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 ”
Sci likes to blog about stimulants like methylphenidate a lot. For those not in the know, methylphenidate is a psychostimulant, marketed as Ritalin or Concerta (and a few other names), and used for treatment of attention-deficit/hyperactivity disorder. It is prescribed to up to 25{9f43b4361d9a125bc126dd2a2d1949be02545ec69880430bc4fed2272fd72da3} of school children in some areas. And we know a lot about it. We know that it increases levels of the neurotransmitters norepinephrine and dopamine, and we know that increases in these neurotransmitters in the brain can increase focus and attention.
But we don’t know HOW. Many people have hypothesized that increases in norepinephrine in the prefrontal cortex are to blame. Some have thought that it might be dopamine in attention and motivation-related brain areas. But we still don’t really KNOW. And knowing how Ritalin works seems pretty important, given that we give it to a very large number of children.
So here, the authors of this study took rats, and injected small amounts of Ritalin into an area of the brain called the lateral amygdala, an area of the brain known for things like learning, particularly fear-learning, but regular learning as well. They they looked at how the rats performed a task, and how the neurons in the amygdala reacted to the presence of the Ritalin.
They found that two distinct mechanisms are responsible for the way the brain responds to Ritalin. And they involve two types of dopamine receptors. The dopamine system has five types of receptors, but they are divided into two main types, the D1 type, and the D2 type. The receptors are part of the neurotransmission process. When dopamine is present, it binds to the receptors, which are in the membranes of neurons. These receptors cause things to happen in a cell when they are stimulated. But in the lateral amygdala, the D1 type and D2 type receptors are doing very different things.
When they tested the rats in response to Ritalin, they saw that the animals performed a difficult task much better than they did previously. They also showed stronger synapses in the lateral amygdala, indicating that Ritalin and the task performance was increasing those synapses. Then they manipulated the D1 and D2 types of receptor to determine which of the receptors was responsible for the learning and the stronger synapses.
And they got something interesting. When they knocked out the D1 receptors, certain synapses were no longer strengthened, and they were the ones that processed the reward learning part of the task, indicating that the D1 receptors were responsible for the reward-related processes that made the rats motivated to perform the task for a reward. Not only that, they found that D2 receptors were responsible for something entirely different, strengthening synapses that allowed the rat to ignore stimuli that were irrelevant to the task.
This is a pretty important finding for HOW Ritalin actually works in the brain, on what neurons it’s acting, and for what purpose. Helping to understand how Ritalin works in the brain and WHERE is important not just for the therapies that are used now, but to come up with other therapies that might be safer or better.
And thus concludes the official SFN neuroblogging. See you next year in San Diego!
