc.) of the brain ?
And if the inhibitive messenger could be turned off, there would in fact be far greater neurogenesis ?
Pardon me if I sound very vague; I'm quite rusty on all this.

tribalbeeyatch · 06-30-2003, 05:04 PM

Quote:

Originally posted by Gurdur
IIRC, isn't neurogenesis shown in recent research to be actually inhibited by the non-neuronal cells (astro-, etc.) of the brain ?

I certainly couldn't rule that out completely, and I would be somewhat surprised if non-neuronal cell types didn't release at least some antiproliferative chemosignals. Some glial types release known proliferative factors like FGFs, though. And, of course, neurons themselves release the anti-proliferative TGF-beta/GDF11, which acts in opposition to FGFs.

Quote:

And if the inhibitive messenger could be turned off, there would in fact be far greater neurogenesis?

That's the way it should go. Either antagonizing the effects of anti-proliferative signals to disinhibit neurogenesis or promoting the effects of proliferative signals themselves should accomplish the same end in theory. In practice, however, there is likely to be one or more inhibitory feedback loops involved that dampen the effect of these sorts of interventions and push the rate of neurogenesis back towards basal.

Quote:

Pardon me if I sound very vague; I'm quite rusty on all this.

Not at all. The literature on this topic is rather vague at this stage, so even the experts are left sounding a bit rusty.

Mageth · 06-30-2003, 05:14 PM

Thanks for the clarifications, Gurder and tribalbeeyatch. Interesting stuff.

And Gurder, you should do something about that cough.

sweep · 06-30-2003, 05:28 PM

Quote:

That's the way it should go. Either antagonizing the effects of anti-proliferative signals to disinhibit neurogenesis or promoting the effects of proliferative signals themselves should accomplish the same end in theory. In practice, however, there is likely to be one or more inhibitory feedback loops involved that dampen the effect of these sorts of interventions and push the rate of neurogenesis back towards basal.

thank fuck for those inhibitor feedback systems. we wouldn't want to feel too much now, would we?

er I mean, that which is inputted quickly is not understood, right?

Gurdur · 06-30-2003, 06:14 PM

Quote:

Originally posted by sweep
.....
er I mean, that which is inputted quickly is not understood, right?

Wham, bam, thank-you ma'am ?

________

Back to the spinal cord:
Anyone here want a trivia question ?
Take a guess at how long the longest neuron cell is in the human body ?

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06-30-2003, 05:14 PM	#48
Mageth Contributor Join Date: Jul 2001 Location: Deep in the heart of mother-lovin' Texas Posts: 29,689	Thanks for the clarifications, Gurder and tribalbeeyatch. Interesting stuff. And Gurder, you should do something about that cough.

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