Prozac, Ritalin, Cognitive Enhancement, and the power of a snappy title

Let it be known that Sci, like many a young, bright-eyed little scientist, tries to keep up on her reading. TRIES is the operative word, but every week Sci gets the Tables of Contents for all the major journals in her field (and all the major ones in her subdisciple) emailed straight to her for her perusal. She scans the title lists, searching for things that are cool in her field, cool to blog, or that might indicate a scoopage of her work (hey, it happens).
And it was in one of these perusals that I came across this article. And this article is on a subject that needs to be blogged. But this article also says a lot about the “selling” of a scientific paper to a high-ranking journal. Biological Psychiatry, the journal in which this paper was published, has a pretty decent impact factor (8.67), and in Sci’s field, is considered to be a pretty hot publication venue.
But before I go into that, let’s take a look at this paper: Steiner et al. “Fluoxetine potentiates methylphenidate-induced gene regulation in addiction-related brain regions: Concerns for use of cognitive enhancers?” Biological Psychiatry, 2010.
cognitive enhancer1.jpg
Sci would like to start by noting that doing an image search for “cognitive enhancer” yields some surprisingly boring results. I was really hoping for something like this:
cognitive enhance2.jpg
Oh well.

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Stress and Anxiety, aka CRF and 5-HT2

Today’s post comes to you from several tweets that Sci received way back in the mists of time (that is…two weeks ago. Three? Something like that). Sci got wind of this paper and has been meaning to blog it for a while, but other things get in the way, like other things will. And when those other things finally get out of the way, Sci sometimes finds that she’s so SLEEPY she doesn’t know if she can make it through any more dry, sciency prose (sciency prose, even at the best of times, is pathetically dry. It’s why Sci blogs for you. See how she cares).
Like right now, when Sci is SO SLEEPY she just wants to lie down next to the cat and sack out. Scicat is currently reclining in a truly relaxed manner on the floor and isn’t making this any easier. But for the sake of stress, anxiety, depression, and a large glad of iced Moroccan mint green tea, SCI BLOGS ON.
bottom biting bug.png
(Sci’s determination very much resembles that of the bottom biting bug pictured here. A friend of mine showed this to me about a year ago, and it may still remain the oddest thing I have ever seen on the internet. Sci also finds it hilarious that every time anyone in Japan apparently trains for ANYTHING, they must at some point sit under a waterfall, and always end by looking determined on the top of Mt. Fuji. It’s like the Rocky Steps of Japan.) Magalhaes, et al. “CRF receptor 1 regulates anxiety behavior via sensitization of 5-HT2 receptor signaling” Nature Neuroscience, 2010.

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Bulimia and the Vaso-Vagal Reflex

This post was chosen as an Editor's Selection for
This is another post in Sci’s investigation into the current studies being performed on eating disorders, particularly binge eating and bulimia. Usually I try to focus on the dysregulation of reward-related systems in these disorders, but this paper will be a little different. Faris et al. “De-Stabilization of the Positive Vago-Vagal Reflex in Bulimia Nervosa” Physiology and Behavior, 2008.
It’s kind of in the nature of an eating disorder that there aren’t any really funny pictures or something that Sci can put in here.
So before we go forward, here’s a kitten.

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A Follow up: Depression, p21, CREB, and more

Everyone once in a while, someone sends Sci email. Often it’s silly. This one, however, was very good in that it asked for some clarification on a series of posts that I’ve been working on looking at clinical depression and possible causes and treatments, including neurogenesis in the hippocampus, cell cycle controls, and CREB.
And luckily, the guy who sent it gave Sci permission to repost, which is good, because it allows me to clarify some stuff. Here goes:

Hi Sci: I read your blog about how antidepressants stimulate neurogenesis in the hippocampus. Since the CREB deficient mice had robust neurogenesis and normal serotonin I wasn’t sure why they were anxious. Apparently they did benefit from antidepressants right away on the tail suspension and forced swim tests so the neurogenesis hypothesis took a bit of a whack. To add to the complexities I just read about MIF (macrophage migration inhibitory factor). Apparently reducing the amount of MIF in the rat hippocampus dramatically reduces neurogenesis and increases anxiety. Do you understand how CREB and MIF are related? I’m trying to get a handle on this whole complex area. Thanks.

