UNDERSTANDING CANNABINOIDS

[Mr. Charlie]

Wow, thanks G.O. Joe...it appears that my decarboxylation procedure is woefully inadequate...which serves to further complicate my thinking. Certainly it explains the lack of psychoactivity in my tinctures, which is a good thing as I am able to be nearly full functioning. But, it clouds the reasons of why my tincture Works for me, and works quite well. Apparently other cannabinoids are at work in my case, and are providing significant relief. Exciting to think that if I were to properly cook my buds, that efficacy may be increased even more. I am with you, Kodiak, I will need some time to fully wrap my brain around all of this data

I am having the same results with my woefully inadequetley created tinctures! They totally work for me as a wonderful euphoric high, anti-depression stimulant. The description that i get from others is that the tincture is more "background", meaning not so psychoactive. I believe it is due to the CBD's and CBN's and the specific properties of the strain used.
I am straining a tincture today that I heated the dried greens in an attempt to activate the THC(five minutes at like 190 degrees) I'll post the info on the results...
I will experiment by making a new tincture today with activated THC and see what happens.
Thanks a lot for this great thread. We all gain by sharing!

 

[jump117]

How it happens:​

... This concentrated mat is hit by UV-B light waves, causing the creation of cannabinoids. ...​

Why Trichomes?​

... They protect the plant from UVB light rays, especially Cannabis plant since THC has very good UV-B light absorption. ...​

This is assumptions but not the proven fact.​

 

[Stevius]

Hey jump117


We did not claim anywhere that all the data is a fact and proven information. I apologize, but all the info is gathered from the internet (mostly). So for me, as an ordinary person and not some kind of chemist or biologist, this is all I can do, to gather the information and put it in one place where EVERYONE can look at it and ADD any useful information to the subject.

I must warn you, as I posted before, English is not my native language therefore it makes the whole search and reading a LOT more difficult.... so please bear with me!


If you have any info's on this subject you posted, I believe that ALL of us would be more than happy to see it shared and learned from it.

 

[G.O. Joe]

One last book recommendation from me:
Handbook of Experimental Pharmacology, Volume 168: Cannabinoids

 

[partcleguy]

Innacuracies

Innacuracies

Not sure if this has been posted earlier in the thread, but there are some inaccuracies in the first post. Again, just trying to keep things as accurate as possible. I went to grad school for a year trying to get my PhD in neuroscience but I decided not to pursue the degree because I found out I did not like research. I was in one lab that worked with cannabinoids and did a rotation in another lab that studied neuroprotection. I wrote a solid grant (it was not turned in- was for practice in a class but was truly subjected to critique by our professors) on cannabinoids in neuroprotection following traumatic brain injury.

Anyway- just some of the things I saw were: the drawings showing the cannabinoids acting on a neuron showed them going from the pre-synaptic cell to the post-synaptic cell. It is believed that cannabinoids act in a reverse mechanism being released from around the synapse of the post-synaptic cell and acting on the pre-synaptic cell. This modulates the pre-synaptic cell's release rate of other neurotransmitters like acetylcholine/dopamine. It can go either way but many neurons decrease their firing when the cannabinoids find their way to the pre-synaptic cell.

Secondly- there is evidence for non-cb1/cb2 type receptors. Neurons are not the only cells in the brain that have receptors. Glial cells (which were thought to mostly form the structure of the brain and hold neurons together but do a whole lot more) also have receptors. Cells called microglial cells are responsible for inflammatory response and for helping to heal the brain after injury. Its been shown these cells may have non-cb1/cb2 receptors on them that are distinctly different. They are implicated in the neuroprotective effects of cannabinoids. Interestingly, cannabinoids are thought to inactivate microglial cells. Microglial cells heal the brain by forming a scar around damaged cells. The cells would normally burst releasing chemicals usually safely packaged in the cells. Release of these chemicals causes cells surrounding the burst cells to die. Microglial cells scar around the damaged cells preventing these chemicals from being released into the surrounding cells. Unfortunately that also means the cells can not grow back like they would in the spinal cord and other places. So in other words, like we've heard before, cannabinoids have anti-inflammatory capabilities that can prevent some neurotoxicity following a brain injury

 

[Kodiak]

Thanks for posting yet another great book G.O. Joe. Those are hard to come by. It will take some time to absorb all the information in those books but they will surely help us along on the road to understanding cannabinoids.

