Friday Weird Science: Coke Bees.

Sci was going to try and stick with the sex this week, but this paper reminded her SO much of this article in the New Yorker, which then reminded her SO much of that awesome YouTube video, and the next thing you knew Sci had to blog bees on crack. It’s how I roll.
But first, let’s get in the mood:

(Nice web, crack spider)
And from the New Yorker:

There’s that fat kid again. I’m going to sting this whole family! “Aah!” They’re running! I’m buzzing, I’m buzzing, I’m buzzing, this is incredible. I’m in the car! I’m in the car. I’m in the car! Everyone’s screaming and flailing and . . .

And let’s go.
Barron et al, 2009. “Effects of cocaine on honey bee dance behaviour” Journal of Experimental Biology, 2009.
(The authors are Australian. I wonder very much if they deliberately put “behavior” in the title so they could spell it like that and get us Americans all ornery. 🙂 )

Immunization for Addiction: the Cocaine Vaccine

Every so often this cocaine vaccine issue rears its head again. I saw it again just the other day. The problem is, of course, the tendency of the media (ain’t it always the media) to say something like “OMG THIS IS TEH CURE FOR EVERYTHING!” in response to one small study. And who knows, the cocaine vaccine may indeed be the cure for everything, but Sci needs to see some big trials before she gets her hopes up. As it is, the studies I have seen provide some interesting clues, but also provide some important warnings.
So, first question first: how the heck do you make a cocaine vaccine?
Haney et al. “Cocaine-specific antibodies blunt the subjective effects of smoked cocaine in humans” Biological Psychiatry, 2009.

Sleep Deprivation Gives Me the Chills

Sci is about to embark on what she suspects will be two or three months with very little sleep, due to various personal and professional matters, and of course, blogging matters. And while she was discussing this with some friends, one of them brought up something very interesting:
She said “does anyone else feel COLD when they don’t get sleep?”
And it occurred to me that she was very right. When I haven’t been sleeping enough, I get COLD. I wake up freezing and end up bundling up in various thick, fuzzy sweatshirts and grasping on to mugs of hot coffee (though the coffee, of course, has a dual purpose). And so we started wondering, is this normal or anecdotal?
Being an awesome scientist herself, my friend hit the Pubmed, and a few moments later, she handed me this:
*pauses for a moment to put on fuzzy slippers*
Vaara et al. “The effect of 60-h sleep deprivation on cardiovascular regulation and body temperature”. European Journal of Applied Physiology, 2009.

Mapping the Glutamate Receptor

So Sci said she wasn’t going to blog this week because of Open Lab and how stressed she is.

(Sci right now, only with better hair and no pocket-protector)
But she lied.
The science, it calls us, precious.
Ah, the power of Twitter. It is indeed powerful, for it hath informed Sci of a new development in SCIENCE. Also, it made her sing. We’ll get to that.
Sobolevsky, Rosconi, Gouaux “X-ray structure, symmetry and mechanism of an AMPA-subtype glutamate receptor” Nature, 2009.

Pretty, huh?

SFN Neuroblogging: Performance-enhancing Ritalin

Sci will admit that blogging SFN has been harder than she thought it would be. This is partially due to the lack of wireless on the poster floor (which would be REALLY hard to remedy), and partially due to…exhaustion. By the end of the second or third day, the posters all begin to blur before your eyes, and you bless anyone who is willing to send you a copy of their poster. This is because your notes, however extensive, become steadily less and less legible (Sci’s netbook is not optimal for this kind of note-taking). So as Sci tries to write about all the cool stuff she’s seen, she ends up squinting curiously at her notes and saying things like “task indecent via 02??? That doesn’t make any sense!!!”
If they keep up this neuroblogging for next year (please do!!!) and if Sci is picked again (Same Sci-time…midnightish…and same Sci url!), Sci wants to start setting up interviews with people who have awesome abstracts, so I can take better notes. Or possibly I could start begging poster copies ahead of time. Many presenters aren’t so good about sending them, and who can blame them? Sci has forgotten many a time. (As to why all poster-presenters don’t hand out copies of their posters, or allow pictures of posters to be taken, well, Sci will save that for another post).
Anyway, I shall forge on, and attempt to decipher my own handwriting! Especially because I recall being very excited about this particular poster and the implications.
K. M. TYE, L. D. TYE, J. J. CONE, E. F. HEKKELMAN, P. H. JANAK, A. BONCI; “Methylphenidate (Ritalin) enhances task performance and learning-induced amygdala plasticity via distinct D1 and D2 receptor mechanisms ”

A Balloon in your Stomach and your Brain

Sci is still tracking her caloric intake every day for the goddess (well, mostly for herself, but also for the goddess). It’s very long, slow haul. Sci still considers days when she eats no more than 2000 calories (preferably a little less) as good days. That may not seem like much of a diet, but compared to my previous intake, it’s quite a big cut. And many days I just don’t make it.
But obviously, this has stayed on my mind. I can’t help thinking about how we register food in the brain, how we tell when we are full, and if there’s a difference between when we know we are full vs when we KNOW we are full. Sci will admit there’s often a big difference between when I feel myself getting full and when I stop eating.
But then I found something that made the issue even more near and dear to my heart. It could have something to do with dopamine!
Tomasi et al. “Association of body mass and brain activation during gastric distention: implications for obesity” PLoS ONE, 2009

