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| Hey. Did any of you read this paper on the role of G9a in cocaine-induced dendritic spine plasticity? No? OK, well did you at least read this summary of the findings in Time? Still no? Fine. The gist is that repeated coke use suppresses a protein called G9a, which slows the growth of dendritic spines in your neurons, which, as Time puts it, “can reflect learning, but in the case of addiction may involve learning to connect a place or person with the desire for more drugs.” If you read that and thought, “Wait a second, is this a potentially beneficial effect of cocaine on your brain that they’re trying to spin as a danger?” then yes you are right. Potentially. There is a well established connection between number of dendritic spines and intelligence as measured by IQ (retarded children have long misshapen dendrites which are unevenly dispersed), but it really has to do with what pathways that extra dendritic power is being used to reinforce. In the case of “bad drugs,” the article just arbitrarily assumes that it would be “the desire for more drugs.” I have always thought what you do on drugs is as important as the drugs themselves, eg people who take LSD and teach themselves to type in a day versus people who stare at a wall in silence, reenforcing the “the stare at a wall in silence” pathway in their limbic system. This is something i think might contribute to permanently “acid burned” people–these are usually the people who are/were least likely to stimulate themselves intellectually while under the influence of a psychedelic. I have no direct evidence for this obviously. Right now it’s just a thought that makes me feel better about using 2C-D to study astronomy for months. It is something, however, I’ve done a bit of research on, mostly in the vein of John Lilly’s “metaprogramming the human biocomputer” or “ketaprogramming” or what not, using NMDA antagonists to enhance neural plasticity. Initially I wanted to sell a line of ketamine-based ADHD treatment tapes but they went the way of my heroin-scented bodyspray and beef-flavored valium schemes. The Lilly book unfortunately doesn’t mention ketamine a single time, but it does mention LSD. Here’s where it ties in to what we were talking about: “Certain chemical substances have programmatic and/or metaprogrammatic effects, i.e., they change the operations of the computer, some at the programmatic level and some at the metaprogrammatic level. Some substances which are of interest at the metaprogrammatic level are those that allow reprogramming, and those that allow and facilitate modifications of the metaprograms…. “For example, the term “reprogramming substances” may be appropriate for compounds like lysergic acid diethylamide. For substances like ethyl alcohol the term “metaprogram-attenuating substances” may be useful.” But this G9a business contradicts Lilly a bit. Although the study only examines cocaine I have no doubt that EVERY psychoactive substance produces structural changes in the brain (beyond the obvious cascade of neurotransmitters and blocking or unblocking of various pores and channels). So alcohol may not be so much a “metaprogram-attenuating substance” as much as a substance which writes a shitty metaprogram. if you look at a neuroscience textbook printed before the early 90s it will say that eurons cannot regenerate. It was not until recently that neuroscientists realized neurogenesis occurs in adults, and even more recently that it is a common effect of SSRI antidepressants which are thought to exert some of their therapeutic effect by inducing neurogenesis in the hippocampus. BUT THEN LISTEN TO THIS: “Caffeine was added to rat neurons in vitro. The dendritic spines taken from the hippocampus grew by 33% and new spines formed. After an hour or two, however, these cells returned to their original shape.” Sound familiar? It’s a bit different in that they are observing the hippocampus and not the NAcc as in the cocaine study, but the basic premise is the same. Now think about the behavioral difference in cocaine users versus caffeine users and what the intend to purpose of their respective drugs is: Caffeine is used to anxiously go to work and take a shit, whereas cocaine is used to engage in impulsive/sexual/self-destructive behavior. The question becomes: Does the behavior make the drug or does the drug make the behavior? It’s a combination of the two. I think all of this comes back to an interesting problem: It’s like the movie Lawnmower Man, when we think of a “smart drug” we think of a pill that effortlessly and instantaneously raises our intelligence, but I think the real key is to understand that you must COOPERATE with the drug. Once you understand this, then a wealth of potent “smart drugs” already exist, eg 2C-D, amphetamines, and (tentatively) ketamine. A “smart drug” allows us to alter our everyday (sober) patterns of learning and concentration for the better by reinforcing activity on these desirable pathways. Whew, anyway now you’ve got me on an adderal rant! (It’s good though, it’s strengthening my rant pathway.) |
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