Thanks for the input partcleguy, interesting stuff. I had to read up a bit on neuroscience at the same time but it was well worth it.

We'll try to work that into the guide. Although the drawing might not be entirely correct, it still illustrates the basic idea.

 

[ChynaRyder]

I am having the same results with my woefully inadequetley created tinctures! They totally work for me as a wonderful euphoric high, anti-depression stimulant. The description that i get from others is that the tincture is more "background", meaning not so psychoactive. I believe it is due to the CBD's and CBN's and the specific properties of the strain used.
I am straining a tincture today that I heated the dried greens in an attempt to activate the THC(five minutes at like 190 degrees) I'll post the info on the results...
I will experiment by making a new tincture today with activated THC and see what happens.
Thanks a lot for this great thread. We all gain by sharing!

Hmmm...So, I made a new tincture last night by placing the buds in the crock pot, this time with the pot on high. Temps were at 250 F, and I left the buds in for 40 minutes....10 min to gain temp, and 30 min to decarboxylate.

I just sampled, and my early opinion is that I like the old way better...but that is prolly cause I overdosed, and am way too stoned to function....My old tinctures were just as Mr. Charlie told me so....soft, uplifting, happy, and the best part, sweetly pain relieving for up to 2 hours, with almost no mental confusion, just a pleasant happiness...we shall see, I will fiddle with dosing over the next few days, but right now I dont think this is the best way for me. I am stoned, stupid, and still hurting....go figure that one out.

 

[ChynaRyder]

AIt is believed that cannabinoids act in a reverse mechanism being released from around the synapse of the post-synaptic cell and acting on the pre-synaptic cell. This modulates the pre-synaptic cell's release rate of other neurotransmitters like acetylcholine/dopamine. It can go either way but many neurons decrease their firing when the cannabinoids find their way to the pre-synaptic cell.

Thanks for this info, partcleguy...I am curious if you know if this activity is uniform for all neurons, or is their a specificity for certain kinds of neurons???(I am an agronomist, and not as familiar with human anatomy as I am with plant, and am not sure if there is indeed a difference between nerve cells that transmit pain and any other nerve cell???) What I am getting at is if this activity can be massaged in any way to make the binding more selective towards the neurons that transmit pain.....it seems to me that decreasing the firing of neurons transmitting pain will dull the sensation of pain, no?...

Secondly- there is evidence for non-cb1/cb2 type receptors. Neurons are not the only cells in the brain that have receptors. Glial cells (which were thought to mostly form the structure of the brain and hold neurons together but do a whole lot more) also have receptors. Cells called microglial cells are responsible for inflammatory response and for helping to heal the brain after injury. Its been shown these cells may have non-cb1/cb2 receptors on them that are distinctly different. They are implicated in the neuroprotective effects of cannabinoids. Interestingly, cannabinoids are thought to inactivate microglial cells. Microglial cells heal the brain by forming a scar around damaged cells. The cells would normally burst releasing chemicals usually safely packaged in the cells. Release of these chemicals causes cells surrounding the burst cells to die. Microglial cells scar around the damaged cells preventing these chemicals from being released into the surrounding cells. Unfortunately that also means the cells can not grow back like they would in the spinal cord and other places. So in other words, like we've heard before, cannabinoids have anti-inflammatory capabilities that can prevent some neurotoxicity following a brain injury

In your experience, is this phenomenon the driving force for the claim of 'neuroprotective' effects of cannabis? Are there other 'neuroprotective' activities in canna? Maybe telling you why I ask will help you understand where I am coming from....I have significant interest in these effects, as I have late stage Chronic Lyme Disease, an illness that has been called a Neuro-Psychiatric condition...I have good control over the musculoskelatal symptoms of the illness, but the slow erosion of my mental faculties, assumed by direct infection of neurons by spirochetes, is deeply disturbing. There is increasing clinical evidence for Alzheimer's type syndromes being connected with spirochetal infection of the brain, and my great fear is that I will end up like many other alzheimer's patients. Are you aware of any activity of cannabinoids that may protect neurons from damage by infection?