Things I like to Blog About: Ritalin

It seems, from the time I first heard about it, there’s been an eternal flare-up about Ritalin, and its similar counterparts, including things like Concerta and Tranquillyn. Issues with who should get it, who HAS attention-deficit/hyperactivity disorder (ADHD), whether or not ADHD is is even a real diagnosis. Issues about whether people who DON’T have ADHD should get Ritalin, and whether it’s ethical to use Ritalin (or other stimulant medications used for ADHD) for things like “cognitive enhancement”, whether it amounts to use of something that is no more harmful than using caffeine, or whether it’s something more sinister.
But that’s not what Sci is going to blog about today. Because I get a lot of people asking me whether Ritalin is bad, mentioning they’ve snorted it once or twice or took it once or twice and it did/didn’t work for them, etc, etc. But Sci’s a scientist. She hopes that people might be able to determine for themselves whether Ritalin is good or bad, once they know how it works.

This is Ritalin, aka Methylphenidate.

In which Sci gets Snarky: Lithium in the Water

This will otherwise be known as “WTF are you doing, Journal of Medical Hypotheses”.
Sci likes Lithium.

(Lithium burns red. Sci thinks this could have applications for lightsabers if applied correctly)
It’s a cool element, interesting in that we’ve used it over the ages for stuff like gout (which, I hear, is making a comeback), prevention of migraine, blocking the effects of excessive anti-diuretic hormone, and of course for bipolar disorder. But what’s really interesting? We don’t know how it works. Not a clue. It may raise serotonin levels over time, it may decrease or increase other monoamine neurotransmitter levels (such as dopamine and norepinephrine). But we have no idea HOW this occurs. In this, as with other psychiatric drugs (such as Ritalin, which increases dopamine and norepinephrine and improves attention, or with selective serotonin reuptake inhibitors, which increase extracellular serotonin and alleviate depression), we don’t know HOW they work. We just know they WORK (though we’re working on that).
And THAT they work is what matters. When you’re dealing with someone who is potentially suicidal, or unable to function successfully due to severe psychiatric disorders, you’ll take what works and isn’t otherwise “bad” for you (that you can tell), and figure out the mechanism later. And some of these drugs, like Lithium, are very old indeed. Lithium has been used to treat mania and depression since the 1870s, and is still used today as one of the most effective treatments for bipolar disorder (a topic which I SWEAR I will cover someday). It goes a long way toward reducing suicide in those with severe bipolar, and can help with mood stabilization as well.
So if it’s been used that long, it must be good right? This means it might do everyone some good, right? Like, you could put it in the water, and it’d be fine?
Terao, et al. “Even very low but sustained lithium intake can prevent suicide in the general population?” Medical Hypotheses, 2009.

Depression Post 4: The Serotonin Theory (and why it’s probably wrong)

Ok, the serotonin theory of depression may not be wrong. But it is definitely incomplete. One might ask why we use serotonergic drugs to treat depression if the theory behind it is wrong. A good question, but to this I say: because it worked.

(I love the Zoloft depressed marshmallow. He’s so cute!)
This is post four of my series on depression. For previous posts on the etiology of depression, the pharmacotherapies for depression, and how depression is evaulated in the lab, please play link hopscotch! I’ve also got a very recent post on the serotonin system which can give you some more background.
The original antidepressants, the monoamine oxidase inhibitors and tricyclic antidepressants, were originally used to treat other diseases, such as tuberculosis and psychosis, and found to be effective for depression as a sideline. Did people know how they worked? Nope, but they appeared to work (though only in a subset of the population), and so they came into use. Some people might get up in arms about this, and yell about how we shouldn’t use drugs unless we know how they work. But if we spent our lives doing that, no one would have ever made asprin. Or morphine. Heck, no one would have patented Ritalin. We know THAT Ritalin works, and we know what Ritalin does in the brain, but do we know why Ritalin calms down people with ADHD when it’s really a stimulant? Not really, no. But it’s still out there, because it works.
And the serotonin-based antidepressants do work in some people. Only in about 60% of patients at best, and at their best, they only perform 30% better than placebo. But the modern selective serotonin reuptake inhibitors (SSRIs) still work in a set of depressed patients, and they do so with far fewer side effects than pre-existing drugs. And what can I say, we haven’t really got anything better yet. Except cocaine. That’s a GREAT antidepressant, but it obviously has some issues.
So where did this serotonin theory of depression come from? And why is it flawed?

Got PMS? Take Two Antidepressants, and Call Me in the Morning

Sci’s going to go ahead and admit, the last few weeks have been a little…brutal. Ok, maybe a LOT brutal. Grad school can be tough at times, and involve days that leave Scicurious wiped. But the posts must go on! And so, today your tough little grad student (YTLGS) is fortifying herself with the best cures imaginable, moose munch and liquor, to bring you today’s post.
(By the way, being poor, Sci accepts gifts to her blogging muse in the form of Moose Munch, dark chocolate of any kind, and liquor of all varieties except NightTrain. Contact her for details).
Todays post brought to you by sugar and…fermented sugars. Also the letter S. And the Journal Club that Sci has to give…soon. Very, very soon.
Landen, et al. “Short onset of action of a serotonin reuptake inhbitior when used to reduce premenstrual irritability.” Neuropsychopharmacology, 2009.