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Over a month ago I was building a website to video-podcast the recorded lectures from the Research Society on Alcoholism's annual conference. While I was making the RSA Lecture Series website, my mentor/P.I. had me purchase the copyright permissions for the figures and graphs the presenters used on their Powerpoint slides so we could post them online. They weren't cheap; anywhere from $30 – $200 bucks a figure,graph, or table. I thought it was somewhat ridiculous that we were buying back “our” own research. I didn’t realize that publishing companies appropriate the rights to everything. My question is, why do we let them get away with this? Twenty years ago they provided a necessary service – the printing and distribution of research. The difference is, now we have the internet, and they don’t have us in a strangle-hold anymore. Yet we keep signing away the rights to our own research. To fully grasp how senseless the current M.O. for publishing research, I offer this useful analogy: We don’t mind paying taxes to build roads, because we need roads. The Tollway builds roads with their own money, and usually there is an incentive to use them instead of the ones that we’ve already purchased with our tax dollars. So we don’t mind paying the toll. It would be pretty crazy if we spent all this tax money building roads, have our state engineers inspect them for quality, and then just hand them over to the Tollway so they can collect a profit every time someone uses them. This is what we do with our research though. It’s because we use grant money to pay for the subscriptions we need, for journals that our university doesn’t subscribe. Essentially, we do the research, write the article, do the peer-review, and hand it over to them; and then buy it back. It’s important to consider - under this system, all the research and all the funding eventually ends up in the hands of the publishing companies. Oh, and the 400 dollar a year price tag on some of these journals? It’s not the ink! TIME magazine costs around 15 dollars for 36 issues, and they actually pay their writers (unlike the Axon).
“In this section, we discuss existing research into red-black trees, vacuum tubes, and courseware [10]. On a similar note, recent work by Takahashi suggests a methodology for providing robust modalities, but does not offer an implementation [9].” - David Phillips and Andrew Kent, Center for Research in Applied Phrenology, Ithaca, New York.
Our peer-reviewed publishing system is built on trust. Trust that authors faithfully carry out their stated experiments, trust that reviewers objectively evaluate said experiments, and trust that publishing companies oversee such processes with an eye toward disseminating legitimate scientific findings. What happens when all three break down?
The excerpt at the top of this article comes from a paper submitted by Philip Davis and Kent Anderson to The Open Information Science Journal. If you find the prose confusing, then you probably went one step further than the publishing company/reviewers – you actually read it. The entire paper, in fact, was constructed using software that creates grammatically correct but nonsensical text. Thus, the complete paper was utter nonsense; a hoax to test the oversight and integrity of an established publishing company. Utter nonsense that Bentham Science Publishing saw fit to publish under the banner of peer-reviewed science. (You can read more about Davis and Kent’s hoax on sspnet).
This clever little stunt exemplifies one of our chief concerns here at OneSci: the business of science publication.
Imagine this scenario: the Internet has fundamentally changed the practical and economic realities of distributing scientific information. For the first time ever, we have the ability to institute a global and interactive representation of human knowledge - collected, cataloged, written, and reviewed by scientists - with the guarantee of worldwide access. Yet, we have a science based on tradition which, as non-idealistic as it sounds, has a fairly good track record of eliminating submissions of random computer generated text. This system, however: 1) costs researchers upwards of 30 billion dollars per year; 2) confiscates the copyright permissions to all scientific research; 3) is accessible almost exclusively to university-affiliated faculty and staff (not the public); and 4) puts all this money into the hands of large multinational publishing corporations (instead of recycling the money back into the scientific process). In turn, these publishing companies essentially provide two things: 1) they organize the peer review process (with no monetary compensation for reviewers, mind you); and 2) they have printing presses. The solution might seem too obvious, but here it is anyway: stop publishing for companies that take copyright permissions from you and your colleagues; start publishing and reviewing for journals that protect the authors' research under a GNU open access license.
We, the undersigned, feel obliged to address the challenges of the Internet as an emerging functional medium for distributing knowledge. Obviously, these developments will be able to significantly modify the nature of scientific publishing as well as the existing system of quality assurance. We know this is a task that will take inside of a decade to accomplish fully. We don't expect established principle investigators to jump right into publishing to online journals.
However, if you too agree that publishing companies are taking too much control and money from the scientific process, and there exists a better solution to the publishing process, here are ways you can help:
Science performed in isolation is useless. Only through rich scientific discourse can we reach our maximum potential for efficiency and progress. Onesci.com was founded on this simple principle and is committed to facilitating communication between scientists of every discipline. We welcome you to join the conversation.