 

[Mr. Charlie]

Hmmm...So, I made a new tincture last night by placing the buds in the crock pot, this time with the pot on high. Temps were at 250 F, and I left the buds in for 40 minutes....10 min to gain temp, and 30 min to decarboxylate.

I just sampled, and my early opinion is that I like the old way better...but that is prolly cause I overdosed, and am way too stoned to function....My old tinctures were just as Mr. Charlie told me so....soft, uplifting, happy, and the best part, sweetly pain relieving for up to 2 hours, with almost no mental confusion, just a pleasant happiness...we shall see, I will fiddle with dosing over the next few days, but right now I dont think this is the best way for me. I am stoned, stupid, and still hurting....go figure that one out.

I hear you ChynaRyder regarding the "old" way. The lack of confusion is a major benefit. I also like the length of the euphoric feeling... almost a bit caffeine-like( go figure, a stimulant).

The batch that I made a few nights ago... I finely chopped(Cuisinart) my dried AAA trim and warmed it in quart mason jars with the lid loosely on for 20 minutes at 270 oven temp. Next add 1 cup grain, 1 cup organic glycerin, 1 cup distilled water. shake for a month and we'll see.
Thanks for sharing your results.

How is your tincture done so quickly?

 

[partcleguy]

ChynaRyder- neurons throughout the brain have different amounts and types of receptors. This is what allows some of the specificity of areas to do certain tasks. Dopamine is mainly produced in two specific areas of the brain for instance- the substantia nigra (which degenerates over time and leads to parkinson's disease- a condition due to insufficient dopamine) and the ventral tegmental area (and axons from these areas spread throughout the brain). With that said, most research has been done on the more familiar CB1 and CB2 receptors and there have been studies to see where these receptors are densely found. CB1 receptors are mainly found in areas controlling motor, cognitive, emotional and sensory functions (hippocampus, basal ganglia, cerebellum, cortex, thalamus, amygdala, and olfactory bulb) with additional areas of high density in nuclei involved in pain reception, body temperature, sleep-wake cycles, and hormone function (brainstem, the hypothalamus, and the pituitary gland). So yes, the cannabinoid system may be involved in pain (and anecdotal evidence from medical marijuana users like yourself adds additional support to this). CB2 receptors and the non-CB1/CB2 receptors are mainly implicated in immune responses and are found on microglial cells and other cells (mast cells etc.).

So anyway- in the peripheral nervous system (where pain messages are transmitted from- outside the brain), nerves serve different functions. Some send signals from the brain to your muscles to move, others send signals to your sensory nerves which inhibits their firing. Its a very finely tuned system. The nerves themselves are very similar- its where they go to or from in the brain and body that differ. Muscle nerves go to the motor cortex of the brain (eventually- they have to go through the brainstem/thalamus/etc. first). They also have a different composition where they touch the muscle fiber compared to sensory nerves which have different specialized components in the skin to sense vibration/crushing (for pain), and other things.

