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02-21-2009, 01:51 PM
So, it was college that made him a drug addict because before going he says he never used tobacco or alcohol till he turned 18 and before using DXM, he was doing "harder" drugs till we went broke because of lack of self-control.
Dumbass kids these days |
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02-21-2009, 02:13 PM
Newton is a small farming community in western Kansas. When I say small, I mean like 3,000.
Thats fucking crazy....just another article. Dxm use has been real heavy in kansas since the mid 90's. With the lack of any other drugs besides (primarily) Meth and shit weed, Kids have seemed to always turn to dxm. Too bad its getting this much attention in this light. |
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02-21-2009, 07:24 PM
Yeah. I guess I can appreciate that the article was pretty benign compared to how it could be portrayed - still I was bothered by some stuff, like:
Quote:
" Ninety years ago I was a freak. Today I'm an amateur. " |
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02-21-2009, 07:43 PM
another reference to it as DMX, awesome
In time I'll seduce you with some heavy "Lay on the banks with me" I cry "Best to breathe on matted grass and reeds" The moons frail light illuminates your silhouette as it submerges in a blanket of darkness |
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02-21-2009, 09:35 PM
Quote:
Quote:
" Ninety years ago I was a freak. Today I'm an amateur. " |
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02-21-2009, 10:36 PM
There are varying types of brain damage.
There is pruning of the dendrites. ( As seen with Meth ) http://www.pnas.org/content/96/7/4073.abstract?ck=nck Perhaps pruning is the effect of down-regulated neuronal terminals being rerouted to a newly adapted neural progenitor cell (NPC). The older neurons are then used less, or do not respond as quickly as they did before. http://www.ncbi.nlm.nih.gov/sites/entrez?D...Search=17034791 There is lesioning ( as seen with Ibotenic acid and DXM/DXO ) Lesioning may be the effect of apoptosis. Sustained abuse of dissociative anesthetics is ill-advised. |
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02-21-2009, 10:38 PM
Keep in mind most studies are done with SubQ injections or sometimes straight into the brain. DXM is not meant to be injected. It is not as toxic as PCP or MK-801 by weight, but it will produce symptoms similar to Dissociative Anesthetic intoxication akin to the aforementioned and Ketamine.
As stated before, these are among the most neurotoxic drugs known. Keep in mind they have also found Mercury in HFCS. ------------------------------------------------------------------------- Oral administration of dextromethorphan does not produce neuronal vacuolation in the rat brain http://www.sciencedirect.com/science?_ob=A...2c4814c1553d5be R.D. Carlissa, Corresponding Author Contact Information, E-mail The Corresponding Author, A. Radovskyb, 1, E-mail The Corresponding Author, C.P. Chengelisb, 1, E-mail The Corresponding Author, T.P. O’Neillb, 1, E-mail The Corresponding Author and D.L. Shueyc, 2, E-mail The Corresponding Author aUniversity of South Alabama, 1504 Springhill Ave SHAC, rm 2309, Mobile, AL 36604, United States bWIL Research Laboratories LLC, 1407 George Road, Ashland, OH 44805-9281, United States cEndo Pharmaceuticals Inc., 100 Endo Blvd., Chadds Ford, PA 19317, United States Received 28 January 2007; accepted 20 March 2007. Available online 6 April 2007. Abstract Dextromethorphan is a widely used antitussive agent, also showing increased recreational abuse. Dextromethorphan and its metabolite dextrorphan are non-competitive antagonists at the N-methyl-d-aspartate (NMDA) receptor ion channel. Single doses of some NMDA receptor antagonists produce neuropathologic changes in neurons of the retrosplenial/posterior cingulate cortices (RS/PC), characterized by vacuolation or neurodegeneration. To determine whether dextromethorphan produces these characteristic lesions, dextromethorphan was administered orally either as a single dose of 120 mg/kg to female rats, or daily for 30 days at doses of 5–400 mg/(kg day) to male rats and 5–120 mg/(kg day) to female rats. Brains were examined microscopically for evidence of neuronal vacuolation (4–6 h postdose) and neurodegeneration (not, vert, similar24 or 48 h postdose). Administration of dextromethorphan at 120 mg/(kg day) in females, and at ≥150 mg/(kg day) in males produced marked behavioral changes, indicative of neurologic effects. Mortality occurred at the highest doses administered. There were no detectable neuropathologic changes following single or repeated oral administration of dextromethorphan at any dose. Administration of MK-801 (9 mg/kg) produced both cytoplasmic vacuolation and neuronal degeneration in neurons of the RS/PC cortex. Thus characteristic neuropathologic changes found with more potent NMDA receptor antagonists do not occur following single or repeated oral administration of dextromethorphan. |
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