Bradley Monakhos and Jeremy Biane
Consult any introductory neuroscience text on the topic of dopamine, and you’re likely to be regaled with how dopaminergic neurons of the midbrain code for the rewarding value of a stimulus. According to this generally accepted theory, midbrain dopamine neurons increase their firing rate in response to a) an unexpected reward; or b) a stimulus that predicts delivery of reward. Conversely, firing rate decreases if reward is withheld following presentation of a reward-predicting stimulus. However, results regarding the response of dopamine neurons in response to adverse stimuli have been conflicting, with some experiments showing increased firing, and others depressed firing. In this week’s edition of Nature, Matsumoto and Hikosaka recorded from distinct classes of dopaminergic neurons that differ based on their response to adverse stimuli – in essence showing that both response patterns exist in the same animal. Interestingly, these separate populations were largely confined to distinct regions of the midbrain, with neurons excited by adverse stimuli found mostly in the dorsolateral midbrain, while those inhibited by adverse stimuli located in ventromedial regions.
While all recorded neurons showed the well-established excitatory response to rewarding stimuli, this study is the first concrete evidence that dopaminergic neurons of the midbrain may not be as homogenous as previously thought, with one population encoding the rewarding value of a stimulus (neurons excited by reward and inhibited by “punishment”), and the other seemingly encoding motivational salience (neurons excited by both rewarding and adverse stimuli).
The authors point out that, based on their location in the midbrain, these distinct populations of neurons can also be differentiated based on their primary target of axonal projection, which may account for the unique information carried by these different classes of neuron. It will also be interesting to see whether the type of dopamine receptors contacted differs by class.
Matsumoto and Hikosaka are quick to point out that their boundaries for classification are rather arbitrary, and in reality there probably exist many distinct categories based on more subtle criteria. Still, the study is a landmark in the reward signaling field, and provides fertile ground for reexamining our rather simple view of dopaminergic signaling.
Jeremy Biane 04:11, 11 June 2009 (UTC)
If you're in the field of neuroscience and for some crazy reason haven't heard of channel rhodopsin-2 (ChR2) yet, you will. It has got to be the sexiest contemporary technique available for the neuroscientist, and one that will probably earn Karl Deisseroth a trip to Stockholm in the future.
A relatively new technique, ChR2 allows for tight temporal control of neuronal activation via photostimulation (optically mediated inhibition can be induced via the halorhodopsin channel). The ability to express ChR2 in specific cell populations via genetic targeting make it far superior to previous methods of neuronal activation. Thus far, ChR2 has mainly been used to study synaptic plasticity and to map functional connections between neurons. However, a new paper in Science is the first to show that ChR2 activation can actually drive behavioral changes in adult mammals. While this result is not all that surprising, it's surely a milestone in the field and a harbinger for many, many studies to come. comments
Jeremy Biane 00:32, 1 June 2009 (UTC)
For many years, selective serotonin reuptake inhibitors (SSRIs) such as prozac have been a favorite pharmalogical treatment for depression. Interestingly, it is often weeks before the psychological effects of these drugs kick in, the cause of this lag period being largely unknown. As the drug is known to increase neurogenesis, some believe this upregulation of newborn cells - and the gradual time it takes for this process to occur - underlies the delayed impact of SSRIs.
In a "recent" study published in Science magazine, Vetencourt et al throw another interpretation into the hat. Their study indicates that under the influence of fluoxetine (aka prozac), the adult rat visual cortex can undergo levels of reorganization typically restricted to developmental periods of life. This enhanced plasticity appears to be mediated by a decrease in inhibitory GABAergic signaling (an increase in which is known to coincide with the end of the critical period during development).
The authors ostensibly focus on how fluoxetine can be used as a treatment for amblyopia, a condition where signaling from one eye is impaired due to input deprivation during development. However, considering many systems-level plastic changes often take weeks to emerge in adult animals, one immediately wonders if reorganization of particular emotional areas of the brain might underlie the mood-enhancing effects of SSRIs (and, if so, why are such effects unipolar in their psychological consequence?). Or perhaps it is an overabundance of inhibitory signaling that SSRIs rectify?
Whatever the case, given what we already know about plasticity and sensory processing, you might consider increasing your vitamin p intake next time you take on a new language (I hear the side effects are pretty tolerable). comments
Jeremy Biane 03:04, 19 May 2009 (UTC)