It sounds to me like you would like to find a way for cannabinoids to more specifically dampen pain. Unfortunately, smoking/vaporizing/imbibing cannabis and all of its cannabinoids simply results in a uniform increase in the amount of cannabinoids in the brain. This might be partially what some anti-medical marijuana doctors are talking about when they say it's not really a medicine. A drug is designed to perform a specific task with minimal side-effects. Its kind of a miracle and a testament to how we already use cannabinoids in our brain that there are so few side-effects from imbibing the stuff. The side-effects we do get (hunger, sleepiness, dry mouth etc.) can be attributed to the receptors throughout the brain. Receptors in the hypothalamus are most likely the reason you get more hungry, the receptors in your brain stem (which regulate alertness/waking/sleeping) are probably responsible for it making you tired, and receptors in the hippocampus (associated with short-term memory and encoding of long-term memory) is probably why you are more forgetful while under the influence. I am not a doctor so I do not know if there are any drugs known that can possibly work as co-agonists with cannabinoids to decrease pain (though I doubt there is anyone researching it due to our governments stance on the plant). In short I do not believe there is enough research done on the topic to specifically target cannabinoid receptors involved in pain

I'm sorry if I'm rambling- its such a huge topic and I'm trying to sum up a lot of things... Let me know if there is anything I need to clarify!

I'll respond to the second part in another post...

 

[partcleguy]

Oh I guess I didn't completely respond to the first part about the reverse action of canninoids being responsible for the inhibition of pre-synaptic cells and whether this is true for all neurons. Here is a wikipedia article I found on what I was talking about: http://en.wikipedia.org/wiki/Depolarization-induced_suppression_of_inhibition

These studies are based on brain slices and using tiny electrodes to measure current/voltage from single cells. Its extremely difficult to see in vivo (like in a living animal) whether cells act in a certain way. So I really don't think anyone knows whether all cannabinoids act through DSI/DSE.

I gotta go to class so I'll respond to the part about neuroprotection later!

 

[partcleguy]

I have an interesting article you might want to read about new areas of research into cannabinoids and pain. Its by Roger G. Pertwee called "Emerging strategies for exploiting cannabinoid receptor agonists as medicines." Its in the British Journal of Pharmacology (2009), issue 156, pg. 397–411. I have a copy if you would like me to send it to you.

Not all the neuroprotective effects of cannabinoids are from activation/inhibition of the microglial cells I talked about. However if you're talking about neuroprotection from invading spirochetes, I don't think any of the other mechanisms of protection would do anything to a targeted attack by a microorganism. The other mechanisms of protection involve mediating the effects of the chemicals released from damaged cells like I talked about in my first post. Calcium is highly regulated in the brain because it does so many things. Cells keep it packaged in certain structures, and excessive release (like a burst cell) can cause cells around the damaged cell to die by apoptosis. Other chemicals like glutamate act in a similar excitoxic mechanism. Additionally, cannabinoids can act as anti-oxidants which prevent cell death as well.

I'm afraid I don't know enough about lyme disease as it is and again I doubt there is much research on using cannabinoids as a therapy in the late stages of the disease. I think the best you can probably do right now is use cannabis as a medicine to relieve symptoms (pain, maybe inflammation) of the disease. I wish the best of luck to you. If you have any questions let me know.

Other great reviews on cannabinoids in the brain- Mario van der stelt et. al "Acute Neuronal Injury, Excitotoxicity, and the Endocannabinoid System" Molecular Neurobiology Volume 26, 2002.

I would post my bibliography for my grant but its a word 2007 file and I only have word 2003 on this computer. So frustrating!

 

[Kodiak]

Thanks for all that information partcleguy.

We had in mind when we started writing this guide that it would partly serve as a portal for discussions relating to the medicinal use of cannabis. We first thought about including a chapter on it but soon realized that we lacked the proper knowledge for it.

With your help and with the help of others, we might be able to make add that chapter to the guide after all.


Regarding the 2007 Word file, you actually have two options. You can either install the Compatibility Pack or try opening it in OpenOffice.

If you have any studies on your computers that you would like to share with us, you can upload the file to a free webserver and post the link here.