All right, I’m going to try this before my first cup of coffee and we’ll see how it goes:

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The Neurogenesis theory of depression and a little guy called CREB

Sci wishes she could begin this post with something clever. But she has a cold. Suffice it to say that this paper is cool and interesting. And also, as Sci has a cold, I expect all of you to read this post out loud to yourselves in suitably stuffy, gluey Sci-voices.
(*sniff*) Gur et al. “cAMP Response Element-Binding Protein Deficiency Allows for Increased Neurogenesis and a Rapid Onset of Antidepressant Response” The Journal of Neuroscience, 2007.
(Yeah, yeah, the title is long and scary. Worry not, Sci will ‘splain.)
And this paper is especially good because it allows Sci to write a post on a topic she’s been meaning to get to even since she did a depression series way back when: the neurogenesis theory of antidepressant responses.
So here we go. And a new neuron is born.
(From Bumpy Brains. Sci thinks the rendition of diapers as glia is hilarious.)

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SFN Neuroblogging: Got Type 2 Diabetes on the Brain

As some of my readers from WAY back (all two of you, hi guys!) may know, diabetes is one of Sci’s favorite things. It’s one of those things that, if she could start her entire little sciency life over, would be something she would heavily consider as a focus. Heck, there’s always another post-doc, right?
Anyway, you might think that diabetes would not be one of the things generally discussed at Society for Neuroscience meetings. But you would be wrong. The symptoms of diabetes, type I or II, stem from not enough insulin, whether that is because you don’t produce any (type I) or you don’t have enough and aren’t sensitive enough to what you have (type II). Insulin isn’t just limited to the gut, pancreas, and muscles, however. It’s also important in the brain. Normally, your brain is pretty responsive to blood levels of glucose, no matter what, because you want your brain to be the last thing to go when your blood sugar levels drop. But insulin still plays an important role, and insensitivity to insulin, like that seen with type II diabetes extends to the brain as well.
This study taught Sci a lot of things that she didn’t necessarily know. First, it taught her that insulin sensitivity is affected by free fatty acid levels. And it taught her that both of these together could have major effects on cognitive impairment. Suddenly the major increases in type II diabetes are looking a little more scary.
V. E. COTERO, E. C. MCNAY “Effect of intrahippocampal FAs with varied saturations on spatial memory in adult Sprague-Dawley rats”
Doesn’t sound like anything to do with type II diabetes, does it? You would be surprised. 🙂

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Best. Modelling Paper. Ever.

The abstract says it all:

Zombies are a popular figure in pop culture/entertainment and they are usually portrayed as being brought about through an outbreak or epidemic. Consequently, we model a zombie attack, using biological assumptions based on popular zombie movies. We introduce a basic model for zombie infection, determine equilibria and their stability, and illustrate the outcome with numerical solutions. We then refine the model to introduce a latent period of zombification, whereby humans are infected, but not infectious, before becoming undead. We then modify the model to include the effects of possible quarantine or a cure. Finally, we examine the impact of regular, impulsive reductions in the number of zombies and derive conditions under which eradication can occur. We show that only quick, aggressive attacks can stave off the doomsday scenario: the collapse of society as zombies overtake us all.

They use the mathematical models applied to outbreaks of infectious diseases to show that — absent a cure or concerted eradication of large proportions of zombies simultaneously — we are well and truly screwed. This realization should in no way detract from the observation that MATH IS COOL. It will be a damn shame when the zombies eat it out of our brains.
Hat-tip: Marginal Revolution