I use http://uploading.com/

 

[Pineydoobey]

Why Trichomes?​

Cannabis and many other plants have evolved resin trichomes for variety of uses. They protect the plant from UVB light rays, especially Cannabis plant since THC has very good UV-B light absorption. It protects the plant from insects and animals and also provides protection for buds from low humidity and harsh winds.​

This is assumptions but not the proven fact.​

I believe I may be able to prove every word of this statement.

Protection From UV-B light
In the flowering stage plants exposed to an ultraviolet light versus those given only say a HPS produce more trichomes.
My opinion in why this happens is that it acts as a sunscreen. As the bud matures the trichomes go through various stages as pictured in the synopsis on the first page. Clear, cloudy, and finally amber.

It would seem that the plant is getting a tan and building it's tolerance to the sun as occurs in humans. Clear, would offer little protection; It would let light pass through. Cloudy would offer more protection; less light penetrates the trichome. Amber would add even greater protection; The light does not penetrate as much and also seems to reflect.

Protection From Bugs
If you have ever seen a picture of a bug on a bud it's usually stuck to it. Not so good for the consumer, because who wants to smoke a bug, am I right? In the case of the plant though, it may have just saved days of growth and allowed the continuation of growth of what would now be residing in the bugs stomach.

Basically, good bud is sticky. Sticky bud is a death trap for insects that would dine on the pungent buds if they could just get past those sticky resin glands.

Protection From Wind And Humidity
This one is a little tougher to explain so try to stay with me.
My dad is a skydiver. When trying to achieve maximum freefall time one creates as much drag as possible by using what is called a "Wing-suit" It's pretty much self-exclamatory as to what that is. If you can't wrap your mind around it though I'll explain.

It's like Redbull.

These wings slow your movement speed. If you had big enough wings you could possibly even save your life

This same principal could easily apply to the bud of the marijuana plant. The trichomes create weight and drag, that in harsh winds, may slow the movement of the bud.

Anyone with the basic knowledge of how the cannabis plant grows would know that the bud is a reproductive organ. That being said it only makes since that the plant would do everything in it's power to protect it's offspring.

aka the seed

With that, I give you this. The resin glands of a healthy mature marijuana plant are very sticky. It seems logical that the only way this is possible is for there to be some amount of water present in the glands. The only way I have ever seen good bud without sticky resin is if it was dried too fast. Even then it was still somewhat sticky. It would appear that it retains moisture very well and could act as a reservoir to help retain water in times of drought or area's with low humidity.

Adding to the "Stickiness" portion; Pollen from a male probably manages to often find itself lodged on a resin gland, being that it is so sticky. If this pollen were to then touch the white pistil hairs it would propagate a seed a seed and further the generation of the species on a whole.

My brain hurts and I don't want to go into this in any more detail than I already have. I hope this makes sense and makes people less skeptical about the benefits of trichomes for both humans and the plant itself.

 

[Sheriff Bart]

I believe I may be able to prove every word of this statement.

Protection From UV-B light
In the flowering stage plants exposed to an ultraviolet light versus those given only say a HPS produce more trichomes.
My opinion in why this happens is that it acts as a sunscreen. As the bud matures the trichomes go through various stages as pictured in the synopsis on the first page. Clear, cloudy, and finally amber.

It would seem that the plant is getting a tan and building it's tolerance to the sun as occurs in humans. Clear, would offer little protection; It would let light pass through. Cloudy would offer more protection; less light penetrates the trichome. Amber would add even greater protection; The light does not penetrate as much and also seems to reflect.

you have to keep in mind, that from the scientific perspective, one can never PROVE anything, one can only preform a reproducible experiment and observe the outcome and then either accept or reject a hypothesis. a hypothesis is just a hypothesis, 'I think this is why this particular thing happens, and this is why I think this...(and the evidence is then presented)'. hypothesis can become theorems if they have a certain amount of certainty and a general consensus about them as to the universal application (the theory of gravity for instance, is persistant, but in the end gravity is still a hypothesis for the reason large objects have attractions towards each other, for instance)

and now you also have to realize that what you see is the visible spectrum. clear, cloudy, amber has nothing to do with the UV or infra-red properties of those compounds, since that is something you cannot see. the color seems to simple be part of the nature of the cannabinoids, or the other products in the glands, and they just take on that visible color. given their relatively close structures as well though its likely they have similar, but still distinct, UV absorption patterns.

and also, sunlight would be the most intense in the summer, during vegatative growth, with decreasing intensity as flowering begins, and when resin production occurs



one way to truly support the hypothesis for UV protection would be to knock out the trichome genes, or cannabinoid synthase genes, so that the plant cannot make trichomes or the cannabinoids. the trichomeless/cannabinoidless plant would then be grown in the same conditions as a plant that can make trichomes/cannabinoids, and one could observe the growth patterns, cellular responses, etc. when UV light is applied to the plants. if the trichomeless/cannabinoidless plants started to grow more poorly, exhibit stress and damaged, then we can accept our hypothesis that the plant is using the glands/cannabinoids for uv-protection. there may still be other reasons for them, but that is at least one function that has evolved over time.

i know that there are grants for the research on cannabis with this exact aim, to create a trichomeless cannabis plant. the thc synthase gene has already been identified amoung with many of the others. so its only a matter of time until it gets done/published. but also cannabis is not a model organism, and so research in general on it is very minimal compared to the other plant model organisms used like arabidopsis or tobacco.

 

[partcleguy]

Bibliography

Bibliography

Thanks for the advice on opening word 2007 files! Here is my bibliography (sorry if the formatting is weird):

Literature cited
1. van der Stelt, M., Veldhuis, W. B., Maccaronne, M., Bär, P. R., Nicolay, K., Veldink, G. A., et al. (2002). Acute neuronal injury, excitotoxicity, and the endocannabinoids system. Molecular Neurobiology, 26(2-3): p. 317-46.

2. Kreutz, S., Koch, M., Böttger, C., Ghadban, C., Korf, H., & Dehghani, F. (2009). 2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal cannabidiol-sensitive receptors on microglial cells. Glia, 57: p. 286-94.

3. Zhang, J., & Chen, C. (2008). Endocannabinoid 2-Arachidonoylglycerol protects neurons by limiting COX-2 elevation. J. Biol. Chem., 283(33): p. 22601-11.

4. Biegon, A. (2004). Cannabinoids as neuroprotective agents in traumatic brain injury. Current Pharmaceutical Design, 10: p. 2177-83.

5. Pertwee, R. G. (2009). Emerging strategies for exploiting cannabinoid receptor agonists as medicines. British Journal of pharmacology, 156: p. 397-411.

6. Herkenham, M., Lynn, A. B., Little, M. D., Johnson, M. R., Melvin, L. S., De Costa, B. R., et al. (1990). Cannabinoid receptor localization in brain. Proc. Natl. Acad. Sci., 87: p. 1932-6.

7. Hill, E. L., Gallopin, T., Férézou, I., Cauli, B., Rossier, J., Schweitzer, P., & Lambolez, B. (2007). Functional CB1 receptors are broadly expressed in neocortical GABAergic and glutamatergic neurons. J. Neurophysiol., 97(4): p. 2580-9.

8. Howlett, A. C., Breivogel, C. S., Childers, S. R., Deadwyler, S. A., Hampson, R. E., & Porrino, L. J. (2004). Neuropharmacology, 47: p. 345-58.

9. Khaspekov, L. G., Brenz Verca, M. S., Frumkina, L. E., Hermann, H., Marsicano, G., & Lutz, B. (2004). Involvement of brain-derived neurotrophic factor in cannabinoid receptor-dependent protection against excitotoxicity. Eur. J. Neurosci., 19(7): p. 1691-8.

10. Rahn, E. J., Zvonok, A. M., Thakur, G. A., Khanolkar, A. D., Makriyannis, A., & Hohmann, A. G. (2008). Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception induced by treatment with the chemotherapeutic agent paclitaxel in rats. J. Pharmacol. Exp. Ther., 327(2): 584-91.

11. Hampson, A. J., Bornheim, L. M., Scanziani, M., Yost, C. S., Gray, A. T., Hansen, B. M., et al. (1998). Duel effects of anandamide on NMDA receptor-mediated responses and neurotransmission. Journal of Neurochemistry, 70: p. 671-6.

12. Nagayama, T., Sinor, A. D., Simon, R. P., Chen, J., Graham, S. H., Jin, K., & Greenberg, D. A. (1999). Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures. J. Neurosci., 19(8): 2987-95.

13. Sinor, A. D., Irvin, S. M., & Greenberg, D. A. (2000). Endocannabinoids protect cerebral cortical neurons from in vitro ischemia in rats. Neuroscience Letters, 278: 157-60.

14. Louw, D. F., Yang, F. W., & Sutherland, G. R. (2000). The effect of Δ-9-tetrahydrocannabinol on forebrain ischemia in rat. Brain Research, 857: 183-7.

15. Hallam, T. M., Floyd, C. L., Folkerts, M. M., Lee, L. L., Gong, Q.-Z., Lyeth, B. G., et al. (2004). Comparison of behavioral deficits and acute neuronal degeneration in rat lateral fluid percussion and weight-drop brain injury models. Journal of Neurotrauma, 21: p. 521-39.

16. Center for Disease Control. (2007). “Traumatic Brain Injury.” National Center for Injury Prevention and Control. <http://www.cdc.gov/ncipc/factsheets/tbi.htm>. Last visited 1 May, 2009.

17. Royo, N. C., Conte, V., Saatman, K. E., Shimizu, S., Belfield, C. M., Soltesz, K. M., et al. (2006). Hippocampal vulnerability following traumatic brain injury: a potential role for neurotrophin-4/5 in pyramidal cell neuroprotection. European Journal of Neuroscience, 23: p. 1089-1102.

18. Bigler, E. D., Anderson, C. V., & Blatter, D. D. (2002). Temporal lobe morphology in normal aging and traumatic brain injury. Am. J. Neuroradiol., 23(2): p. 255-66.

19. Yan, H. Q., Ma, X., Chen, X., Li, Y., Shao, L., & Dixon, C. E. (2007). Delayed increase of tyrosine hydroxylase expression in rat nigrostriatal system after traumatic brain injury. Brain Research, 1134(1): p. 171-9.

20. Wagner, A. K., Drewencki, L. L., Chen, X., Santos, F. R., Khan, A. S., Harun, R., et al. (2009). Chronic methylphenidate treatment enhances striatal dopamine neurotransmission after experimental traumatic brain injury. Journal of Neurochemistry, 108: 986-97.

21. Wagner, A. K., Sokoloski, J. E., Ren, D., Chen, X., Khan, A. S., Zafonte, R. D., et al. (2005). Controlled cortical impact injury affects dopaminergic transmission in the rat striatum. Journal of Neurochemistry, 95: 457-65.

22. Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., et al. (2001). Nature, 413: p. 527-31.

23. Van der Stelt, M., Veldhuis, W. B., van Haaften, G. W., Fezza, F., Bisogno, T., Bar, P. R., et al. Exogenous anandamide protects rat brain against acute neuronal injury in vivo. J. Neurosci., 21(22): 8765-71.

24. McIntosh, T. K., Vink, R., Noble, L., et al. (1989). Traumatic brain injury in the rat: characterization of a lateral fluid-percussion model. Neuroscience, 28, 233-44.

Also about uploading the files- does anyone know a free one that lets you upload multiple files at a time? I really don't want to wait, upload, and copy and paste the url for each of the 24 files :/

Also forgot to mention (as you can see in article 3) cannabinoids can be anti-inflammatory by limiting COX-2 elevation after an injury. You may remember Vioxx and the scandal following the findings about its side-effects and blood pressure. Vioxx was a COX-2 inhibitor. COX-2 is an enzyme responsible for causing inflammation and pain.

 

[ChynaRyder]

How is your tincture done so quickly?

I make them with grain alcohol, and cooked bud ground in a coffee grinder. Not much seems to change potency wise after a couple hours...longer soaks just seem to extract more chlorophyll.

I can say that after using the new tincture for several days, and adjusting the dose, it is effective for pain, but in a different way than the low temp tincture...its an in your face kinda thing...surprisingly psychoactive...but the dosage is far less. The combination of the 2 tinctures results in even better effects, quite good to be honest...my assumption is that I am ingesting larger doses of other cannabinoides with the old tinctures, because I am not limited in dosage by psychoactivity like I am with the higher temp method. 2-3 mL's for the high temp and any more and I am too stoned to function, and about 6 mL's with the lower temp was a standard dose, so I was injesting 2-3 x the amount of other cannabinoides with the low temp.

I suppose it is possible that some ephemeral component that was providing relief in the low temp stuff could have volatilized in the higher temp...I would love an opportunity to use some of minilab's little cannabinoid analyzers to actually see what I am making....I hate screwing around in the dark like this.

partcle guy...wow I have some reading to do

 

[Kodiak]

There are a few things that speak for the theory that UVB increases potency in cannabis plants, although it's perhaps not that straight forward.

Take a look at this diagram.

1. The absorbance of an object quantifies how much of the incident light (energy) is absorbed by it. It has been said that cannabinoids show an absorption maximum between 270 and 280 nm in the ultraviolet region.

2. It has also been said that the highly energetic UVB photons are needed to fully energize the photochemical reaction that will produce THC. Less energetic photons from light with a greater wavelength will not do the job properly.


"Pate (1983) indicated that in areas of high ultraviolet radiation exposure, the UVB (280-320 nm) absorption properties of THC may have conferred an evolutionary advantage to Cannabis capable of greater production of this compound."

"The extent to which this production is also influenced by environmental UVB has also been experimentally determined by Lydon et al. (1987)."

"The phytochemical process will not be completely energized with only UVA photons which are more penetrating but less energetic, and the harvested resin spheres will have mostly precursor compounds and not fully realized THC."


I'm still not sure what to think of this.

One way to look at it would be that plants that receive UVB will contain more THC while they are alive, than plants that are grown under artificial light. This might however even out during the curing process when the remaining THCA in the bud decarboxylates into THC.

So I guess the real question is whether or not UVB light actually raises the total amount of THC that a plant can produce or if it just tips the THCA/THC scale in favor of the latter while the plant is still alive.

From a greater perspective I think that UVB-radiation might play a larger role as a stress factor, thereby promoting trichome formation. From that perspective I guess you could say that UVB increases potency because more trichomes equals more cannabinoids and subsequently, more THC.

 

[Mr. Charlie]

Hmmm...So, I made a new tincture last night by placing the buds in the crock pot, this time with the pot on high. Temps were at 250 F, and I left the buds in for 40 minutes....10 min to gain temp, and 30 min to decarboxylate.

Thanks ChynaRyder. I am taking your advise for today's batch. Cooking for 40 minutes in a 270 degree oven to decarboxylate.
I keep you in touch with the results. Cheers

 

[Mr. Charlie]

I would love an opportunity to use some of minilab's little cannabinoid analyzers to actually see what I am making....I hate screwing around in the dark like this.

I agree that an analysis would be great. The People's Choice clinic in Denverwaverops, it is a great clinic!) gave me the info for the Colorado testing facility. www.patientschoiceofcolorado.com, the facility tests CBD, CBN, Delta 9 THC, and Delta 9 THC-A. The paperwork says that it takes a week. I am not clear on how to send them a sample and how much they need for a test. The tests start at $90.
I am wondering if there is any home tests we can do other than experimenting on ourselves and friends/patients.
Nice thread, thanks for sharing your info... Now to catch up on this reading info!!